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Cardiac Arrhythmias:
Interpretation, Diagnosis,
and Treatment
Second Edition
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Cardiac Arrhythmias:
Interpretation, Diagnosis,
and Treatment
Second Edition
Eric N. Prystowsky, MD
Director, Cardiac Arrhythmia Service
St. Vincent Hospital
Indianapolis, Indiana
Consulting Professor of Medicine
Duke University Medical Center
Durham, North Carolina
George J. Klein, MD
Professor of Medicine
Western University
London, Ontario, Canada
James P. Daubert, MD
Professor of Medicine
Director, Cardiac Electrophysiology
Duke University Medical Center
Durham, North Carolina
New York Chicago San Francisco Athens London Madrid Mexkx> Oty
Mlan New Detil Singapore Sydney Toronto
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claim or cause arises in contract, tort or otherwise.
To my wife Bonnie, my constant source oflove and support for over 50 years.
To my sons David and Daniel, whose lives have filled me with pride and joy, and their wives,
Malia and Beth, who are the daughters we never had.
And for my grandchildren, Dylan, Laila, Amber, and Noah, who always bring
boundless joy and sunshine into our lives.
And in loving memory of my parents, Drs. Rose and Milton Prystowsky, compassionate
physicians who taught me that being a physician is not a gift to be wasted.
-Eric N. Prystowsky, MD
To my wife and best friend, Klara.

To my son Ben and daughter-in-law Elissa and their children Adam, Leah, Beth, and Talya,
and to my daughter Anna and son-in-law Mark and their children Lucy, Nate, and Sari,
who are all my real source of pride and joy.
To the memory of my unselfish and giving parents, Paul and Clara.
-George/. Klein, MD
To the memory of my late parents, Dr. James J. Daubert and Irene M. Daubert,
recognizing their inspiration for and support of my education.
To my wife Amy for her tremendous support and wise counsel throughout my medical career.
And to our children, Patrick, Thomas (MD), Mairin, and James.
-James P. Daubert, MD
Contents
PARTI
Basic Electrocardlographlc Observations and Clinical Electrophysiologic Correlates-........- ....•..- · 1
1 Cardiac Conduction ..........-................._,_...........-.......- ...........- .......................- ...........- ..............-·-···......................... 3
2 Electrocardiographic Consequences of Atrial and Ventricular Ectopy..........-..........._,_....................-....... 35
3 Bundle Branch Block......... _................. _,_ ..,...,.... _...,..._........... _....................... _........... _..,........... _,_,,, ....................... 57
4 Apparent Parado.xical Conduction ............................................................................................................................83
5 Mechanisms of Tachycardia .............._,_...........-.......-...........-.......................-...........-.............._,_.......................... 95
George J. Klein, MD
PARTll
A1Th-ythmfas ..............~··········.....••••••••.....••••••......••••••••.....••••••......·······~··········.....••••••••.....••••••......••••••••.....······" 111
6 Supraventricular Tachycardia ..........._,_...........-.......-...........-.......................-...........-.............._,_....................... 113
George J. Klein, MD
7 Preexcitation Syndromes-................. _,_ ...........-.......-...........-.......................-...........-.............. _,_....................... 139
8 Ventrlcular Tachycardia....................................................................................................................................................... 171
9 Atrial Fibrillation ................................................................................................................................................................................. 213
10 Bradycardia: Causes of Pauses ........._,_...........-.......-...........-.......................-...........-.............._,_....................... 235
George J. Klein, MD
PARTlll
Clinical Presentations ......................................................................................................................................... 253
11 Electrocardiographic Abnormalities in Asymptomatic Individuals...-...........-..........._,_....................-.... 255
George J. Klein, MD
12 Narrow QRS Tachycardia._................._,_..,........-......._..........._......................._..........._..,..........._,_,,..................... 287
George J. Klein, MD
13 Wide QRS Tachycardia ................................................................................................................................................. 301
George J. Klein, MD
vii
viii CONTENTS
14 Undiagnosed Syncope, Dizzy Spells, Palpitations ............................................................................................ 323

George J. Klein, MD
15 Sudden Cardiac Arrest/Sudden Cardiac Death .................................................................................................. 341
PART IV
Methods and Therapy........................................................................................................................................ 371
16 Electrophysiologic Testing and Diagnostic Maneuvers .................................................................................. 373
17 Catheter Ablation ofSupraventricularTachycardias ........................................................................................ 401
18 Catheter Ablation ofVentricularTachyarrhythmias ......................................................................................... 447
19 Cardiac Implantable Electronic Devices ............................................................................................................... 479
lndex ........................................................................................................................................................................................... 501
Preface
Twenty-five years ago, Drs. Pryst.owsky and Klein authored the first edition ofthis textbook. Our
purpose was to "write a comprehensive textbook on an integrated approach to cardiac arrhyth-
mias for individuals without a background in clinical electrophysiology.' While we hoped clini-
cal electrophysiologist.s would find our book useful, our intent was to educate the broader field
of clinicians, for example, medical students, house staff, primary care physicians, cardiologists,
and nurses, on the diagnosis and treatment of patients with cardiac arrhythmias. Thousands of
copies of the book were sold, and we hope those readers found it useful. We received much feed-
back from our colleagues and trainees over the years and discussed with each other some altera-
tions to consider when we wrote a second edition. While othe.r textbooks on cardiac arrhythmias
are available, we felt there remained a void in providing our practical application ofelectrophys-
iological principles and electrocardiographic correlations to the broader community involved
in caring for patients as well as the clinical electropbysiologist. This motivated us to pursue a
second edition of our book. We welcome our new co-author, Dr. James Daubert, also a Duh-
trained electrophysiology fellow. and long-standing friend and colleague.
There has been a sea change in the last 25 years to our therapy of cardiac arrhythmias. Surgery
to cure arrhythmias is nearly extinct, and new antiarrhythmic drug development has been stag-
nant At the same time, the.re have been remarkable advances in catheter ablation technology and
its application to treat a wide variety of cardiac: arrhythmias, as well as development of newer
implantable cardiac electrical devices and indications for their use. The content of our second
edition reflects these changes in our field, and we have deleted specific chapters on arrhyth-
mias in acute myocardial infarction, pharmacologic therapy, operative therapy of arrhythmias,
and noninvasive methods. Important information on drug therapy and noninvasive methods
is covered in other chapters. Further, we have added new chapters on atrial fibrillation, cath-
eter ablation of supraventricular tachycardia, catheter ablation of ventricular tachycardia, and
provide a major update in the chapters on sudden cardiac death and device therapy. Many new
figures and information have been added to the existing chapters. To allow for easier reading,
there is some deliberate overlap of information between various chapters. Key references of
c:lassic and up-to-date articles are provided for each chapter.
Like the first edition, this book represents our personal approach to patients with cardiac
arrhythmias. Nonetheless, it would be unrealistic to expect 3 electrophysiologists to have
entirely uniform approaches to diagnosis and therapy. Hence, the primary author's views
in individual chapters prevailed when there were minor differences in approach. Each of us
reviewed all the chapters and made recommendations for change. In the end, we did not feel
there were any substantial differences in our approach to patient care and were comfortable in
signing off on the total content
ix
x PREFACE
The book is divided into 4 parts. Part I is Basic Electrocardiographic Observations and Clinical
Electrophysiologic Correlates. There are in-depth discussions of cardiac conduction with major
additions on the effects of alterations in autonomic tone, effects of premature atrial and ventric-
ular ectopy on conduction and automaticity, concealed conduction and apparent paradoxical
conduction, bundle branch block, and mechanisms of tachycardia Part II focuses on specific
arrhythmias. It begins with an in-depth chapter on a clinical classification of supraventricular
tachycardia and includes chapters on the preexcitation syndrome (Wolff-Parkinson-White),
ventricular tachycardia, atrial fibrillation, and bradycardia. Diagnostic information from
patient history, physical examination, and laboratory tests is given, as well as an approach to
therapy for each arrhythmia. Part III includes chapters on common clinical presentations of
arrhythmias. An approach is given for patients who are asymptomatic but have electrocardio-
graphic abnormalities, and for those who present with a narrow QRS tachycardia, wide QRS
tachycardia, syncope, dizziness, palpitations, or who have survived a cardiac arrest. Part IV
consists of chapters on diagnostic techniques and therapeutic modalities. Included are methods
of electrophysiologic testing and diagnostic pacing maneuvers, catheter ablation of supraven-
tricular tachycardia, catheter ablation of ventricular tachycardia, and device therapy.
Acknowledgements: Dr. Prystowsky thanks Mrs. Jane Gilmore, CMI, for her outstanding
artwork.
George J. Klein, MD
PART
Basic Electrocardiographic
Observations and Clinical
Electrophysiologic Correlates
Chapter 1 Cardiac Conduction
Chapter 2 Electrocardiographic Consequences of Atrial and Ventricular Ectopy
Chapter 3 Bundle Branch Block
Chapter 4 Apparent Paradoxical Conduction
Chapter 5 Mechanisms of Tachycardia
Cardiac Conduction
GENERAL CONCEPTS
The normal cardiac: impulse originates in the sinus node, a crescent-shaped structure
approximately 9 to 15 mm long that is located at the juncture of the superior vena cava
and right atrium (Figure 1-1).1 After the electrical impulse exits the sinus node, it pro-
ceeds to activate the right and left atria. Activation of the atria is responsible for the P wave
recorded on the electrocardiogram (ECG) (Figure 1-1, orange color). Activation of the nor-
mal human atria takes approximately 90 to 100 ms, the right atrium being activated within
approximately 65 ms.2 The last area to be activated is the left atrial appendage, although
atrial tissue near the left inferior pulmonary vein can also be activated very late. It should be
noted that as the spread of atrial activation occurs, some sections of the right and left atria
are activated at the same time.2
A controversy has existed for decades concerning the existence of specialized internodal path-
ways for conduction between the sinoatrial (SA) node and the atrioventricular (AV) node. The
essence of this controversy is whether preferential atrial conduction between the SA and AV
nodes occurs over specialized pathways or whether the activation wavefront proceeds through
nonspecialized or ordinary atrial myocardium.1" Most data strongly suggest that no specialized
pathways of conduction exist. The observed preferential conduction of atrial impulses along
various anatomical routes can be explained adequately by various factors, such as the complex
anatomy of the right atrium, which includes multiple "holes" such as the orifices of the inferior
and superior venae cavae and coronary sinus ostium, as well as the orientation of atrial fibers
in longitudinal and perpendicular directions, with conduction being faster in the longitudinal
direction.'
The PR interval in the ECG encompasses activation in the atria, AV node, His-Purldnje system,
and ventricles (Figure 1-1). The AV node is a complex structure that includes the compact
node and its posterior extensions.5 The AV node was initially considered to be subdivided into
3 functional zones: the AN, N, and NH zones.0 The N zone appears to be the most common
area where block occurs in the AV node. However, a more recent microelectrode mapping of
the AV node suggests that it includes 6 different cell types.9 Slow conduction through the AV
node is multifactorial, in part related to the complex arrangement of nodal cells and connective
tissue, reduced electrical cellular coupling, and action potentials that are dependent on the
4 CARDIAC ARRHYTHMIAS: INTERPRETATION, DIAGNOSIS, AND TREATMENT
Sinus node
(pacemaker)
I
(
Atrioventricular node
(delay)
Purkinje fibers
(activation)
FIGURE 1·1 • Schematic of the electrocardiogram and cardiac conduction 5Y$tem. The pink color represents the electrical sy:stem,
orange activation of the atria, and green activation of the ventticles. (See text for details.)
slow inward calcium current.10 The impulses exit from the AV node into the ventricular spe-
cialized conduction system that has more rapid conduction properties, which consists of the
His bundle, the left and right bundle branches with their subdivisions, and the peripheral
network of Purkinje fibers, which terminate into ventricular myocardium. The left bun-
dle branch is often described as having two primary f u.nctional divisions, the anterior and
posterior fascicles. However, as early as 1906, Tawara11 identified a third fascicle of the left
bundle branch that enters into the left interventricular septum, an observation confirmed
by others (Figure 1-2).' In a classic study by Durrer et al.2 on excitation of the human heart,
3 endocardial areas were consistently shown to be excited synchronously 0 to S ms after the
CHAPTER 1 • Cardiac Conduction S
acd-------
mpa--·
FIGURE 1-2 • Photomiaogr.iph demonstrating the distribution of the left bundle branch in the human heart taken from the
original publication ofTawara. (Reproduced wtth permission from Tawara S. Dos Relzteltungssymm des Sougetlerherzens. Jena,
Germany: Fischer; 1906J
beginning of the left ventricular cavity potential. giving credence to the concept of a functional
trifascicular left bundle branch system.
In the absence of bundle branch block. ventricular activation is quire rapid. usually less than 100 ms,
and is represented on the electrocardiogram. by the QRS complex (Figure 1-1, green color).
Examples of ventricular epicardial activation in normal hearts of patients undergoing swge.ry
for ablation ofthe accessorypathwa:yin the Wolff-Parkinson-White syndrome are demonstrated
in Figures 1-3 through 1-5. These maps were computer generated during activation of 1 QRS
complex. using a 56-electrode array sock. Figure 1-3 shows normal ventricular activation; right
bundle branch block and left bundle branch block are noted in Figures 1-4 and 1-5, respectively.
ELECTROPHYSIOLOGIC-ELECTROCARDIOGRAPHIC CORRELATIONS
Electrophysiologic studies utilize several multipolar electrode catheters positioned at various
locations in the heart (Figure 1-6). These catheters make it possible to record electrical poten-
tials from within the heart and to stimulate various cardiac chambers in the diagnosis and
management of cardiac arrhythmias. Whereas the electrocardiographer analyzes the surface
electrocardiogram, the clinical electrophysiologist peers through this tracing to analyze its
component parts (Figure 1-7). In essence, the more one knows about intracardiac events, the
easier it is to analyze the surface electrocardiogram.
ANTERIOR
FIGURE 1·3 • Normal eplcardlal ventTlcular activation. The format for Rgures 1·3, 1-4, and 1·S Is the same. At the time of surgery,
a 56-electrode array sock was positioned on the epicardlal surface of the heart; during 1 QRS compleX', ventrlcular activation was
obtained at all sites. Each site Is noted by a letter and number that designate the electrode position and, undemeath, the local
activation time. using the initiation of the surface QRS complex as time 0. The left anterior descending (LAO) coronary artery is
schematically represented in the anterior view and the posterior descending {PDA) coronary artery is represented similarly in the
posterior view. These are approximate posltlOI\$ as noted during surgery. In thb figure, note the rapid ac:ttvatlon of the entire right
and left venuldes. The last area activated Is the base of the right ventrlc!e, and activation time Is complete within 78 ms. The right
ventricle In the anterior view Is to the left of the LAO and In the posterior view to the right of the PDA. This method of dlsplayf ng
the heart assumes that the posterior aux of the heart Is dMded and the ventricles are then laid out flat The base of the heart with
the atria removed is at the top of the figure and the apex (electrodes A1 through AS) is at the bottom. It is not that critical to ana-
lyze each point but rather to realize that the entire epicardial surface of the ventricle is activated relatively quickly.
PR Interval
Figure 1-8 demonstrates int.racardiac electrophysiologic events.1'·u The top tracing is surface
ECG lead V1; simultaneous intra.cardiac recordings are from 1 catheter in the high right atrium
(HRA) and from another positioned across the tricuspid valve to record electrical signals com-
ing from the AV junction near the His bundle electrogram (HBE). This was a quadripolar
catheter, and the proximal 2 electrodes (HBE PROX) are closer to the atrial side ofthis juncture,
recording a large atrial (A) depolarization along with a His bundle deflection (H) and a ven-
tricular (V) electrogram that represents activation of the high ventricular septum. The distal
bipolar electrode pair (HBE DIST) is situated more into the ventricle, and this enabled the
recording of a right bundle branch (RB) potential.
The PA interval, a measure of atrial conduction, is taken from the onset of the surface P wave to
local atrial activation in the His bundle electrogram. In our opinion, this interval is of minimal
value, since it only records atrial activation through a part of the right atriwn. More important
measurements are the atrio-His (AH) .interval, which is an approximation of AV nodal con-
duction time, and the His-ventricle (HV) interval, which reflects conduction through the His-
Purkinje system. Measurement of the AH interval is taken from the first rapid deflection in the
CHAPTER 1 • Cardiac Conduction 7
ANTERIOR
FIGURE 1·4 • Eplcardlal ventricular activation during right bundle branch block. (See Figure 1-3 f'or details of mapping methods.)
Note that the left ventricle, represented by electrodes 8 through D, is activated in a nonnal fashion and relatively quickly. However,
ttie right ventrfde, represented by electrodes Ettirough G, Is ac:ttva'ted late, as would be expected In right bundle branch block.
Point F, Is activated 115 ms after the Initiation of the surface QRS complex. Compare this acttvatlon with that noted In Figure 1-3.
ANTERIOR
FIGURE 1·5 • Eplcardlal ventrlcular activation In left bundle branch block. (See Figure 1-3 for dmlls of mapping.) In contrast to
Agure 1-4, the earilest activated sites In this patient are on the right ventricle and the latter activated points on the left ventricle,
as expected with left bundle branch block. Right ventricular points are prlmarily noted by G and E, which are left of the LAD In the
antEt'lor view and right of ttie PDA In the posterior view. Note that the last area to be activated Is on the left ventricle at 02 (117 ms}, In
contrast to the last area activated during right bundle branch block. which is on the right ventricular epicaRlial surface {see Figure 1-4).
FIGURE 1-t • Radlograph of endocardlal atheter placement. (Key: RA= rtght atrium; CS= coronary sinus; RV= rlghtventrlde;
H =His bundle area.)
~~
d
~
AH V
=== i:::_ -_~ p R
FIGURE 1·7 • A cllnlal electrophyslologlst's view of the electroCllrdlogram.

FIGURE 1-8 • lntracardlac electrophyslologlc conduction Intervals during the PR Interval. {See text for detalls.) {Key: HRA =high
right atrium; HBE {Prox) =proximal His bundle electrode pair; HBE (Dlst) = dlstal His bundle electrode pair; A= atria~ H =His;
V =ventricle; RB= right bundle.)
atrial electrogram on the His bwidle 1racing to the onset of the His bundle defledion.14 The first
rapid deflection represents local atrial activation in the vicinity of the AV node, but the earliest
ident:illable His bundle activity is chosen because the measurement ofinterest is conduction time
through the AV node-not conduction time to a speciflc local area in the His bundle. In other
words, when the His bundle act:iv:ity is seen. conduction through the AV node is confirmed. In
contrast. the HV interval is measured from the earliest identifiable His deflection to the earli-
est onset of ventricular acti:v.ity recorded from either an .intra.cardiac electrogram or any surface
QRS complex. For this measurement the desired conduction time is from the earliest evidence of
acti:v.ity in the His bwidle to any point conmming ventricular activity, regardless of the area from
which this activity is generated. We consider an AH interval between 60 and 120 ms and an HV
interval between 35 and 55 ms recorded during sinus rhythm as normal for our laboratories.
.Abnormalities of AV conduction are discussed in more detail in Chapters 3 and 10, but some
examples are offered here to illustrate the usefulness of intracardiac recordings in defining the
location of conduction disturbances. In Figure 1-9, first-degree AV block (since no atrial acti-
vation is actually "blocked" from conducting to the ventricles. we prefer the term first-degree
conduction delay) is demonstrated by a PR interval of 220 ms (0.22 s) and conduction of every
P wave. The QRS duration is 90 ms. which is normal. The cause offirst-degree conduction delay
is noted in the His bundle electrogram. The AH interval measured 155 ms. which is markedly
prolonged. However, in Figure 1-10, the prolonged PR interval in a patient with first-degree
AV conduction delay and left bundle branch block is due to a severe conduction abnormality
in the His-Purkinje system. as demonstrated by an HV interval of 165 ms. This latter situation
represents a more aitical cardiac conduction disturbance, as discussed in more detail in Chapter 10.
A third example of first-degree AV conduction delay is shown in Figure 1-11. This patient
RV--t
FIGURE 1.. • First-degree AV block due to abnormal conduction in the AV node. (Key: RV= right ventricle. See Figure 1-8 for other
abbrevlrtlons. TI me llnes: each major dfvlslon =50 ms.}
has a PR interval of 210 ms and left bundle branch block. However, the HV interval is only
moderately prolonged to 65 ms, but a combination of all conduction times still yields an ECG
pattern of first-degree AV conduction delay. Finally. first-degree AV conduction delay can be
due to conduction abnormalities in both the AV node and His-Purkinje system (Figure 1-12).
ThePRintervalrecm:dedduringsinusrhythm.usuallydemonst:ra:resminimalvariabilit.yunlessmarlced
changes in autonomic tone occur (see "Autonomic Nervous System Effects;' later in chaprer). Thus,
the appearance of 2 distinctly different stable PR intErvals during electrocardiographic recording
I 11 i i 1 1 1 1111
1
PR2SO
Ill
HRA
A H
/i 0
~1 ~m11-----1-"'---"
70 165
FIGURE 1·10 • First-degree AV block and left bundle branch block with a markedly prolonged HV interval. (See text for details.)
111 11111 1111 111111 II 1 11 1111111 111 11 111 I 11 111 11 1111111111
11-......__, .__ _ _ ___,_ _, .__ _ ____,,_ _
III ---"V-------"V------~
HRA--4 ~ AH85
HB£--')h-il·---A HV0i4i~ 1
FIGURE 1·11 • First-degree AV block with left bundle branch blockand minimal intracardi;ac conduction abnonnalities.
II
v v v
Ill
v v v
aVF
V1
v,
HRA
A H v
AH 130
HV95
HBE
FIGURE 1·12 • First-degree AV block with combined AV nodal and Hls-PurklnJe conduction abnormalltles.
..
f+ . II) ti 1 j )Jj I , ..., f [
I.. -· .; lr· Iii; ' !J 1
~fi· .. I ~- JE H·l
·~'
,. !
.J 2. _l , I' Jlr'rt L.t1~:. . L-'-'
LL.l_j_ ....J...JL
: l j1 rL
J
...u...lLU..U.Ju..J. • ~J
Il JI L
PllMllA
FIGURE 1·13 • Two separate and stable PR intervals. This patient had stable PR intervals that were either normal {A) or long (8).
(Reproduced with permission from KelleyWN,ed. Ttxtbookoflntemaf Medfdnt. Phlladefphla, PA: Lippincott 1989.)
strongly suggests the existence of 2 functionally separate anterograde conduction pa1hways. both
preswnably in the AV node (Figure 1-13). The PR interval in panel A is 180 ms and in panel B
400 ms. This patient had dual AV nodal physiology; as illustrated in Figure l-l4.1s.19 In this figure,
the first 3 PR intervals represent AV nodal conduction over the slowly conducting pathway, and the
1111 l llllrl1n1111 r11n II I 1111 l IIii ii iii i 11 iii Ii ii i I iiii i If ii IIii I itmrffm'l'll I I II 11m'ffTTTlfm
v1 - -
HRA -J\--------.1\oo------..Jfpa--~
AH290 S2 AH80
~ 1~t---H~H~
Rv-t----it----t' t r t-
FIGURE 1·14 • Dual AV nodal physiology demonstrated at electrophysiologic study. (See text for details.} {Reproduced with per-
mission fA>m PrystewSky EN, Page RL Elearophysiologyofthe Sino-Atriof ondAtriovetlttkuforNodes. New York. NY: Alan R. US$; 1988.)
i+-t--+~----t-1~
1 2 3
i
FIGURE 1·15 • Schematic ofWenckebach AV nodal block during incremental atTial pacing.
AH .interval is 290 ms. A premature atrial stimulus (S1) -was inttoduced into the high right atrium
and blocbd in the AV node (no His depolarization after atrial premature compla). .Attioventricular
nodal c.onducti.on resumed over the fast conducting pathway. as shown in the last 3 complexes on this
tracing and demonstrated by a normal PR.interval and an AH conduction time of80 ms.
Attfoventrlcular nodal block
Incremental atrial pacing is used to evaluate AV nodal function in the electrophysiology labora-
tory. Amal pacing is started at a rate slightly faster than the spontaneous sinU8 rate and is progres-
sively increased until AV nodal block occurs. The AH interval increases with faster-paced rates
as shown schematically in Figure 1-15. This is an example of 3:2 Wenckebach block. Complex 1
is the baseline interval and conducts with relatively minimal AV nodal delay; complex 2 shows a
substantial increase in the AH int.erval; and complex 3 fails to conduct to the His bundle. Records
from a patient are demonstrated in Figure 1-16. Not.e in ECG lead II a progressive increase in the
PR int.erval for the first 3 paced beats, followed by a P wave without conduction to the ven1Jicle;
conduction resumes with the last paced beat, and the PR interval is shorter than the PR int.erval
of the last conducted beat prior to block. The first PR increment is the largest of the sequence
(30 vs 10 ms). consistent with Wenckebach behavior. This pattern of conduction abnormality is
referred to as Wenckebach. or Mobitz type I serond-degree, AV block. The changes in PR interval
in this example occur within the AV node, as demonstrated by the progressive increase in the AH
interval from 70 to 110 ms without change in the HV interval. Not.e that in the fourth paced beat
the a1Jial depolarization in the HBE tracing is not followed by a His bundle deflection, confirming
bloclc: within the AV node. Conduction resumes with an AH interval of 70 ms.
In very unusual instances it is difficult to detect a measurable increase in the PR interval prior
to block. An example of this is noted in Figure 1-17. This patient had spontaneous episodes
while awake of nonconducted Pwaves with minimal or no prior PR prolongation. Figure 1-17Awas
recorded upon electroph}'5iologic study at a routine ECG paper speed of25 mm/s. There is only
I I Ii I I Ii I I I Ii II II I I ii Ii T'r"M'T"!Trl"l"'M' r I Ii Ii r II II r I I I I 11'TTTT'T'I' Ii ii I ii I I II I 'l'T'TT'
II
v, ~
HRA
RV _.. . ._. r-----r-o----ir---------r- AH A
FIGURE 1·16 • Wenckebach AV nodal block. {See text for detalls.) Arrow points to nonconducted P wave.
a minimal change in the PR interval measurable in this example. Analysis of the intracardiac
electrograms reveals conduction block in the AV node. with a mere 10 to 15 ms increase in
the AH interval prior to the nonconducted P wave (Figure l-17B). This recording was done
at a 100-mm/s paper speed. where more precise measurements can be obtained. The normal
25mm/s
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FIGURE 1·17 • Wenckebach AV nodal block with mlnlmal PR prolongation prior to block. (A) Wenckebach block during routine
ECG recording. (8) Wenckebach AV nodal block demonstrated at electrophysiologic study. (See text for dmils.}
II
Ill
Ve
HAA~~~1-00--------..~~----~~-:cf.-~~------:n,...-----~
AH
s
~ 700
110
H
s! t
RV --f-----.i..---
~ - - --,a,--
~ f---4
200ms
Panel B
FIGURE 1-17 • (Conrfnued)
QRS complex strongly suggests that block will be in the AV node or His bundle, not below the
His bundle. However, one should suspect block with.in the His bundle in cases ofWenc:ktbach
or 2:1 block with baseline normal PR and QRS intervals with minimal changes in PR interval
before block (Flgute l-18A). Note in this example of 2:1 block the normal PR and QRS inter-
vals on the conducted complexes, and the intrac:ardiac: electrograms showing a split His poten-
tial with block after the first His deflection, or intraHis block (Figure l-18B.C).
On occasion, a Wenckebach conduction pattern can occur in the His-Purkin.je system

(F1gu.re 1-19). At electrophysiologic study during inc.remental atrial pacing, there was a progres-
sive increase in the PR interval, as noted in ECG lead II. Analysis of conduction times in the His
bundle elec:trogram shows a progressive inc.rease in the HV interval from 130 to 165 ms prior to a
nonconducted P wave. The AH interval.remained constant. Note that the fifth paced atrial complex.
demonstrates activation of the His bundle but no conduction beyond this point. Thus, conduction
block is infra-His, which represents a severe form ofconduction disturbance. Note that the patient
has a right bundle branch block pattern. Even with a bundle branch block pattern, a Wenckebach
conduction sequence most commonly implies conduction delay and block in the AV node.
Testing of the AV nodal conduction system with incremental atrial pacing in the el.ectrophysiology
laboratory yields a wide range ofatrial paced cycle lengths at which Wenckebach AV nodal block
occurs. In the resting state during electrophysiologic testing, we consider AV nodal conduction
to be normal if 1:1 conduction is present to a right atrial paced cycle length ofless than 505 ms.20
Of particular interest is that even though Wenckebach block may occur at a wide range of cycle
lengths, the AV nodal function curve is physiologically similar for all patients. This is demon-
strated in Figure 1-20, which shows the lengthening of the AH interval, noted on the ordinate,
aVR V1 V4
II aVL V2 vs
Ill aVF V3
II
L-il9
PlntlA
1 1--------~--~-------------~
1111------------_...___________
11$1--------------"------------
v1 1--------~r-----~r-~---------.1
Panela
.. . ... . ' .... . . . . . . . . . . . . . . . . . ... . ... . ... . . . . . . . .
....
1 1---~~--"--~------~----~--~A
11 $ t-----'"'------......-----------'\..---"
~-----
1111------A"----------------A"-----
v11---------r----~-------------"\ r~---
PanelC
FIGURE 1·1 I • (A) ECG wlU'l 2:1 AV block with nonnal PRand QRS Intervals. (8) Simultaneous tracings of ECG leads 1-3 and V1, and
lntracardlac electro grams from the dlstal (HBED} and proxlmal (HBEP) His bundle areas from same patient The second complex Is
premature and shows a spilt His after the atrial electrogram. {C) Block would always occur after the first His elec:trogram as seen In
U'le middle atria I complex wlU'lout conduction to the second His electrogram, or lntraHls block. (See text for more detBlls.)
r11i11•11"'f fl"l1l1" /~I'·"!" Icp1r ~·I· JJJ.pr1•fi17'"'M11,F1l'fcil'i''l'111'fl'r1'9""H1~t''l'~ml8'~1ilf1'l111f:j-fllit:l111'111r ,mlfZ1111'111M'llf11 p:·~ll" ·11 ·I

1 ~·~~..r-~~~-.r'-~~__,r--~--~...r"-'-~~~----~-..1
II
Ill
FIGURE 1-19 • Wenckebac:h block conduction pattem with Infra-His block. (See text for details.)
as a function of shortening of the atrial pacing cycle length (increased heart rate), noted on the
abscissa.21 Each line represents a group of patients with Wenckebach block occurring at different
cycle lengths. For example, the curve on the far right includes patients in whom Wenclcebach block
occurs at cycle lengths greater than 500 ms. whereas the curve on the far left represents patients in
whom Wenclcebach o«:urs at paced cycle lengths less than 300 ms. Each curve is divided into sep-
arate segments, with the most distal segment represented by A. Analysis of these data showed that
the curves were progressively shi&d to the left as shorter atrial paced cycle lengths were required
to yield Wenclcebach block. but the slopes of each part of the curves were similar for all curves. In
essence, only minimal to moderate prolongation of the AH interval o«:urs until the Wenclcebach
cycle length is approached. As a corollary, drugs that demonstrate negative dromotroplc effects,
0
300 500 600
Right A1rlll Pacing Cycfe Length {mMC)
FIGURE 1-20 • Famlly of AV nodal function curves obtained during electrophyslologlc testing. From top to bottom the curves
represent patients who hed shortest 1:1 atrlel pacing cyde length <600 ms but :!!SOO ms; <500 ms but :!!400 ms; <400 ms but :!!300 ms;
and <300 ms. (Reproduced with pennls.slon from Jackman WM, Prystowsky EN, Naa:arellr GV, et al. Reevaluatlon of enhanced atrloven-
tricular nod;il mnduction: evidence to suggest a continuum of nonnal allioventricular nodal physiology. Circuhmon. 1983;67:441.)
+Breath Holding
111111 I 11 I 111 1111111 I 111 111 t 111 1111 I 11 I II I II I 11 I 111 I 11 111 I I 111111 1111 111 111 I 111 I II I I I I 111 I
FIGURE 1-21 • Effect of Increased vagal tone with brealtl hold Ing to tennlnate atrlcwentJlcular re-entry with retrograde conduc-
tion over a left free wall accessory pathway. Note tachycardia terminates with an atJlal electrogram (A) without conduction over I.tie
AV node. Simultaneous tJacings are ECG leads 1-3 and V1; high right atrium (HRA); HBE; proximal (PCS) and distal (OCS) coronary
sinus; and right ventride (RV).
that is, depress conduction, on the AV node-such as verapamil or beta-adrenergic blockers-

minimally affect condition on the flat portion of these curves but have a marked effect on the
stressed. portion (part A) ofthe curve. Since AV re-entry and AV node re-entry conduct near the
Wenckebach point during tachycardia. it is not surprising that a briefincrease in vagal tone with a
maneuver such as breath holding (Figure 1-21) can terminate the arrhythmia.
RETROGRADE CONDUCTION
Incremental ventricular pacing and introduction of premature ventricular extrastimuli are
used to evaluate retrograde conduction during electrophfiiologic testing. Figure 1-22 shows
a schematic of possible paths of ventriculoatrial (VA) conduction. Eccentric retrograde atrial
activation, that is, VA conduction during ventricular pacing or tachycardia that occurs earliest
in the right or left atria typically reflects conduction over a right- or left-sided accessory path-
way (AP), respectively. whereas concentric VA conduction can be over an AP in the septum or
over the normal VA conduction system (His-Purkinje system and AV node, VACS). Incremen-
tal ventricular pacing typically generates VA curves seen in Figure 1-23. Conduction over an
AP normally has minimal conduction delay but may show some delay at fast rates. However,
many patients with conduction over the normal VACS show only 30 to 40 ms delay in this
curve, and thus incremental pacing is not the best technique to differentiate concentric retro-
grade conduction over an AP from the normal VACS.
Right atrium Septum Left atrium
Right ventricle Left ventricle
FIGURE 1·22 • Schematic of possible paths of retrograde conduction. (See text for details.)
Extrastimulus testing during ventricular pacing can clearly differentiate conduction over an AP
from the normal VACS. In Figure l-24A, a premature interval (SlS2) of300 ms during 600 ms
right ventricular (RV) pacing cycle length (100/min) is followed by a retrograde His deflection
and atrial activation (HA 42 ms). The His deflection after ventricular activation results from
retrograde block in the right bundle branch (RBB) with transseptal conduction and subsequent
activation of the His bundle over the left bundle branch (LBB). In Figure l-24B, the S 1S2 inter-
val is shortened to 260 ms, resulting in slower retrograde conduction with an increase in the V
to His interval from 130 to 168 ms, but the HA interval remains constant, a finding that only
occurs with retrograde conduction over the normal VACS. The reason for the relatively con-
stant H 2A 2 interval with progressive increases in the V to His interval during extrastimuli test-
ing (V2H 2) is shown in the graph in Figure 1-25. Note that as the ventricular coupling intervals
VA Interval During Incremental V Pacing
150
f of VA - 30 msec
'ii"
I VACS
!. 100
~ AP
o---~~~~~~~~~~~~~~~~~~~~~~~
0 100 200 300 400 500 600 700 800

Ventricular Pacing CL (maec)
FIGURE 1-23 • Schematic of retrograde conduction curves over the normal ventrlculoatrlal (VPJ conduction system (VACS) and
an accessory pathway (APJ. (See text for details.)
II
Ill
V1
HRA
HBE
HBE
ms
RV
S1 600 600
I
C·14
Panel A
II
Ill
V1
HRA
HBE
HBE
~168ms
RV
S1 595 S1 800 S1 260 S2
C-14
PlnelB
FIGURE 1-24 • Ventrlcular extrastlmulus testing In a patfent with conduction over the normal VACS with S1S2 300 ms (A) and
260 ms (8). (See text for dmils.}
(V1V2 ) progressively shorten, the conduction to the His bundle (V2H2) increases as well. Thus,
by prolonging the V2H2 interval, the AV node is not subject to a progressively shorter interval,
and the H,.A:i interval remains relatively constant.
A very different pattern occurs with retrograde conduction over an AP (Figure 1-26). During
RV pacing at 600 ms cycle length. there is a retrograde His deflection noted on the HBE lead
just before local ventricular activation, with a HA interval of 82 ms. This His is conducted over
60
50
~
.s"'
40
30
•• •• • •
<"' 20
"'
:I:
10
0
175
......
0
150 ......
3!
.s 125 ... ...
"'
:I:
>"' 100
o~ 0 225 250 275 300 325 350
v1 v2 (msec)
C·14
FIGURE 1·25 • Graph of retrograde V2H2 inteMls and H2A2 intervals from patient shown in Figure 1-24. (See text for details.}
the RBB. An extra.stimulus (S1S2) of 280 ms causes retrograde RBB block with conduction to
the His over the LBB. However, the HA interval now shortens to 24 ms, which cannot occur
with conduction over the norm.al VACS, confirming conduction over an AP. Retrograde con-
duction over the AP remains nearly the same in both complexes.
I
II
Ill
V1
HRA
HBE 24ms
HBE
PCS
MCS
MCS
DCS
600 600
RV
E12
FIGURE 1·26 • Ventrlcular extrasttmulus testing In a patient wld'I reuograde conductton over an accessory pathway. (See text for
details.)
AUTONOMIC NERVOUS SYSTEM EFFECTS

Sinus Node
The sinus node is richly supplied with nerves from the parasympathetic and sympathetic ner-
vous systems.1 At rest, humans are "vagal animals" with regard to sinus nodal behavior. That is,
although the sympathetic nervous system affects the sinus node tonically, the parasympathetic
nervous system is prepotent. Experimental studies, including those in humans, demonstrate
that when both sympathetic and parasympathetic inputs to the sinus node are blocked, the
resultant sinus nodal rate substantially increases.D.23 Since sympathetic blockade decreases and
parasympathetic blockade increases sinus rate, a faster rate during autonomic blockade con-
firms the predominant effect of vagal tone.
The interaction of parasympathetic and sympathetic influences on the sinus node is often quite
complex; these influences act in concert to alter the sinus rate. For example, the change to a
standing from a reclining position or from relaxation to exercise results in parasympathetic
withdrawal as well as increased sympathetic tone. Figure 1-27 shows the resultant sinus rate
after a variety of maneuvers that affect the autonomic nervous system. Note that sinus tachycar-
dia occurs in the resting supine state, which was usual for this patient with inappropriate sinus
tachycardia (discussed later in the book), but is a decidedly abnormal fmding. Even though
this patient had a persistent sinus tachycardia, he still responded appropriately to a variety of
maneuvers with an increased rate while standing; an increased sinus rate during phase two of
the Valsalva maneuver, with subsequent sinus slowing during phase four; and sinus nodal slow-
ing during immersion of his face in ice water-a situation that markedly enhances vagal tone.
The sinus rate results from an interplay of the individual's intrinsic sinus nodal automaticity,
the background tonic influences of the autonomic nervous system, and perturbations in the
environment that reflexively change the autonomic input to the sinus node. An example of the
effects of a brief increase in systolic blood pressure on sinus nodal automaticity is demonstrated
in Figure 1-28. The left-hand portion of this figure demonstrates a resting sinus cycle length of
675 ms (89/min). The bottom half of the figure shows the blood pressure, which is approximately
91 mmHg systolic at rest. A 200-µg intravenous bolus of phenylephrine was given to increase
systolic pressure, which was approximately 116 mmHg at its peak. The increase in systolic blood
pressure results in a short period of enhanced vagal tone that prolongs the sinus cycle length to
a maximum of 1110 ms (54/min), but this effect soon dissipates, and sinus rate returns to con-
trol values shortly thereafter. Sinus rate also varies with respiration; it typically increases with
inspiration and slows with expiration-an effect modulated by the parasympathetic nervous
system.24-26 In fact, lack of respiratory variability in sinus rate has been noted in patients with
long-standing diabetes mellitus who have autonomic dysfunction.27 It has also been correlated
with a worse prognosis after acute myocardial infarction,28.29 possibly because of a beneficial
effect of vagal tone on preventing the emergence oflife-threatening ventricular arrhythmias.
An interesting arrhythmia seen in patients with variable degrees ofheart block is ventriculophasic
sinus arrhythmia (Figure 1-29). Note the characteristically shorter P-P intervals that surround a
QRS complex compared with the longer P-P intervals without an intervening QRS complex. The
explanation for this phenomenon stems at least in part from alterations in sinus nodal automatic-
ity resulting from changes in blood pressure. For example, ventricular electrical systole is followed
by a rise in systolic blood pressure that would tend to slow the sinus cycle length, as demonstrated
STANDING
VALSALVA
. I
ICE WATER
I ..
I
~ I
. ," .._ ....
h
'\ ,,. ..,J
l .. .. ..
I
it-tt--
1-. _t +'
I I
I I
- '
i I
J•
lJ \
, ... '
-~1-1·. -~-
1.. J1 I
,,.
.
·- 1 - · .
.. ,_ II.I.A.. ~ }
tt~ "..
I
_,__
I
-
F - ·- .... ...:c
.I L
-
! ·1J r~t ~ -
- -- -- -·- - -·-_,_Ti-
- ·-
-..-
1-1-
1-0-
- '-• - - -- -
-I -- -
FIGURE 1·27 • Effect of various autonomic manelM!fs on sinus nodal automaticlty. (See text f'or details.)
in Figure 1-28. However, if the systolic rise in blood pressure occurs too late to affect the next
sinus-generated P wave, it may still slow the subsequent sinus impulse. In Figure 1-29, this would
cause the P wave immediately following the QRS complex to occur on time but the next P wave
to be delayed, yielding a longer P-P interval without an intervening QRS complex. Since the effect
of heightened blood pressure is short-lived, the P wave immediately after the QRS complex is not
delayed and therefore the P-P interval surrounding the QRS complex is relatively short That this
mechanism is operative is strengthened by the observation noted in Figure 1-30.
The data in Figure 1-30 were generated from a patient undergoing autonomic testing by means
of neck-collar suction.'o.s1 With the patient in a supine position, this is accomplished by the
Control 200 µg Phenylephrfne

111111 111 11 1111111 11 111 11 11111111 1111 1111111 11 111 111111111111111111111 11 1111111111111111 1111111111111111111111111111 111111111 1111111111
1: ~~
Ill -Jl..-.-.....--1.-......--JI.-__..-.
±:t j
V1 ~
0 ,,
\
FIGURE 1·.28 • Slowlng of sinus rate as result of enhanced vagal tone followlng an lncrNse In systolic blood pressure during
phenylephrlne Infusion. (See text for detallsJ
placement of a malleable lead collar, resembling an ordinary neck brace, around the patient's
neck with an airtight seal The collar has 2 ports, 1 for intracollar pressure readings and the
other to be connected to a vacuum source. Negative intracollar pressure of -60 mmHg for a
duration of 600 ms is initiated at various points throughout the sinus cycle, and the resultant
increase in P-P interval is plotted as a function of the time that neck suction is initiated prior
to the anticipated onset of the sinus P wave. The neck suction imposed through the collar
creates a deformation of the carotid sinus, mimicking a sudden increase in blood pressure and
thus producing increased vagal tone. This technique can be used to detennine the earliest time
possible prior to an anticipated sinus impulse at which a sudden increase in vagal tone can
: I I I ! I :,:
.! l I ·I : ·i
i !. : II
: I
; 990I '"1·
: !
I·.
I
'I
. I I
' I I . I
· ·: ·i r-·1
:Ii !
! ·! !. I '' '
I l-.
J I l
l
I
I ' ' i ...I : I
I ;
I '
FIGURE 1-29 • Vennlculophaslc sinus arrhythmia In a patient with 2:1 AV block. {See text for details.)
500
400
100
•
1000 900 800 700 600 500 400 300 200
Stlmulu&--(antlclpatad) P wave, ms
FIGURE 1-30 • Example of a baroreflex lnhlbltlon curve of the sinus node obtained during pulses of neck-collar suction of-60 mmHg
for 600 ms throughout the c.ardlac cycle. (See text for detalls.)
affect sinus nodal automaticity. It can also be used to demonstrate for that individual the fun-
ing of the peak effect and when the vagal tone will dissipate. In this 22-year-old patient, the
latency-that is, the fune before the anticipated P wave when the imposed vagal tone did not
affect sinus nodal automaticity-was approximately 200 ms. A substantial effect was seen only
after 500 ms prior to the onset of the P wave. The latency tends to increase with age, and it is
not uncommon for patients in their fifth and sixth decades to have latencies of 400 to 500 ms. 32
Reevaluation of Figure 1-29 reveals an approximate 500 ms interval between the QRS complex
and P wave immediately following this complex. It is quite possible in this older individual that
the expected enhanced vagal tone following cardiac contraction fell within the latency period
of the next sinus impulse and thus produced no effect on the sinus rate. However, the increased
vagal tone could clearly have depressed automaticity of the subsequent sinus impulse, produc-
ing a prolonged P-P interval.
AV Node
Unlike the sinus node, the AV node in humans at rest appears to have a relatively balanced
input from the parasympathetic and sympathetic nervous systems.23 But in patients who have
abnormal AV nodal conduction, a preponderance of vagal effect may be noted at rest.2° Con-
duction time through the AV node depends on a combination of the direct effects of heart rate
and the indirect effects of changes in autonomic tone. The direct effect ofheart rate on AV node
conduction is shown in Figure 1-20 at electrophysiologic study. At relatively slow atrial pacing
rates the AH interval is near baseline, but there is a progressive increase in AH conduction
time with faster-paced rates and eventual Wenckebach block. The direct effect of increased
sympathetic tone on AV node conduction is seen in Figure 1-31.33 At electrophysiologic study,
atrial pacing at the same relatively slow and fast rate for each patient occurred at control and in
the presence of isoproterenol infusion. Note the shortening of AH interval with isoproterenol
for the slow and faster heart rate, and this shortening was most pronounced at faster rates;
atropine can have the same effect. However, an increase in vagal tone can have the opposite
Effect of lsoproterenol (1 tJg/min) on Paced AH Interval
• Control
160 • lsoproterenol
'U'
=
.§. 120 I
ll.63 msec*
~
f
::c
80 L
oC
40
*P<0.05
0
141:t75 650:t112
Atrtal Paced Cycle Length (maec)
FIGURE 1-31 • Effect of isoproterenol to shorten AH interval more at faster than slower atrial paced rates at electrophysiologic
study. (See text for details.)
effect as shown in Figure 1-32. In this study, tonic parasympathetic tone was increased during
a constant infusion of phenylephrine that increased blood pressure34 and its effect on AV node
conduction evaluated at a relatively constant slow and fast rate for each patient (Figure 1-32).
There was some increase in AH interval at the slower-paced rates, but a much more prominent
prolongation at the faster-paced rates. It is not surprising that a brief increase in vagal tone can
terminate an AV node-dependent tachycardia whose heart rate is near the Wenckebach point
(Figure 1-21) yet the same maneuver has minimal effect on AV node conduction at rest.
280
240 0 Baseline
200 • Phenylephrine
n = 10
~
.!!
.5
::c
160
120
MHs
(msec) r~·
127:t40
oC
102:t48} !:..AHL
80 84:t24 (msec)
40
0
A1-A1 = 575:t209 A1-A1=845±132
FIGURE 1-32 • Effect of enhanced reflex parasympathetic tone during phenytephrine infusion to prolong AH interval at relatively slow
and faster atrial paced rates. (See text for details.) (Reproduced with pennission from Page RL, Tang ASL, Prystowsky EN. Effect of continu-
ous enhanced vagal tone on atrioventricular nodal and sinoatrial nodal function in humans. arc Res. 1991 ;68:1614-1620.)
Ef1'11cte of HR and ANS on AV Nodal Conduction

Long
Exen:I•
PR Interval
(mMC)
Indirect ANS eft'ect
Heart nlte
FIGURE 1·33 • Schematic of Interaction of effi!ct5 of heart rate and autonomic tone on AH and PR Intervals. (See text for detallsJ
The interaction of heart rate and autonomic tone is shown in Figure 1-33. Under usual clrcwn-
stances, for example, eurdse, the direct effect offaster heart rates to prolong AH or PR interval
is offset by the increase in sympathetic and reduction of parasympathetic tone, which facilitates
AV node conduction, and the PR interval remains about the same (middle curve). A constant
PR interval is important for optimum hemodynamics, and evaluation of the PR interval during
exercise testing shows how well this system works. A sudden increase in heart rate because of
an atrial tachycardia typically is associated with a prolonged PR interval. often a differential clue
regarding sinus tachycardia versus atrial tachycardia. A common observation noted at times of
expected high vagal tone-for example, during sleep-is Wenckebach AV nodal block in the
presence of a relatively slow rate (Figure 1-34). This figure is from a patient with normal sinus
and AV nodal function. Note the telltale finding of a progressive increase in the length of the
sinus cycle prior to the nonconducted P wave. A combination of sinus slowing and Wenckebach
AV block strongly suggests the mechanism. to be enhanced parasympathetic tone, a normal
physiologic event that tends to occur during sleep. We stress that this is not an abnormal find-
ing and, by itself. should never be an indication for permanent pacemaker implantation.
. ," ':~in'. li1i !!:: ::;! :;;; ": . ~ -.fh '·', .:.:.:... . . . ... . - '/ l/ ~
I;, !: 1 , :;' 1:38. m,", ,:;, •:.' • 1.44 -;-~ - 1.48 ' 1.40
FIGURE 1·34 • Wenclcebach AV nodal block during sleep. Arraw points to non conducted P wave. The Intervals represent the timing
between P waves. (See text for demlls.)
FIGURE 1·35 • High-grade AV block during sleep apnea. (See text for details.)
Another manifestation ofdisturbed AV nodal conduction, at least in part related to autonomic

perturbations, is high-degree heart block during sleep apnea (Figure 1-35).35.16 Experimental
data have shown that conduction disturbances and sinus nodal abnormalities during apnea can
be ameliorated with supplemental oxygen delivery but can also be prevented with atropine.
This suggests that the effect on the AV node during this pathophysiologic state is mediated via
the parasympathetic nervous system. Increased vagal tone during vomiting appears to ha:ve a
more pronounced effect on AV node conduction than sinus node automaticity, although the
sinus rate typically slows some (Figure 1-36).
As noted earlier, increased sympathetic tone or decreased parasympathetic tone can facilitate
conduction through the AV node, as shown in this patient with SVT and a change in 2:1 to 1:1
conduction with vagal withdrawal (Figure 1-37). In some patients, we have noted that admin-
istration of intravenous isoproterenol or atropine can alter automaticity in junctional tissue
prior to affecting sinus nodal automaticity (Figure 1-38). This patient was given an intravenous
infusion of 3 µglmin of isoproterenoL Note in the left-hand portion of the figure a junctional
tachycardia, with a His bundle deflection occurring before each QRS complex and retrograde
atrial activity. The sinus rate accelerates and the sixth QRS complex is generated by the sinus
node and not the junction. Thus, although the primary effects of increased sympathetic and
decreased parasympathetic tone on the AV node are usually manifest through changes in AV
nodal conduction, on occasion enhanced automaticity may predominate.
His-Purkinje System
Most data suggest that normal His-Purkinje conduction is minimally affected by sympathetic
and parasympathetic input However, other observations suggest that abnormal His-Purkinje
FIGURE 1·36 • ECG rhythm strip obtained when the patient was vomiting. While there was some slowing of sinus rate, the
predominate effect was on the AV node, with several nonconducted P waves.
..1:...
.
I
II ·1 ~l·' :. .
• ::
·1 , , ...
! ·.. :1··· !'.
• .... L"
Pln•IA
•• 1 ;
I
• 1<' : :II • II!'
1
Pln•IB
FIGURE 1-S7 • ECG rhythm strips of an allfal tachycardia with a cycle length of approximately 320 ms with the patient at rest and
3:1 conduction (A) and with activity with 1:1 conduction (B).
conduction-for example, Mobitz type II block-can be worsened with beta-adrenergic block-

ade and improved with atropine.l7 The mechanism for these effects is atill unclear. However, as
with AV nodal physiology. changes in autonomic tone can have a direct effect on His-Purkinje
conduction and an indirect effect mediated by a change in sinus rate. An example of this is
shown in Figure 1-39. In the top tracing (panel A), during sinus rhythm at rest in the electro-
phY5iology laboratory, the HV interval is 70 ms, which is prolonged in a patient with underlying
left bundle branch block and 1:1 AV conduction. In panel B, the sinus rate has substantially
increased during atropine infusion from a cycle length of 1175 ms (51/min) to 770 ms (78/min)
but 1:1 AV conduction is still present, although the HV interval has increased to 80 ms. Note,
however, the shortening of AH interval from 100 to 60 ms, demonstrating that the predom-
inant effect of atropine on AV nodal function was a direct one that countered the expected
lengthening of AH interval due to the increased heart rate. In panel C, Mobitz type II AV block
is present after an increased amount of atropine was given that shortens the sinus cycle length
to 550 ms (109/min) and results in a rate fast enough to cause infra-His block. Thus, atro-
pine has been shown to improve diseased His-Purkinje conduction during electrophY5iologic
study32; however, when the sinus rate increases to a critical point during atropine administra-
tion, Mobitz type 11 block will occur because of the overriding stressful influence of increased
heart rate on tenuous conduction in the His-Purkinje system.
lsoproterenol 3.0 1o11>'min
II
Ill
1----i
200ms
FIGURE 1·38 • Accelerated junctional tachycardia during isoproterenol infusion. The first 4 complexes demon mate a junctional
tachycardia with a His deflection (artowheod) preceding each <lRS complex and with atrial activation being retrograde and noted
first in the His bundle lead followed by the high right atrial lead. There are no P waves identified on the surface ECG. In beat 4, there
appears to be some activation of the atrfa by the sinus node, although the QRS complex Is generated by the juncUonal focus. Note
the slfght alteratlon of the beginning of the <lRS complex, representing atrlal activity that Is different from the flrst 3 beau. Beat
S demonstrates capture of the atrium prlmarily by the sinus focus, but the QRS complex Is most likely still generated from the
Junctlonal focus. The sixth QRS complex Is generated by the sinus node, which results In the high right atrium being activated flm,
followed by His bundle (septal) atrial activation and then conduction through the AV node and Hi5-Purkinje system. The proximal
coronary sinus (PCS) and distal coronary sinus (OCS) represent left atrial activation that occurs after that of the right atrium.
A clinical counterpart of this phenomenon is heart block that occurs during exercise testing,
usually in patients with bundle branch. block. This is almost invariably due to block in the
His-Purkinje system and bnplies a markedly abnormal situation that often requires pacemaker
implantation. On rare occasions we have noted this phenomenon in patients with a narrow
QRS complex. and block in these individuals has usually been within the His bundle itself.
When heart block is noted during exercise testing and the mechanism is unclear, electrophysi-
ologic evaluation is indicated. However, AV nodal block would be distinctly uncommon during
exercise because the autonomic alterations of both vagal withdrawal and enhanced sympathetic
activity have a salutary effect on AV nodal conduction.
Atrium and Ventricle

Both the atrium and ventricle receive input from the parasympathetic and sympathetic ner-
vous systems. In general. increased vagal tone has a more marked effect on atrial tissue than
on ventricular tissue in humans. In our experience, increased parasympathetic tone shortens
atrial refractoriness but may lengthen ventricular refractoriness.2s.sa Increased sympathetic tone
tends to shorten refractoriness in both types of tissue. In the absence of anti.arrhytlunic drug
therapy, changes in autonomic tone minimally affect the rate of sustained monomorphic ven-
tricular tachycardia, although exceptions do occur (Figure 1-40).
VasovagalPhenomenon
In most situations, alterations in autonomic tone provide a fine-tuning effect on cardiac elec-
trophysiologic properties. The potential magnitude of the effects of increased parasympathetic
Control
1111111111111111111 lll ll ll ll lllli11i l l
11 - - - - - - ' " ' - - - - - - -- -------' ......___ _ _ __
111 - - - - " - - - - - - - - - - - . - . . . . - - - - - -
v,
HRA ------w--~---'-
11~7~
5 -----'lrl~-----~
AH100
HBE ~~~l1l-HV_10_ _ _~\J'j /\,.___
•I
Panel A
Atropine lmg IV
770
Atropine 1.5 mg IV
v, AA.75
HV75
-y~-
1
1100
RV ---.t~-----------,"
1
PanelC
FIGURE 1·3' • The effects on His.-Purkinje conduction of increased heart rate due to atropine infusion. (See text for details.)
tone can be observed during a vasovagal episode. a period ofimposition ofimmense vagal tone
on the heart that can have devastating results, such as total asystole and syncope (Figure 1-41).
During a vasovagal episode in this patient. there was no sinus nodal activity or any junctional
or His-Purkinje escape rhytlun for over 7 s; we have seen asystolic episodes last longer than 15 s.
The lack of automatici.ty in any subsidiary pacemaker during one of these episodes should
remove any doubt that the parasympathetic nervous system can have a significant effect on
His-Purkinje and ventricular tissue.
LYING
STANDING
FIGURE 1-40 • The effects of posture on tfte cycle length of ventricular tachycardia. In this unusual patient. the rate of ventricular
tachycilrdia substantially increased when the patient rose from the supine position. It is unclear whether this was due primarily to
changes in autonomic activity, such as parasympathetic withdrawal and increased sympathetic tone, changes in ventricular filling, or
both. Most patients with ventricular tachycardia have minimal changes In wntrtcular tachycardia rate with changes In body position.
ll!MffflfffflffM!lflftfllffflfltftflffffilffilfffflfftfflllllffillmfllftlll~ffiflftllfflftlfllflllftlltMlllHftiiliiiiliiilililinmft•Ul!ll•lllllllllllllllllllH!llll!lilllliliiiiliiiiliiliiliiilllmft!ffiliilftlfllflll!MI
1----------4
I sec
II
FIGURE 1-41 • Vasovagal episode with no evidence of sinus nodal or subsidiary pacemaket' function. (See text for details.)
REFERENCBS
1. StraU88 HC, PrystowU:y EN, Selle.Inman MM, et al Sino-atrial and atrial electroge.neela. Prog CardiOYasc DU. 1977;
14(5):385.
2. Durrer D., T. Th VUIDam, GE Freud. et aL Total eJ:Citt&tion of the lsolt&Se<l human heart. CimURtion. 1970;41;899.
3. VanDamlmi,JameMJ.Activationoftheheart.In:MadulanePW;LawrieTDV. ed.s.ComprelrmsivtI!lectroavdiology:
TMmy tmd Pnidia in Hi:o1t1i "1Ul Diu:tue.. New Yotk, NY: Pcrgamon Pr:e.a:lOl-127.
4. Spach MS, Lieberman M., Scott JG, et al. Bxdtation sequence of the atrial septum and AV node in illola.ted heam
of the dog and the rabbit. Cite Ru. 1971;29:156.
5. Inoue S, Becker AE. Posterior me.oslons of the hum.an compact atrlove.ntricula.r node: a neglected anatomic
feature of poten1ial cllnlcal slgniftcance. Circullmtm. 1998;97:188-193.
6. Paes de Carvilho A, de Almeida DF. Spread ofactmtythrough the atrioventricularnode. Res. 1960;8:801. cm
7. Anderson RH, Jame MJ, wn Capelle PJ, et al. A combined mozphological and electrophynological study of the
atrloventrlcular node of the rabbit heart. cm Ra. 1974;35:909.
8. JBillette. MJ Janae, F)' van Capelle. et aL Cycle-length depende.nt propertiu of AV nodal adiwtian Jn rabbit hearts.
Ami PltyJlot 1976;231:1129.
9. .BWette J. Atriowntricular nodal activation during perl.odl.c premature stimulation of the atrium.. Am J Phytlot
1987;252:H163-Hl73.
10. Temple IP, lnadaS., DobrzynskiH., et al. Connexins and the atrioventricular node. Heart Rhythm. 2013;10:298-304.
11. Tawara S. Das Reizleihmgssystem des Saugetierherzeris: Eine Anatomisch-Histologische Studie uber das Atrioven-
trikurbundel und die Purkinjeschen Faden. Jena, Germany: Fischer; 1906.
12. Demoulin JC, Kulbertus HE. Histopathological examination of the concept of left hemiblock. Br Heart ].
1972;34:807.
13. Benjamin J. Scher Lag, Sun H. Lau, Richanrd H. Helfant, et al. Catheter technique for recording His bundle activity
in man. Circulation. 1969;39: 13.
14. Prystowsky, EN. Electrophysiologic testing. In: Kelley WN, ed. Textbook of Internal Medicine. Philadelphia, PA:
Lippincott; 1989:344-353.
15. Prystowsky EN, Page RL. Electrophysiology and autonomic influences of the human atrioventricular node. In:
Electrophysiology of the Sino-Atrial and Atria-ventricular Nodes. New York, NY: Alan R. Liss; 1988:259-277.
16. Moe GK, Preston JB, Burlington H., et al Physiologic evidence ofa dual A-V transmission system. Circ Res. 1956;6:357.
17. Rosenblueth A. Ventricular •echoes." Am l PhysioL 1958;195:53.
18. Mendez C, Moe GK. Demonstration of a dual A-V nodal conduction system in the isolated rabbit heart. Cin: Res.
1966;19:378.
19. Pablo Denes, Delon WU, Ramesh C. Dhingra, et al Demonstration of dual A-V nodal pathways in patients with
paroxysmal supraventricular tachycardia. Circulation. 1973;48:549.
20. Rahilly GT, Zipes DP, Naccarelli GV, et al Autonomic blockade in patients with normal and abnormal atrioven-
tricular nodal function. Am J Cardiol. 1982;49:898.
21. Jaclcman WM, Prystowsky EN, Naccarelli GV, et al. Reevaluation of enhanced atrioventricular nodal conduction:
evidence to suggest a continuum of normal atrioventricular nodal physiology. Circulation. 1983;67:441.
22. Levy MN, Zieske H. Autonomic control of cardiac pacemaker activity and atrioventricular transmission./ Appl
PhysioL 1969;27:465.
23. Prystowsky EN, Jaclc.man WM, Rinkenberger RL, et al. Effect of autonomic blockade on ventricular refractori-
ness and atrioventricular nodal conduction in humans. Circ Res. 1981 ;49:511.
24. Katona P, Jih F. Respiratory sinus arrhythmia: noninvasive measure of parasympathetic cardiac control. l Appl
PhysioL 1975;39:801.
25. Katona PG, Poitras rw, Barnett GO, et al. Cardiac vagal efferent activity and heart period in the carotid sinus
reflex. Am JPhysiol 1970;218:1030.
26. R. Coker, A. Koziell, C. Oliver, et al. Does the sympathetic nervous system influence sinus arrhythmia in man?
Evidence from combined autonomic blockade./ Physiol 1984;356:459.
27. Ewing DJ, Neilson JM, Travis P. et al. New method for assessing cardiac paruympathetic activity u.ing 24 hour
electrocardiograms. Br Heart]. 1984;52:396.
28. Wolf MM, Varigos GA, Hunt D., et al Sinus arrhythmia in acute myocardial infarction. Med J Aust. 1978;2:52.
29. Kleiger RB et al Heart rate variability: a variable predicting mortality following acute myocardial infarction. /Am
Coll Cardiol. 1984;3:547A.
30. Prystowsky EN, Zipes DP. Postvagal tachycardia. Am J Cardiol 1985;55:995.
31. Eckberg DL, Cavanaugh MS, Mark AL, et al. A simplified neck suction device for activation of carotid baroreceptors.
l Lab Clin Med. 1975;85:167.
32. Prystowsky EN, Sheta M., Adams D., et al Carotid baroreflex abnormalities and end-organ responsiveness in
patients with diabetes mellitus. /Am Coll CardioL 1986;7:126A.
33. Kammerling JM, Miles WM, Prystowsky EN. Effects of graded isoproterenol infusions on human cardiac electro-
physiologic properties. Circulation. 1985;72:1II-252.
34. Page RL, Tang ASL, Prystowsky EN. Effect ofcontinuous enhanced vagal tone on atrioventricular nodal and sinoa-
trial nodal function in humans. Circ Res. 1991;68:1614-1620.
35. Prystowsky EN, Klein GJ. Arrhythmias in chronic lung disease. In: Rubin LJ, ed. Pulmonary Heart Disease. Boston,
MA: Martinus Nijhoff Publishing; 1984:273-283.
36. Zwillich C., Devlin T., White D., et al. Bradycardia during sleep apnea-characteristics and mechanism. l Clin
Invest. 1982;69:1286.
37. Markel ML, Miles WM, Zipes DP, et al. Parasympathetic and sympathetic alterations of Mobitz type II heart block.
JAm Coll Cardiol. 1988;11:271.
38. Prystowsky EN, Naccarelli GV, Jackman WM, et al. Enhanced parasympathetic tone shortens atrial refractoriness
in man. Am I CardioL 1983;51 :96.
Electrocardiographic
Consequences of Atrial and
Ventricular Ectopy
Ectopic complexes arise from areas other than the sinus node and, when manifest, disturb
the normal sequence of automaticity and conduction in the heart. Premature complexes most
commonly originate in the ventricles and atria but may also occur in the atrioventricular (AV)
junction. Regarding terminology. ectopic does not refer to a mechanism but to the origin of the
complex outside the sinus nodal area. Mechanisms include automaticity and reentry and are
discussed in more detail in Chapter 5. These abnormal complexes are often referred to as beats,
although technically a beat suggests a stroke or pulsation of the pulse o.r heart, whereas PVCs
and PACs are actually electrical events and may not be coupled with contraction. Regardless,
premature beats is a term so ingrained in the literature that it is not worth altering merely for
semantics. This chapter discusses the elect.rocardiographic (ECG) consequences of premature
complexes.
PREMATURE ATRIAL COMPLEXES

Effects on Sinus Nodal Function
Premature atrial complexes (PACs) can affect sinus nodal automati.clty and conduction. The
ECG events are a result of conduction from the PAC that is "concealed;' but the results of which
are manifest.H Figure 2--1 is a schematic illustrating some of these general principles. PACs
may result in a compensatory pause. reset, or are interpolated (Figure 2-1).M A compensatory
pause occurs when an atrial complex fails to conduct ret.rogradely into the sinus node and does
not allow the regular sinus impulse to manifest itself because of refractoriness of the tissue
after the PAC. The subsequent sinus impulse is on time and conducts normally to the atrium
(Figure 2-1. I). Thus. the interval from the spontaneous atrial complex (A1) preceding the PAC
(A,_) plus the time from the PAC to the subsequent sinus beat (AJ after the PAC (A,,A,, + A,A)
equals twice the spontaneous sinus interval (2 x A1A1). Further, the return cycle length (R1).
or A,A, in this example is greater than the spontaneous sinus cycle length. The second return
cycle (R,), or A,A,, will equal the basic (B) sinus cycle length ifthere has been no disturbance
of sinus nodal automatidty and the sinus rate has minimal normal variability. An example of a
compensatory pause produced at electrophysiologic testing is shown in Figure 2-2.
Reset occurs when a PAC conducts through the atriosinus junction and depolarizes the sinus
nodal pacemaker (Figure 2-1, Il).5.6 In unusual circumstances. a PAC can cause reset without
actual capture of the sinus nodal pacemaker.7·9 Reset tends to happen with a PAC that occurs
I. Compensatory Pause
II. Reset
\ .\ :~ ~\ :~ A1 A2 +~Aa=2 XA1A 1
¥3>A1A1
:~
A1 ~+~Aa<2 XA1A1
\ .\.( R, \ ¥3>A1A1
Ill. Interpolation
\ .\/~1 A1 ~ + ~ Aa = or> A 1A 1
~>A1A1
FIGURE :Z-1 • Schematic of effects of premature atrial complexes on sinus nodal automaticity. The ladder diagram represents con-
duction from the sinus node {S) to the atrium (A) showing conduction time by the diagonal line connecting S with A. Block is repre-
sented by a small horizontal line perpendicular to the normal conduction line. With interpolation, tne tnird sinus impulse conducts
without Increased anterograde delay from the sinus node to the atrium, as represented by the solid line, or with some addltlonal
conduction delay shown by the dotted line. (Key: Basic cycle length = B; premature cycle lengtn = P; first return cycle = R1; second
return cycle length= ff,.) (See text for further details.)
at 70 percent or less of the spontaneous sinus cycle length. Mathematically, reset is defined as
the sum of A 1~ plus ~A3 being less than twice A1A1 with the A2A3 interval greater than A1A1•
Reset is an excellent example of concealed conduction. The PAC is manifest but its conduc-
tion into the sinus nodal region is not apparent on the ECG. However, reset demonstrates that
the PAC affected the sinus nodal pacemaker, yielding an earlier-than-expected return complex
(AJ Assuming no change in sinus nodal automaticity caused by the PAC, A3A• will approxi-
mately equal A1 A1 (Figure 2-3).
Interpolation is present when a PAC neither enters the sinus node to reset the pacemaker nor
prevents the spontaneous sinus depolarization from activating the atrium (Figure 2-1, III).
Complete interpolation, which is relatively rare, occurs when the PAC has no influence on
sinus nodal automaticity or sinoatrial conduction and therefore the A 1A2 plus A2A3 interval
equals the spontaneous sinus interval, A1A1• The ~A3 interval necessarily must be less than
A1 A1 in this instance. More commonly, a PAC will affect automaticity, conduction, or both,
and the A1 ~ plus A2A3 interval is greater than A1A1; this is referred to as incomplete interpo-
lation (Figure 2-4). In Figure 2-4, the second return cycle (A3A4) is substantially longer than
expected, presumably due to depression of sinus nodal automaticity by the PAC-another
manifestation of concealed conduction.1°'11 Sinus node reentry may also occur when a very
early PAC conducts into the sinus node and produces one or more re-entrant complexes. 1i- 16
With one re-entrant complex, the A1 A2 plus ~A3 interval is less than the basic A1A 1 sinus cycle
length. Spontaneous sinus node echo beats are rarely observed on a routine 12-lead ECG or
CHAPTER 2 • Electrocardiographic Consequences of Atrial and Ventricular Ectopy 37
III I II II II Ill II II II II II I II II II III II II II II III II II II II III II II II IIII I II I
690 600 790 700
FIGURE 2-2 • Complete compensatory pause following a premature atrial complex. Simultaneous recordings of surface ECG and
intracardiac electrograms from the right atrium and His bundle area (top to bottom). The sinus cycle length (A1A1) is 690 ms with a
premature atrlal complex (.\) Introduced at an A1A2 Interval of 600 ms. The return sinus complex ~) has an AA Interval of 790 ms,
yielding a complete compensatory pause (790 + 600 = 1390 ms). The second return cycle CA,AJ essentially equals A,A,, demon-
strating no effect on sinus nodal automaticity from A,_. (See text for further details.)
even during 24-h ambulatory recordings. Sinus node echo beats and short runs of sinus node
reentry are occasionally initiated at electrophysiologic study; but sinus node reentry is rarely a
significant clinical problem.
Effects on Atrioventricular Conduction

PACs can conduct to the ventricles with or without prolongation of the PR interval or may
be blocked in the AV node or less commonly the His-Purkinje system (HPS). Conduction of
a PAC over the AV conduction system depends on several factors, including the prematurity
of the ectopic complex, the sinus cycle length, and conduction characteristics of the AV node
and HPS. Bundle branch block and aberrancy are discussed in greater detail in Chapter 3. In
general, only PACs that occur late in diastole are able to conduct with no increase in the PR
interval When conduction delay occurs, it is usually in the AV node (Figure 2-5). In this example,
the P wave of the PAC is inscribed on the preceding T wave (P on T). Note that AV nodal
conduction time represented by the AH interval is longer in the PAC than the normal sinus
complexes. In this example, the actual PR interval of the PAC is difficult to determine from the
surface electrocardiogram because the P wave is obscured by the preceding T wave. AV nodal
delay with a PAC is clearly identified from the intracardiac His bundle electrogram (HBE)
recording. 11- 19 One measurement that is sometimes useful to identify AV delay with a PAC is
1111111 11111111111111 I I I I I I I I I I I I I I I I 111111111111111111111111111111
A, 700 A, 440 Ai. 850 730
FIG URE 2-3 • Sinus nodal reset with premature atriaI complex In same patient noted In Figure 2-2. An ea rifer PAC with an A1A,_
interval of440 ms is followed byan A2A, return cycle of850 ms demonstrating sinus nodal reset. The interval A,A, = 1290 ms, con-
siderably shorter than 1,400 ms expected with a complete compensatory pause. A,A. is essentially unchanged.
a comparison of the isoelectric segment between the end of the T wave and the beginning of
the QRS complex of the PAC with the isoelectric segment of the PR interval of the preceding
sinus complex. Although the end of the P wave is not certain in many of these instances, a
longer isoelectric interval of the PAC compared with the normal PR interval certainly suggests
AV conduction delay as seen in Figure 2-5. Examples of conducted and blocked PACs in the
same patient are shown in Figure 2-6. In ECG strip A, PACs are responsible for the fifth and
eighth QRS depolarizations. A blocked PAC occurs in ECG strip B, as noted by the arrowhead.
ECG recording C is complex and demonstrates Mobitz type I second-degree AV block with a
blocked PAC noted by the arrow. In this example, there are 2 consecutively nonconducted
P waves, the frrst due to AV nodal Wenckebach block and the second caused by a PAC. Of note,
the interval between the sinus P wave and PAC in ECG strip C is similar to the PAC interval in
ECG recording A (Figure 2-6).
In some instances block may occur in the HPS. This can be physiologic, for example, in a
patient with excellent AV nodal conduction who has a slow heart rate in which a relatively early
PAC conducts through the AV node but blocks in or below the His bundle (see Chapter 3). In
some patients with abnormal His-Purkinje conduction, a PAC can block within the HPS at a
relatively long premature interval even in the presence of a normal or accelerated supraventric-
ular rate (Figure 2-7).19-21 A relatively rare example of infra-His block in a patient during atrial
fibrillation is shown in Figure 2-8.
lli1l IIIIlldl IIIIll1il IIIIlli1l IIIIllT1l IIIIlliil 1111 lliil IIIIlli1l IIIIllil
A, 690 A, 800 770

350
FIGURE 2-4 • Interpolated premature atrial complex in same patient demonstrated in Figure 2-2. A premature atrial complex
is introduced with an A,A, interval of 350 ms and the subsequent sinus impulse occurs with an A,A, interval of 480 ms. The com-
bined A, to A, interval of 830 ms is greater than the baseline cycle length of 690 ms, demonstrating incomplete interpolation.
This is probably due to depression of sinus nodal automaticity with some delay in the sinus nodal impulse following A,. and sinus
nodal depression Is demonstrated by the prolonged A,A4 and even A 4A, Intervals compared with A 1A 1• Some contribution from an
increase in sinoatrial conduction time might also have contributed to the greater-than-expected A,A, interval had this been com-
pletely interpolated.
I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I 111111111111111111111111111111
~~-.1A .......A...---- A~~~-
II
Ill A.
~ A
V1 v v v v
HRA--4-
~ v
*t v t
HBE
* ·t A4 ~~
•
I ··t-
t T
FIGURE 2-5 • Prolonged AV nodal conduction time with a premature atrial complex. The star represents the PAC and the arrow
demonstrates an Increase In AH Interval (AV nodal conduction time) compared with the preceding 2 complexes. (Key: HRA = hlg h
right atrium; HBE = His bundle electrogram.)
Panel A
PanelB
PanelC
FIGURE 2-6 • Electrocardiographic rhythm strips in a patient with conducted and blocked premature atrial complexes. The arrows
In Panel A demonstrate conducted PACs. The arrow In Panel B shows a nonconducted PAC. In Panel C. a PAC (arrow) follows a non-
conducted Pwave that Is the cul mlnation of an AV nodal Wenckebach sequence.
11111 l I l I I l I "1111 l I I l I l I I l I I l I I I I l I I l I I tl 1111111111111
II
Ill
V1
HRA~, S1
A1
600
V1
.J .J' 510
~
H1 H2
HBE
FIG URE 2-7 • Premature atrial complex with block below the recorded His potential. This patient had baseline right bundle
branch block with left anterior fascicular block and the high right atrium (HRA) was paced for 8 beats at 600 ms (100/min). A PAC
was Introduced at an Interval of 510 ms and on the HBE block ls noted after His depolarization (H2 ). Block below the Hls bundle at
this heart rate and with such a long premature Interval Is abnormal and Identifies pathology In the HPS.
I IIIIIII IIIIIIIIIIIIII IIIIIII IIIIIIIIIIIIII IIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIII
II_,.._ _..,
Ill - - - - " l l l ' - - - - - - - 1 , 1 - - - - - - - - - " ' 1... -----'ll...___
H H
HBE
I
'f ..I
FIGURE 2-8 • Block below the His bundle potential during atrial fibrillation. Note on the HBE in a patient with right bundle branch
block with left anterior fasclcular block that conduction block occurs below some His potentials. This relatively rare observation sig-
nifies marked abnormality of the HPS. Of note, this patient had a history of syncope and required permanent ventricular pacing.
Concealed conduction can also occur with a blocked PAC (Figure 2-9). In this example, taken
from an electrophysiologic study, the right atrium is initially paced at cycle length 400 ms
(150/min), and 2:1 AV nodal block is present. Note on the HBE that the second and fourth
atrial impulses are not followed by an His bundle depolarization, indicating block in the AV
node. The conducted beats have an AV node conduction time of 100 ms. The last 2 paced
complexes are at cycle length 800 ms, or twice that of the preceding cycle length. Conduction
of each atrial complex occurs, and the AH interval is now 80 ms, or 20 ms shorter than con-
ducted atrial beats during the 2:1 conduction pattern on the left-hand side ohhis figure. The
prolonged AH interval in the presence of 2: 1 block is due to penetration of the nonconducted
I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I I 111111111111111111111111111111
II
Ill
FIGURE 2-9 • Demonstration of anterograde concealed AV nodal conduction during atrial pacing techniques. (See text for details.)
atrial complex into the AV node, resulting in a wake of refractoriness that is encountered by
the next conducted beat, causing a prolongation of AV nodal conduction time. This is a classic
example of anterograde concealed AV nodal conduction.3.21.22 Concealed conduction of a PAC
into an accessory pathway is noted in Figure 2-10.23
S1
2
f-----440 ----l
Panel A
PanelB
FIGURE 2-10 • Anterograde concealed conduction into an accessory pathway. Panel A, An atrial premature complex (52 ) after the basic
drive beat (51) is blocked. A second premature complex CS~ with a 5153 interval of440 ms is also blocked. Note the marked pre-excitation
on the drive beats. Panel B, The 52 ls omitted, and now the 53 with the same 5153 Interval of 440 ms conducts over the accessory pathway.
This finding suggests concealed conduction of 52 into the accessory pathway in panel A. (Reproduced with permission from Klein GJ et al.
Orculation. 1984;70:402.)
PREMATURE JUNCTIONAL COMPLEXES

Premature junctional complexes originate from areas of the AV node and His bundle that are
capable of automaticity. In a given patient, it is not possible to identify the precise origin ofthese
complexes even with intracardiac electrograms. Most junctional premature beats are manifest
and produce a retrograde P wave, QRS complex, or both. Concealed junctional premature com-
plexes can occur and produce many interesting ECG phenomena.24.is
Figure 2-11 shows 2 ECG abnormalities resulting from junctional premature beats. The first arrow
points to a retrograde P wave occurring near the end of the T wave. It would not be possible to
diagnose this deflection conclusively as a P wave unless other areas of the ECG strip demon-
strated normal T-wave morphology, as noted in QRS complexes four and five on the right.
Under most circumstances, one would designate these as PACs, but an alternative explanation
should be considered after analysis of the entire ECG recording. Note the sudden, unexpected
PR prolongation (2nd arrow) in the fifth conducted QRS complex. There is no sudden change
in the sinus rate, and autonomic influences rarely cause such a sudden isolated change in the
PR interval without affecting the sinus rate (see Chapter l).26.27 Thus, a likely diagnosis for both
phenomena is junctional premature complexes with retrograde conduction to the atrium mani-
festing as P waves on the ECG (first three QRS complexes) and a concealed junctional premature
complex that does not conduct to the ventricle or atrium but causes conduction delay in the
AV node with sudden PR prolongation (fifth QRS complex). Confirmation of this diagnosis is
shown with His bundle electrocardiography (Figure 2-12). Further ECG clues that the "PACs"
might be coming from the junction are the fact that they are late in diastole and yet are "blocked;'
and the P waves are very narrow, consistent with originating in the anterior septa! space.
Junctional premature complexes often occur in patients with underlying His-Purkinje disease
and can simulate Mobitz type II second-degree AV block (Figure 2-13). In this simultaneously
-~~' j ,. r•· n- 1•· ·m ... .. rn . ., c::

;,
j j ·- : ·~
:J *. H=l Ff! ll ill
... ..
~
·- ·~
I<
:b
L ..U µ
"
c; HA• f" r'"' .d.
ff : :: ~ i c;r.
:
~. UC +
,,
m
,..
~
f = ,:
~·
,.,. !:); < i:+f 1"' ' ::;;.
~
: :!:!:" :±± '=" ~ .: f. : :
.,
: II
- I
-
:r ~
t!' '
- ~
I :1 ;:
.. ' ...
'
t : ~ : ~ ': !± :±J ~ ::
=
= ~ !n ~
- IJ: ·~ j:: ~ : ; ,._, : ~

=
FIGURE 2·11 • Junctlonal premature complexes with retrograde atrial activation (first arrow) and concealed conduction with manifest
prolonged PR interval (second arrow). (See text for details.)
1-----------~-------~---.---~-----~--~-------~-------.-~
ll---A1...,-----A\..-----A"'w_ _ _ __.
111~--~ '\....- - - - - \ - - - - - \ , . . . . - - - - " \ - - - """_ _ _ _ _ _,,,
aVF
V1
Va
H~~4------A~i----~ir-----+~-----+-----~~--~
H'A250A
HBE.--'IH-oJr'---r-..,,_..,....,....~--"ll"l~lll"------11'+-..lr-~...,._~-----~~---'l.rf--J
85 H'
200ms
FIGURE 2-12 • Junctlonal premature complexes diagnosed at electrophyslologlc study. Same patient as In Figure 2-11. The first
corn plex conducts with a normal AH Interval of 85 ms. A Junctlona I premature complex (H 1 conducts neither to the atrium nor
ventricle but prolongs AV nodal refractoriness with a sudden prolongation of the PR interval and AH interval of the next sinus-
conducted complex. A second junctional premature complex is noted, with anterograde conduction yielding the fifth QRS complex
in this tracing.The H' A interval of 190 ms is too short to allow recovery of AV nodal conduction such that the next sinus impulse
blocks In the AV node. Note that only anterograde conduction occurred with thIs premature beat.
99
II
Ill
aVR
aVL
aVF
V1
V2
V3
V4
Vs
Va
FIG URE 2-13 • Twelve-lead simultaneous ECG demonstrating sudden loss of conduction and a junctional premature complex.
(See text for details.)
I
II ./\.. /\..-----~---~~~~---~
Ill I\, ,/\,~----~~~-----,1\,---
aVF /\.. /\,~------~~~---/'\r---
V1 ...
v v v--
V6 ~ --~~~~~~~~~~~
/"".,..
HRA Ai ~ ~
H'A 225
A H
HBE
85 H'
200ms
FIGURE 2-14 • Electrophysiologic correlation of apparent heart block seen in Figure 2-13. Note tnat following tne second sinus
conducted beat, a •concealed" premature junctlonal complex (H 1 ls present wltnout conduction retrograde to tne atrium or antero-
grade to tne ventricles. Tne H' A interval of 225 ms is too short to al low recovery of anterograde AV nodal conduction and thus tne
next sinus Pwave blocks in tne AVnode.Tnis simulates Mobitz type II second-degree neart block. The last AH interval of75 ms is
sligntly shorter tnan tne baseline AH interval of 85 ms. This was probably due to some recovery of AV nodal conduction after the
prolonged pause, but one cannot rule out with certainty a junctional complex that occurred fortuitously 1Oms earlier tnan when
normal conduction would have been expected. The former explanation is more likely.
recorded 12-lead ECG, note that the fourth P wave does not conduct to the ventricles and the
preceding PR intervals are constant. This is consistent with Mobitz type II second-degree AV
block, but further analysis of this ECG shows that the fifth QRS complex is a junctional pre-
mature beat. Thus, a reasonable alternative diagnosis is AV block due to a concealed junctional
premature complex, confirmed by His bundle electrocardiography (Figure 2-14).
PREMATURE VENTRICULAR COMPLEXES

Premature ventricular complexes (PVCs) are ubiquitous and increase in frequency with age and
the presence and degree of heart disease. We do not recommend therapy to suppress PVCs unless
they produce intolerable symptoms, which is unusual or cause a cardiomyopathy. A PVC can con-
duct retrogradely over the ventriculoatrial conduction system to the atrium or can be blocked in
the AV node or, less commonly, in the HPS. Even when a PVC activates the atrium retrogradely,
it is uncommon to have reset of the sinus node. Thus, under most circumstances a PVC yields a
compensatory pause, as noted below. The inability of a PVC to reset the sinus node is due to the
conduction times involved. As an example, suppose a PVC occurs 400 ms after the last conducted
QRS complex in a patient with a sinus cycle length of 840 ms (71/min). If the PR interval of the
beat prior to the PVC is 160 ms, then a total of 560 ms has already elapsed and the next sinus
impulse is expected in approximately 280 ms. Retrograde conduction times are highly variable,
but for this example we will allow 120 ms for the PVC to activate the atrial septum and another
30 ms to reach the high right atrium near the sinus node. By these calculations, the atriwn near
the sinus node is prematurely activated approximately 130 ms prior to activation ofthis area by the
ATRIUM
AV NODE
HPS
VENTRICLE
VERP
-----
Zone of
interpolation
FIGURE Z·15 • Schematic representation of ECG consequences of PVCs. These are noted by lines starting in the ventricle with
retrograde conduction block In the HPS (green) and AV node (orange and purplt). Block Is represented by a short perpendlcular llne.
(Key: VERP =ventricular effi!ctM! refractory period.) Each retrograde line Is paired wtth a subsequent slmllar llne denoting antefo-
grade conduction. (See text for detalls.)
next sinus complex. It would be highly unlikely for an atrial depolarization this late to effect reset
in the sinus node, and therefore a complete compensatory pause would ensue. Depending on the
circumstances. it would certainly be possible for some PVCs to produce a noncompensatorypause.
Figure 2-15 demonstrates the effect of PVCs on subsequent AV conduction. When a PVC
blocks retrogradely in the AV node. complete interpolation is rare, and incomplete interpolation
is uncommon. but concealed conduction is often present Concealed conduction occurs when
the PVC enters the HPS and AV node retrogradely but does not conduct to the atrium.<1.21.a8-30
There is an increase in refractoriness of these tissues and the next sinus impulse either does not
conduct to the ventricle or conducts with PR prolongation. Without doubt, the most com-
mon area of anterograde block following a PVC is in the AV node (Figure 2-16). Note in
this example that the PVC does not conduct to the atrium and the next sinus impulse blocks
without depolarization ofthe His bundle, confirming block in the AV node. Very uncommonly
in our experience, anterograde block following a PVC occurs below the recorded His bundle
potential (Figure 2-17). Note that in this example the nonconducted second sinus complex has
an increase in the AH interval (arrow). demonstrating concealed conduction of the PVC not
only into the HPS but also into the AV node. Another demonstration of concealed conduction
is shown in Figure 2-18. The initial three QRS complexes are ventricular paced beats. Note
that the PR interval after the third paced QRS complex is prolonged, compared with the subse-
quent PR interval. The presumption is that the paced ventricular complex conducted into the
AV node and HPS system retrogradely, which is concealed, and the subsequent prolonged PR
interval is a manifestation of the concealed conduction. The concept ofconcealed conduction is
very important and explains many ECG phenomena. It can be studied in detail at electrophys-
iologic study,30 an example of which is shown in Figure 2-19.
As previously stated, interpolated PVCs are uncommon, as explained by a more in-depth analy-
sis of Figure 2-15. Several requisite conditions must be present for interpolation to occur. These
II
HRA -t--t--~--~- FIGURE 2-16 • Premature ventricular complex with

complete compensatory pause. Followlng the PVC,
the slnus complex does not conduct to the His bundle,
demonstrating increased refractoriness in the AV node
and block due to concealed conduction from the PVC
into this structure.
HBE
RV L
1"
~ ... lr
'
FIGURE 2-17 • Premature ventricular complex with complete compensatory pause. A PVC introduced at electrophysiologic study
ls followed by a sinus lmpu lse that conducts through the AV node with an Increase ln the AH Interval (arrow) but subsequent block
below the His potential. (Key: RV= right ventricle electrogram.) (See text for details.)
. ·•·
'7 ~
:: .,, ., < H ·: tii

~
, :
.. ::l
=
re;
'TI 1 -
""
.. .. ~ :-;;- : .· ... I. .i. ~ ht: tu
~ ~
err
"' ..
f: :: I;'.;: ::: t::
F: ~
I R'IH"I
-
FIGURE 2-18 • Concealed conduction during ventricular paced rhythm. (See text for details.)
t
... ++- t:1 tt+

±±:
; m F: ~
include retrograde block of the PVC, a close-coupled PVC, a relatively slow sinus rate, and reason-
ably good anterograde AV conduction. As noted in Figure 2-15, there is a relatively narrow poten-
tial zone of interpolation, with ventricular refractoriness defining the inner limits and concealed
conduction with subsequent anterograde block closing the outer limits (purple line). Slower heart
rates will prolong ventricular refractoriness by a small amount, disallowing earlier PVCs; in our
experience, however, the increase in ventricular refractoriness is relatively minor compared with the
resultant longer time for recovery of anterograde AV refractoriness and subsequent interpolation
l lllll ll Ill lllllll Ill ll lllll lllll lllll ll II II Ill Ill If I Ill Ill Ill 11111111
Panel A PanelB
FIGURE 2-19 • Retrograde concealed c.onductlon demonstrated by electrophyslologlc pacing techniques. Slmultaneous tracings
from top to bottom are ECG leads I, II, Ill, and VI, with lntracardlac tracings from the HRA, H BE, and RV. In Panel A, the right atrium
and right ventricle are paced simultaneously for an &-beat drive train and a premature ventricular complex (S2) is introduced at an
interval of 320 ms. The PVC is followed by a atrial paced complex (S,) with an interval from S, to S, of 700 ms. The arrow points to
s,
retrograde His activation and undoubtedly subsequent conduction into the AV node. The complex has an AH interval of 160 ms.
In panel 8, the last beat of the drlvetraln ls noted butS2 was deleted. The 515 3 Interval was kept constant and the AH Interval ofS3
rs now 80 ms, 80 ms shorter than noted when 52 is present (panel A). The only difference in Panel B is the lack of the PVC, and this
demonstrates conclusively that the PVC did conduct into the AV node.
CHAPTER 2 • Electrocardtographlc Consequences of Atrial and Ventricular Ectopy 49
II
Ill
v,
HAA~-tf--..r--~-tt--.1~~~,._.~~-
HBE
A' VA 190 A' VA 190
270
11111 1 1111 11 11 11 111111 1 11111 1 11
Panel A PanelB
FIGURE 2·20 • Concealed conduction Into the AV node prevents Initiation of AV reentry (Panel A) that ls Induced when block
occurs below the His bundle (Panel B). (See text for detalls.)
during slower rates. For these reasons it is unusual to observe interpolated PVCs in the presence of
relatively fast sinus rates. In fact. we have observed this many times in the electrophys:l.ologylabora-
tory when induced PVCs are interpolated with relatively slow but not taster sinus rates.
Concealed conduction of a PVC into the AV node can affect induction of AV reentry
(Figure 2-20). During ventricular pacing at 500 ms (120/min). a premature extrastimulus (S1)
is introduced at 280 ms (Figure 2-20A). Note the eccentric retrograde activation with initial
atrial activity on the distal CS lead resulting from activation over a left free wall accessory
pathway. The arrow points to a retrograde His deflection and concealed conduction into the
AV node prevents initiation of AV reentry. In Figure 2-20B, a premature extrastimulus interval
of270 ms now results in retrograde block below the His (arrow without His deflection) and no
conduction into the AV node. allowing AV reentry to occur. Note that the VA time is constant at
190 ms with the same retrograde activation pattern.
Incomplete interpolation is shown in Figure 2-21. Sinus arrhythmia is present with the first
A1A1 interval of 1350 ms (44/min). Note that the AH interval after the PVC is 225 ms, com-
pared with 165 ms for the normal sinus complex. The increase in AH interval is a manifestation
of concealed conduction of the PVC into the AV node and would be represented schematically
by the orange line in Figure 2-15. For complete interpolation to occur, there would have to be
full recovery of AV node and His-Purkinje refractoriness, which is represented by the green line
of Figure 2-15. This is rare in our experience.
It has been known for decades that an inverse relationship exists between the interval from
the PVC to the next P wave (RP) and the subsequent PR interval. Thus, the shorter the RP
111111111111111111111111111111111111 nninrnrnrhrrrrrrrfffnnfnnnn,,
V1 ----l r----------"' ,..___
HRA~~·--v-~~~~~~~ •
IAH AH
165 225
FIGURE 2-21 • Interpolated premature ventricular complex with concealed conduction into the AV node. (See text for details.)
interval, the longer the next PR interval. The prolongation of the PR interval is due to ret-
rograde concealed conduction from the PVC into the AV conduction system, almost always
dependent upon changes in refractoriness in the AV node and not HPS. This relationship is
demonstrated in Figure 2-22. These data were obtained from a patient during electrophysio-
logic study in which premature ventricular complexes were initiated at variable times during
the cardiac cycle. In panel A, the premature complex, S2, is introduced very early in diastole and
the ventriculoatrial (VA) interval is 405 ms. The VA interval is the intracardiac representation
of the RP interval on the surface ECG. The AH interval is 120 ms, considerably longer than the
preceding AH interval of the sinus conducted impulses without concealed retrograde conduc-
tion. In panel B, S2 is introduced later in diastole and the VA interval is 355 ms, with an increase
in the AH interval to 135 ms. In panel C, a later PVC activates the ventricles very close to the
next anticipated sinus QRS complex, with a VA interval of275 ms and subsequent anterograde
conduction block in the AV node.
In this patient, no PVC ever yielded complete interpolation, as discussed above. The concept of
RP to PR or VA to AV intervals depends on a PVC and is not operative when a PAC conducts
to the ventricle.31 In this situation, the PAC might prolong the PR interval, shifting ventricular
activation closer to the next sinus beat. However, conduction of the next sinus complex is not
affected by the preceding ventricular activation but only by whatever AV refractoriness remains
from the PAC. In other words, retrograde concealed conduction occurs with an impulse that
originates below the AV node and not one originating from the atrium.
The normal AV node has a relatively rapid recovery of conduction time after prolongation of
refractoriness due to retrograde concealed conduction (Figure 2-23). 21.32•33 In this illustration
v,
Panel A
HBE
~ .J-:-:-~:-5----j+-
PanalB
v,
HBE
~--t---------11r----SJl
f------l ~ i-----VA 275
200 ms
PanalC
FIGURE 2-22 • Demonstration of the effect of varying the ventrlculoatrlal Interval with a PVC on subsequent anterograde AV nodal
conduction tlme. There ls a progressive increase in the premature ventricular stlmulus (S) interval from panel A to C. The deflection
between the V, and A on the HBE lead in Panel C was an artifact and not reproducible. (Key: VA= ventriculoatrial.) (See text for details.)
from a patient undergoing electrophysiologic study, the first 2 normally conducted sinus
complexes are followed by an induced PVC. The next sinus complex conducts with a pro-
longed PR interval, which is manifest on the surface ECG by a prolonged isoelectric interval
from the end of the T wave of the PVC to the beginning of the QRS complex, as described
earlier. The His bundle electrogram clearly demonstrates the increase in AV nodal conduc-
tion time with an AH interval of 240 ms, compared with 80 ms during normal conduction.
Note that within one complex AV nodal conduction time nearly returns to normal, with an
AH interval of 100 ms, and is essentially at baseline by the last complex in this figure. As part
1___,..~----~~---"-~--'
II --..J'\.-------'~---...,,
Ill ---'\.-------11.--~
HBE
RV--1r~------...-r-~-. . t. . . . .-t~_......,_..~ 1-200_,

ms
FIGURE 2-23 • Normal rapid recovery of AV nodal conduction time after prolonged conduction due to retrograde concealed
conduction. (See text for details.)
of each electrophysiologic study, we routinely introduce PVCs into sinus rhythm and, after
studying thousands of patients, have found that the observation noted in Figure 2-23 is almost
universal. Thus, persistence of a markedly prolonged PR interval following a PVC strongly
suggests the presence of dual AV nodal physiology, as discussed in Chapter 1. An example of
this is demonstrated in Figure 2-24.
This patient demonstrated dual AV nodal physiology during premature atrial stimulation tech-
niques but was unable to have AV node re-entrant tachycardia because of poor retrograde con-
duction. Figure 2-24 was obtained during electrophysiologic evaluation while pacing the atrium
at a constant cycle length of 700 ms (SJ The AH interval is 105 ms during baseline pacing, as
noted by the first complex. A PVC (S2) was introduced, with a VA interval of 270 ms measured
FIGURE 2-24 • Persistence of prolonged PR Interval after a PVC demonstrating dual AV nodal physiology. (See text for detalls.)
CHAPTER 2 • Electrocardtographlc Consequences of Atrial and Ventricular Ectopy 53
to the next atrial depolarlzatio.n in the His bundle lead. The subsequent AH interval markedly
increased to 420 ms and remained long, with some variation between 420 and 510 ms, until
at.rial padng was discontinued. In our experience, this persistence of marked AH or PR prolon-
gation is diagnostic of dual AV nodal physiology. Concealed retrograde conduction into the AV
node fast pathway from the slow anterograde pathway is a likcl.y aplanation for this finding.
Retrograde concealed conduction can also occur in accessory pathways (AP). In Figw.'e 2-25A,
RV pacing is performed in a patient without VA conduction. Note that the initial paced beat is
1 1----........,.,.-----ae-~,.._-----~""-4M---~-J~---~5-~~/~
II 1----+/'-~ , _ ___,,/\r-.-......_-...-v-----.1 \.---~'---.._,,....,
111 1----.J'--_.,...___ _, v-~--" ____.........__ _,.______----.J1'--
v1 1---~-v-~~--~
V2 ,,___ __
HRA 1--~--------'l------------'I------------'>--~
RV
S1 S1 S1
M·S3
Panel A
Sinus beat
AVN
\ ib
RV\~
Paced
Prolonged A-H lntarval Shorter A-H lntarval
no AP conduction preexctted QRS
Panel B
FIGURE 2·25 • Retrograde concealed conduction into an accessory pathway and the AV node. Panel A, intrac:ardiac tracings and ECG
recordl"9$ during wnl'rk:ular pacing. Panel 8, Schema'dc of die 4dl (left) and Sth (right) ORS complexes In Panel A. {See text for decalls.)
a fusion complex, but the next 2 capture the ventricle (the last stimulus occurs in the ventricular
refractory period and does not activate the RV pacing site). The third sinus complex conducts
with a prolonged AH interval compared with the fourth complex at the end of the tracing,
demonstrating retrograde concealed conduction into the AV node. The fourth sinus complex
conducts over an AP and the AV node. The reason for lack of anterograde preexcitation in
the third sinus complex is because the previous RV paced beat conducted into the AP, that is,
concealed AP retrograde conduction. Figure 2-25B is a schematic of electrophysiologic events
for the third and fourth sinus complexes. The third beat on the left shows retrograde invasion
(yellow color) into the AV node and AP, but the AV node can still conduct but with a relatively
long AH interval. The fourth beat on the right demonstrates anterograde conduction over the
AV node, with a shorter AH interval, and the AP, for there was no RV paced beat preceding it.
Anterograde conduction is shown in red.
REFERENCES
1. Engelmann TW. Beobachtungen und Versuche am suspendirten Herzen. Pflugers Arch. 1894;56:149.
2. Erlanger J. On the physiology of heart-block in mammals, with especial reference to the causation of Stokes-Adams
disease. JExp Med. 1905;7:676.
3. Lewis T, Master AM. Observations upon conduction in the mammalian heart. Heart. 1925;12:209.
4. Langendorf R. Concealed A-V conduction: the effect of blocked impulses on the formation and conduction of
subsequent impulses. Am Heart/. l 948;35:542.
5. Langendorf R, Lesser ME, Plotkin P, Levin B. Atrial parasystole with interpolation. Observations on prolonged
sinoatrial conduction. Am Heart/. 1962;63:649.
6. Strauss HC, Saroff AL, Bigger JT Jr, Giardina BG. Premature atrial stimulation as a key to the understanding of
sinoatrial conduction in man. Presentation of data and critical review of the literature. Circulation. 1973;47:86.
7. Prystowsky EN, Grant AO, Wallace AG, Strauss HC. An analysis of the effects ofacetylcholine on conduction and
refractoriness in the rabbit sinus node. Gire Res. 1979;44:112.
8. Miller HC, Strauss HC. Measurement of sinoatrial conduction time by premature atrial stimulation in the rabbit.
Circ Res. 1974;35:935.
9. Steinbeck G, Allessie MA, Bonke FI, Lammers WG. Sinus node response to premature atrial stimulation in the
rabbit studied with multiple microelectrode impalements. Circ Res. 1978;43:695.
10. Bonke FI, Bouman LN, Schopmen FJ. Effect of an early atrial premature beat on activity of the sinoatrial node and
atrial rhythm in the rabbit. Gire Res. 1971 ;29:704.
11. Breithardt G, Seipel L. The effects of premature atrial depolarization on sinus node automati.city in man. Circulation.
1976;53:920.
12. Barker PS, Wilson FN, Johnston FD. The mechanism ofauricular paroxysmal tachycardia. Am Heart J. 1943;26:435.
13. Han J, Malozzi AM, Moe GK. Sinoatrial reciprocation in the isolated rabbit heart. Cin: Res. 1968;22:355.
14. Paulay KL, Varghese PJ, Damato AM. Sinus node re-entry: an in vivo demonstration in the dog. Gire Res.
1973;32:455.
15. NarulaOS. Sinus node re-entry. Circulation. 1974;50:1114.
16. Allessie MA, Bonke FIM. Direct demonstration of sinus node reentry in the rabbit heart. Gire Res. 1979;44:557.
17. Damato AN, Lau SH, Helfant R, et al. Study of heart block in man using His bundle recordings. Circulation.
1969;39:297.
18. Narula OS, Cohen LS, Samet P, Lister JW, Scherlag B, Hildner FM. Localization of A-V conduction defects in man
by recording of the His bundle electrogram. Am J CardioL 1970;25:228.
19. Damato AN, Lau SH, Patton RD, Steiner C, Berkowitz WD. A study of atrioventricular conduction in man using
premature atrial stimulation and His bundle recordings. Circulation 1969;40:61.
20. Wit AL, Weiss MB, Berkowitz WD, Rosen KM, Steiner C, Damato AN. Patterns of atrioventricular conduction in
the human heart. Circ Res. l 970;27:345.
21. Prystowsky EN, Page RL. Electrophysiology and autonomic influences of the human atrioventricular node. In:
Electrophysiology of the Sino-atrial and Atrioventricular Nodes. New York: Liss; 1988: 259.
22. Steinman RT, Lehmann MH. Beat-to-beat changes in atrioventricular nodal excitability and its modulation by
concealed conduction during functional 2:1 block in man. Circulation. 1987;76:759.
23. Klein GJ, Yee R, Sharma AD. Concealed conduction in accessory pathways: an important determinant of the
expression of arrhythmias in patients with Wolff-Parkinson-White syndrome. Circulation. 1984;70:402.
CHAPTER 2 • Electrocardiographic Consequences of Atrial and Ventricular Ectopy SS
24. Langerdorf R, Mehlman JS. Blocked (non-conducted) A-V nodal premature systoles imitating first and second
degree A-V block. Am Hearl]. 1947;34:500.
25. Rosen KM, Rahimtoola SH, Gunnar RM. Pseudo A-V block secondary to premature non-propagated His bundle
depolarizations: documentation by His bundle electrocardiography. Circulation. 1970;42:367.
26. Prystowgky EN, Jackman WM, Rinkenberger RL, Heger JJ, Zipes DP. Effect of autonomic blockade on ventricular
refractoriness and atrioventricular nodal conduction in humans: evidence supporting a direct cholinergic action
on ventricular muscle refractoriness. Circ Res. 1981;49:511.
27. Page RL, Tang AS, Prystowsky EN. Effect of continuous enhanced vaga1 tone on atrioventricular nodal and sinoa-
trial nodal function in humans. Circ Res. 1991;68:1614.
28. Moe GK, Mendez C, Han J. Aberrant A-V impulse propagation in the dog heart: a study of functional bundle
branch block. Circ Res. 1965;16:261.
29. Moore EN. Microelectrode studies on retrograde concealment of multiple premature ventricular responses. Circ
Res. 1967;10:88.
30. Schuilenburg RM. Patterns of V-A conduction in the human heart in the presence of normal and abnonnal A-V
conduction. In: Wellens HJJ, Lie Kl, Janse MJ, eds. The Conduction System of the Heart. Philadelphia, PA: Lea and
Febiger; 1976:485.
31. Moe GK, Childers RW, Merideth J. An appraisal of usupernonnal~ A-V conduction. Circulation. 1968;38:5.
32. Meijler FL, Heethaar RM, Harmg FMA, et al. Comparative atrioventricular conduction and its consequences for
atrial fibrillation in man. In: Kulbertus HE, Olsson SB, Schlepper M. eds. Atrial Fibrillation. Molndal, Sweden:
Hassle; 1981:72.
33. Langendorf R, Pick A. Concealed conduction in the A-V junction. In: Dreifus and Llkoff eds. Mechanism and
Therapy of Cardiac Arrhythmias. New York: Grune & Stratton; 1966:395.
Bundle Branch Block
Eric N. Prystowsk.y, MD
The anatomy of the His-Purkinje system is discussed in Chapter 1. In brief, the His bundle
divides into two major fascicles, the right bundle branch and left bundle branch. The left bun-
dle branch subdivides into the left anterior division, right posterior division, and septal inputs.
Bundle branch block can be permanent (fixed) or functional, that is, present only under cer-
tain conditions. Permanent bundle branch block implies that supraventricular impulses cannot
conduct over that fascicle at any time to activate the ventricle. Ofnote, although we use the term
bundle branch block, an alternative explanation in some patients may actually be very slow con-
duction in the apparently blocked bundle, which prevents the supraventricular impulse from
activating the ventricle early enough in comparison with the other conducting fascicles. Thus,
the electrocardiographic (ECG) pattern will appear as ifblock were present when actually very
slow conduction has occurred. It is not generally possible to make this distinction, and for prac-
tical purposes the term bundle branch block will be used unless it is clearly demonstrated that a
functional conduction delay is present, as discussed later in this chapter.
PERMANENT BUNDLE BRANCH BLOCK

Right Bundle Branch Block
Under normal circumstances, initial activation of the interventricular septum starts on the left
side and proceeds rightward.1 Activation of the right ventricular endocardial surface occurs
at least 5 to 10 ms after activation of the left side of the septum.1 Thus, in a patient with right
bundle branch block. initial activation occurs normally and proceeds from left to right across
the interventricular septum; then activation of the left ventricle occurs and activation of the
right ventricle is last (Figure 1-4, Chapter 1). The ECG representation of right bundle branch
block is shown in Figure 3-1. The duration of the QRS complex is approximately 130 to 140 ms,
and initial left-to-right septal activation results in a small r wave in lead V1, followed by an
S wave reflecting left ventricular activation, and finally by a predominant R' wave representing
activation of the right ventricle. ECG leads I, Vs, and V~ typically demonstrate a wide S wave,
reflecting terminal activation away from the left ventricle (Table 3-1).2
Endocardial catheter mapping of limited sites in the right ventricle was performed by Kastor
et al3 They found that the average interval from the onset of ventric:ular depolamation to
activation of the right ventricular apex, inflow tract, and outflow tract was 18 ms, 23 ms. and
.. ·- I 1 1 I
w -
I "f ' t at
,... I I
'~
I
ll
.. -
~
,... I
"'
Imm
..
·m.., _ I
I
-
:-
•
II I s~
,
.... ... I
-
a aa ., _
...
"
,_ ... - ' I
11-
"' t "\'1
-
FIGURE J-1 • Twelve-lead ECG of right bundle branch block.
I I
- I ,... - -
I I
40 ms, respectively, in patients with normal QRS duration, but it was 54 ms, 49 ms, and 78 ms,
respectively, in patients with right bundle branch block.
The right bundle branch is a subendocardial structure that runs down the right side of the inter-
ventricular septum and is therefore prone to mechanical trauma-for example, catheter-induced
right bundle branch block during electrophysiologic study or passage of a Swan-Ganz catheter.'
Anatomic damage to the right bundle branch has been demonstrated at pathologic examina-
tion of the conduction system in patients with ECG evidence of right bundle branch block."'5 In
one study ofpatients with ECG documentation of right bundle branch block, significant lesions
of the right bundle branch were demonstrated in all patients but, interestingly, total anatomic
disruption was not demonstrated in mosl5 Whether this represents very slow conduction of
the right bundle branch with the inability to activate the right ventricle prior to activation of
the ventricles by the left bundle branch system, as stated earlier, or indeed complete conduction
disruption is not known.
TABLE 3-1 Criteria for bundle branch block.2

Right bundle branch block
QRS duration ;z:O.12 s (120 ms)
V, or V1 : rsr', rsR', rSR'
I and V6 : wide S wave
V,: R peak time >0.05 s (50 ms)
Left bundle branch block
QRS duration ;z:O.12 s
V,, V,,. I, aVL: broad notched or slurred Rwaves
V5, V,,. I: absence of Q waves
V5 andV6 : Rpeak time >0.06 s
CHAPTER 3 • Bundle Branch Block 59
Right bundle branch block (RBBB) is usually associated with organic heart disease. However, it
can occur in apparently normal individuals, and Hiss et al. 6 reported an incidence of right bun-
dle branch block of 1.8 per 1000 in seemingly normal U.S. Air Force personnel. In this study,
the incidence ofRBBB increased with age. 6 Ericksson et al.7 also showed the prevalence ofbun-
dle branch block was greater with advanced age in 855 men followed for 30 years, with 0.8%
and 11.3% in patients aged 50 and 80 years, respectively. The prognosis with RBBB depends on the
presence or absence of associated cardiovascular disease. Rotman and Triebwasser8 reported on
394 people with RBBB at the U.S. School of Aerospace Medicine; during a mean follow-up period
of 10.8 years, new cases of coronary heart disease and hypertension occurred in 6 percent of these
patients, and 4 percent died. Similar observations were reported by Fleg et al.9 The Framingham
study evaluated 70 people who developed complete RBBB during an 18-year follow-up. 10 In this
study, the mean age at the onset of RBBB was 60 years, and in 70 percent of cases at least one
cardiovascular abnormality preceded the onset of RBBB. Cardiovascular mortality was approx-
imately 3 times greater in the patients who developed RBBB than in age-matched persons with-
out RBBB. A recent meta-analysis of the prognostic significance of RBBB concluded that the
presence of RBBB was associated with an increase in all-cause mortality.11 In summary, the data
suggest that mortality is related to the development of organic heart disease and not specifically
to the conduction defect of the right bundle branch.
Left Bundle Branch Block

The sequence of initial ventricular activation is significantly altered in left bundle branch block
(LBBB), and activation occurs first on the right septal surface near the base of the anterior
papillary muscle ofthe right ventricle. Therefore, activation overall will primarily proceed from
right to left, explaining the absence of the normal "septal" Q wave in ECG leads I, V5, and V/
As noted in Table 3-1, the duration of the QRS complex is 120 ms or more and terminal activa-
tion of the epicardial surface of the left ventricle occurs near the posterolateral base {Figure 1-5,
Chapter I).
A 12-lead ECG in a patient with complete LBBB is illustrated in Figure 3-2. Endocardial cath-
eter mapping data from 18 patients with LBBB who had either (1) no obvious organic heart
disease, (2) cardiomyopathy, or (3) coronary artery disease revealed the left ventricular endo-
cardial activation sequence to be variable. 12 However, most of the endocardial surface of the left
ventricle was not mapped in this study, thus precluding more precise determination of left ven-
tricular endocardial activation. The observation of variable activation sequences may explain
the differences noted in the ECG manifestations of LBBB in patients.
Pathology studies in patients with complete LBBB demonstrate destruction of a substantial

proportion of the septal fibers of the left bundle branch.4 Lev et al.13 evaluated the anatomic
basis for the ECG demonstration of complete LBBB in 8 cases, 6 with left axis deviation and 2
with normal axis. The QRS duration varied from 0.12 to 0.20 s, and 7 of 8 patients had athero-
sclerotic heart disease. There was substantial damage at the junction point of the left bundle
branch with the bundle of His in all hearts. Of note, the pathologic findings were similar in
patients with normal axis and left axis deviation.
It is estimated that LBBB occurs in < 1% of the general population. 14 Similar to RBBB, the
prevalence of LBBB increases with age.7.a The prevalence of LBBB was 0.05% in a study of over
200,000 airmen< 30 years old, 90% without apparent structural heart disease.8 In the study of
FIGURE 3-:Z • Twelve-lead ECG of left bundle branch block.
Eriksson et al.,7 LBBB was noted in 0.4%, 2.3%, and 5. 7% of the general population aged 50, 75,
and 80 years old, respectively. Organic heart disease is the rule in patients with LBBB, although
no definable structural heart disease may be present in some individuals.14•15 Hypertension and
coronary artery disease are the most common disorders associated with LBBB. 16-19
The prognosis of patients who have complete LBBB, as with those who have RBBB, depends
on the presence or absence of coexisting heart disease.8•1a. 20 Rotman and Triebwasser8 eval-
uated 125 individuals with LBBB with a mean follow-up of 8.8 years. At entry, 89% of indi-
viduals had no evidence of cardiovascular disease. Coronary artery disease and hypertension
during follow-up occurred in 5% and 8%, respectively, and 8% died. In contrast, data from
the Framingham study revealed that development of LBBB was associated with cardiovascular
abnormalities in most patients, and 50% of patients died from cardiovascular disease within
10 years after LBBB was identified.18 Sudden cardiac death due to ventricular fibrillation and
not heart block has been recognized in patients with cardiovascular disease and LBBB, 19.20 and
this may relate to the severity of heart disease in these patients.
In some patients, the ECG suggests the presence of isolated fascicular block-for example, left
anterior or left posterior fascicular block. Although it has been well-demonstrated that the
endocardial surface of the left ventricular septum is activated by a trifascicular system, the
concept of "hemiblocks" forwarded by Rosenbaum 21 does appear to have ECG correlation. We
prefer the terms kft anterior or left posterior fasdcular block in lieu of kft anterior or left poste-
rior hemiblock.2 Suggested criteria for left anterior fascicular block are (1) left-axis deviation of
-45° to -90°; (2) a qR pattern in ECG lead aVL; (3) an R peak time in lead aVL ~0.045 s; and (4)
QRS duration <0.12 s.2 Because of the superiorly oriented QRS forces, there is often an rS com-
plex in the inferior leads. Recommended diagnostic criteria for isolated left posterior fascicular
I I I I
I I I I I I
I I I~ I II. I I
I I ~
I I
I I .. ·~
, I et I et I et! 1*1m1ct1ct1ct1111 I I I
FIGURE 3-3 • Twelve-lead ECG of right bundle branch block and left anterior fasclcular block.
block are (1) frontal plane QRS axis of +90° to + 180°; (2) rS in ECG leads I and aVL with qR in
inferior leads, with Q waves in leads III and aVF (S1-Q3 pattern); and (3) QRS duration <0.12 s.2
Figures 3-3 and 3-4 are examples of RBBB with left anterior fascicular block and left posterior
fascicular block, respectively, and Figure 3-5 shows LBBB with left axis.
I
.... I
,__ __
' ·.- - v -
--- ,__ __
,_,___ ,__ __ ·'
II
I
·' - I
I
I
a·n I
:.. ·'-
-,-
I I
ml
I I
• I ,_
I - I
-- I ,___ ,__
m
I
I · -.~
l
I
I I
• I
I
I
I
I
I
-- fm
I I I
II I
I
I
I
' ' '
FIGURE 3-4 • Twelve-lead ECG of right bundle branch block with left posterior fasclcu lar block. Note that the patient has 2:1 heart
block, demonstrating the severity of His-Purkinje disease in this patient. A permanent pacemaker was required.
FIGURE 3-5 • Twelve-lead ECG of left bundle branch block with left axis deviation.
Abnormal left axis deviation is not uncommon and in many cases is probably due to left
anterior fascicular block. However, isolated left posterior fascicular block rarely occurs and is
usually associated with RBBB in a patient who has suffered a myocardial infarction. Various
combinations of bundle branch block and fascicular blocks may occur, as noted in Figures 3-3
and 3-5.
FUNCTIONAL BUNDLE BRANCH BLOCK

Premature Atrial Complexes and Bundle Branch Block Aberrancy
Refractoriness of cardiac tissue is cycle length-dependent and for His-Purkinje tissue refrac-
toriness decreases as the cycle length shortens or heart rate increases.22-28 This concept is illus-
trated in Figure 3-6. At a relatively slow sinus cycle length of 950 ms (63/min), a premature
atrial stimulus (S2 ) yielding an H 1H2 interval of 490 ms results in RBBB, as noted by the charac-
teristic rsR' configuration in ECG lead V 1 (Figure 3-6A). Later in the electrophysiologic study,
this patient's heart rate increased to 86/min (cycle length 700 ms). Premature atrial stimuli were
reintroduced and a shorter H 1H 2 of 420 ms conducts without RBBB (Figure 3-6B). Thus, the
faster heart rate caused a decrease in right bundle branch refractoriness.
The effects of changes in heart rate on atrioventricular (AV) nodal refractoriness unrelated to
alterations in autonomic tone are not as predictable. For example, Denes et al. 25 showed that
the effective refractory period of the human AV node lengthened significantly as heart rate
increased. However, in some patients, AV nodal effective refractory period changes minimally
or even shortens with faster atrial paced rates.2s.i6 The typical lengthening of AV nodal refracto-
riness at faster heart rates relates to the slow channel activity of AV nodal tissue compared with
fast channel activity of atrium, ventricle, and His-Purkinje system.
II _ _, __ ""----.1
' .l
1 '
t----950 490----j
Panel A
mmrrirfml'nlfnrmnnTmrm 1llfflTflrfl
II
Ill
HBE
RV
PanalB
f---700
t
I 42~
I ,
l
1
FIGURE 3-6 • Effect of heart rate on right bundle branch block refractoriness. Panel A, A premature atrial stimulus (S,) during a
relatively slow sinus rate results in right bundle branch block. Panel B, A closer-coupled premature atrial complex during a faster
heart rate conducts without right bundle branch block. (See text for detai Is.)
1111 I I I I I I I I I I I I 111111111111111111111111111111
II
Ill
FIG URE 3-7 • Right bundle branch block aberrancy as a consequence of a sudden lengthening of the preceding cycle length
(long-short sequence). The patient has an atrial tachyarrhythmla that was Initiated at electrophyslologlc study. Note that His bun-
dle depolarlzatlons are clearly seen with each conducted QRS complex but are not apparent during the pause between the second
and third QRS complex, which signifies block in the AV node. (See text for details.)
From the above discussion it is apparent why slower heart rates increase the chances for a pre-
mature atrial complex to be conducted with bundle branch block aberrancy. In this situation,
the effective refractory period of the His-Purkinje system tends to be relatively long whereas
refractoriness of the AV node is relatively short-conditions that favor an atrial premature
complex conducting through the AV node and reaching at least part of the bundle branch sys-
tem before recovery from refractoriness. In fact, this was elegantly demonstrated by Moe and
colleagues23 in a classic study of aberrant AV conduction. These authors" noted that premature
atrial stimuli introduced at relatively slow heart rates could conduct through the AV node and
cause RBBB. As the atrial paced rate increased, refractoriness of the right bundle branch sys-
tem became less than that of the AV node, which precluded an atrial premature stimulus from
conducting to the right bundle branch system during its refractory period. The above physi-
ology also explains the relatively frequent finding of bundle branch block aberrancy, usually
right bundle branch block, that occurs during supraventricular tachycardia with variable cycle
lengths. 29.3° Figure 3-7 illustrates RBBB aberrancy during an atrial tachyarrhythmia initiated at
electrophysiologic study. The first 2 QRS complexes are conducted normally to the ventricles.
A relatively long pause ensues due to persistence of AV nodal block (no His deflections on
His bundle lead), and the third QRS complex closes the long pause. The next QRS complex is
conducted with incomplete RBBB aberrancy due to the long preceding pause, which increased
right bundle branch refractoriness, and the subsequent relatively short conducting interval
between the third and fourth QRS complexes (long-short sequence or Ashman phenomenon).
Although LBBB aberrancy can also occur with a long-short sequence, at slower heart rates
refractoriness of the left bundle branch is usually shorter than that of the right bundle branch.27
To complicate matters further, Denker et al.31 demonstrated that cycle lengths of conducted
QRS complexes preceding a pause may also affect the chance for aberrancy after the pause.
In their study, bundle branch aberrancy was facilitated by shorter cycle lengths preceding the
pause, compared with longer cycle lengths. In summary, the chance for bundle branch block
aberrancy to occur during variations in cycle length depends on a critical interplay between the
500
(j)'
.s
"'
400
~
,, ,, ,,
,,
___ , ,,_,,__
~ ..
I
300
,, ,,
I " 6. RBBB
0 LBBB
A <LBBB
200 e <RBBB
o~
500 600 700 800 900 1000
H1 - H1 (ms)
FIGURE 3·1 • Right and left bundle branch block aberrancy at different heart rates. In patients In whom bodi right and left bun·
die branch block aberrancy occurred. the refractory period of die right bundle branch was longer at the slower heart rates, and the
left bundle branch refractoriness was longer at the faster heart rates. Measured on the ordinate Is the H1H2 Interval, which ls the
premature Interval that Is pertinent to the bundle branch system and not the A1Ai interval. The filled circle and filled triangle were
not actual measured points in this study but were postulated from the observations. and the dashed lines represent presumed
shortening of refractoriness of die respective bundle branch systems at different heart rate$. (See text for detalls.) (Reproduced
with permission from Chilson DA et al. Am J c.ardlol. 1984;.545:31 lJ
cycle length preceding a pause, the duration of the pause, and the degree of prematurity of the
R-R interval after the pause.
Patients may demonstrate both LBBB and RBBB aberrancy with a premature atrial complex,
but they usually do so at different heart rates. Chilson and colleagues27 investigated this phe-
nomenon and showed in humans that under usual circumstances the relative refractory period
of the right bundle branch exceeds that of the left bundle branch at slower heart rates, but the
reverse occurs at faster heart rates (Figure 3-8). ln some instances, right and left bundle branch
block aberrancy may occur at a similar heart rate, but LBBB aberrancy almost always occurs
with prolongation of the HV interval, suggesting concomitant conduction delay in the right
bundle branch. Figure 3-9 shows RBBB aberrancy and LBBB aberrancy in a patient with min-
imal change in heart rate. The first 2 QRS complexes are conducted normally and a premature
PR 220 280
p.p 920 420 940
FIGURE 3·9 • Premature atria! complexes with a fixed P.P Interval, producing both right and left bundle branch block aberrancy.
(See text for details.)
1
l l l l I I I I I I I I I l l l l l l l l l l l l I I I I l l l l TT l I I I I I I l l l l l
11 1 11 11 11 11 11 11 11 1 11 1 11 11 1 1 1 11 11 11 11
11---.1·--~
Ill---\..--------------/\.---.. . . .- -
A1
HRA......,1r--~-------------'l~,_.__,,___...u1~~---------
FIGURE 3-10 • Premature atrial stimulus with left bundle branch block aberrancy and prolonged His-Purkinje conduction time.
Note that the H2V2 Interval of the premature complex Is markedly prolonged at 115 ms, representing conduction delay below the
H Is bundle deflection. It Is not possible In this example to diagnose whether conduction delay occurred solely In the dlstal His bun-
dle or in the His bundle and right bundle branch system, but right bundle branch conduction delay was most likely present
atrial depolarization is conducted with RBBB aberrancy. The PR interval of the premature com-
plex is 220 ms, and the P-P interval is 420 ms. Later in the rhythm strip another premature atrial
complex occurs with a similar P-P coupling interval. However, this atrial complex is conducted
with LBBB aberrancy with a PR interval of 280 ms. The prolongation in PR interval most likely
reflects conduction delay in the His-Purkinje system, because there is nothing to suggest any
autonomic perturbation that would prolong conduction through the AV node. Obviously, from
the surface ECG it is impossible to identify the exact reason for prolonged conduction delay,
but prolonged His-Purkinje conduction with LBBB aberrancy is the rule in these situations
(Figure 3-10).
Rate-Dependent Bundle Branch Block Aberrancy

Increases or decreases in heart rate in a particular patient may be accompanied by develop-
ment of bundle branch block aberrancy. 28.32-38 Several terms have been used to describe this
phenomenon, including tachycardia-dependent and bradycardia-dependent block, phase-3 and
phase-4 block, and acceleration-dependent and deceleration-dependent block, respectively. We
favor the terms acceleration-dependent to denote block that occurs as heart rate increases and
deceleration-dependent for block that appears during slowing of heart rate because the actual
heart rates at which block happens may be in the range of normal sinus rates or only relative
bradycardia or tachycardia, as noted below.
Denes et al.33 evaluated 15 patients at electrophysiologic study who demonstrated acceleration-

dependent bundle branch block. Of these, 10 had LBBB and 5 RBBB. Of note, complete LBBB
occurred at a range of cycle lengths from 429 to 800 ms and complete RBBB was noted at cycle
lengths from 450 to 1OOO ms. These ranges of cycle lengths clearly demonstrate that block can
occur in a particular patient at a relatively fast rate but one that is still considered normal sinus
rhythm. A typical finding demonstrated by these authors was a hysteresis curve for the occur-
rence and disappearance of bundle branch block during atrial pacing. In other words, as the
atrial paced rate is progressively increased, bundle branch block appears (e.g., at 100/min); but
FIGURE 3-11 • Acceleration-dependent left bundle branch block. The first ORS complexes In this tracing demonstrate left bundle
branch block aberrancy. Carotid sinus massage was performed and the sinus rate slowed, with concomitant narrowing of the ORS
complex. As the sin us rate increased, left bundle branch block aberrancy reemerged at the end of the rhythm strip.
as the atrial paced rate gradually slows, disappearance of bundle branch block occurs at a paced
rate slower than the rate required to produce block initially (e.g., at 90/min). Similar findings
have been noted by others. 34.35 The reason that bundle branch block disappears at slower rates
than it occurs is not defmitely known, but several explanations have been proposed, including
"fatigue" of the bundle branch during the faster-paced rates that requires some recovery for
normal conduction to occur, or possibly disappearance of concealed transseptal conduction
that was necessary for perpetuation of the bundle branch block at the faster rates (see below).
The exact electrophysiologic mechanism for this hysteresis loop is not known.
Acceleration-dependent bundle branch block appears to occur much more commonly in the
left bundle branch system.33-35 Also, although not universal, the presence ofheart disease is com-
mon in this situation.35 Examples of acceleration-dependent bundle branch block are shown in
Figures 3-11through3-13. In our experience, deceleration-dependent bundle branch block.is
relatively rare compared with acceleration-dependent bundle branch block.
In 40 patients with rate-related intermittent bundle branch block aberrancy, 4 different pat-
terns of recovery from block were characterized by Nau et al.36 These authors evaluated
multiple R-R intervals during bundle branch block aberrancy and resumption of normal
QRS complex conduction. Type A recovery was considered normal and demonstrated a
30- to 50-ms time period as the heart rate slowed where incomplete bundle branch block
occurred. Type B recovery showed a greater range of heart rates over which complete bun-
dle branch block persisted compared with type A, but there was still a short time period of
incomplete bundle branch block prior to recovery of the normal QRS morphology. Type C
was noted to have an extension of heart rates with complete bundle branch block, but no
intermittent bundle branch block was seen prior to normalization of the QRS complex. Type D
was characterized by a prolonged range of heart rates for both complete bundle branch
block and incomplete bundle branch block. In other words, there appeared to be a critical
range of heart rates at which bundle branch block would occur, and this range could be
prolonged either due to complete bundle branch block alone or to both complete bundle
branch block and incomplete bundle branch block. Importantly, the clinical significance
of this observation remains to be determined. In another study from these investigators,37
it was shown that intermittent bundle branch block per se is not predictive of development
of complete irreversible bundle branch block. In fact, the authors present 1 patient with 18 years
of intermittent bundle branch block without development of complete bundle branch block.
Likewise, identification of bundle branch block at one point in time at a specific heart rate
Panel A
=> "'l ...- :i:i = "" ':it'
''" "''" ''., ~ ~ t
hil IC"
"' llW I I 'U tt
!! llW I
::
.I .I , " li
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~
t lt .'=1 f. : ±m
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- -
I
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=-
:1 '11' ·mim:t ff
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" Filf '"' "' ·= oil'#
PanelB
[ :;;;tt;;m
:" :;;
:" :;;
:!!Im"
H+i'4 ~"·"" !! ""'" h...._t Ldt
'tt [tt' [tt'
It tt
tt !! Jmll..
~
if
""""" • "
tt =
:::!l:fiiilf I
"'" m
"I
kH
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* •
,:,::J; tit '" I
'""
,,.
~ '" II
-
PanelC
ta# *"
"'
*" lt 1::
tt tt tt . tt tt
1::
FIGURE 3-12 • Acceleration-dependent left bundle branch block aberrancy during atrial flbrlllatlon. In rhythm strips shown In
Panels A, B, and C, whenever the R-R interval shortens sufficiently, bundle branch block aberrancy occurs and normal ventricular
conduction resumes when the pause is long enough after the last bundle branch block aberrant complex. One must differentiate
this observation from premature ventricular complexes or nonsustained ventricular tachycardia. Analysis of long ECG rhythm strips
usually enables one to do this, and there will be a range of heart rates over which the bundle branch block aberrancy will emerge.
Further, there is no consistent coupling interval between the narrow QRS complex and the first bundle branch block complex, and
grossly irregular R-R intervals are apparent between the aberrantly conducted R-R complexes. All of these strongly favor aberrancy
over ventricular ectopy.
does not confrrm that bundle branch block will subsequently be present, and the presence
of fixed bundle branch block can be confirmed only with multiple ECG observations over a
substantial period of time.
The mechanism of acceleration-dependent bundle branch block aberrancy probably does

not correlate in most patients with the actual duration of the bundle branch action potential.
Rather, it may represent postrepolarization refractoriness-that is, refractoriness that outlasts
the duration of the action potential that can occur in diseased Purkinje tissue.39 If one postu-
lated that acceleration-dependent block was due only to a prolonged duration of the action
potential, then this duration would have to be enormously lengthened in some patients, because
block can occur at relatively slow rates-for example, 60/min {1000 ms). Evidence support-
ing postrepolarization refractoriness as the mechanism for acceleration-dependent block was
presented by Davidenko and Antzelevitch.39 These investigators examined Purkinje fibers in a
I ' 11 11 11 1111 111 I I 1 111 1

''I 11 1111 11111 1 11 I 11 11 11
0 1000 2000
II
Ill J\ /' ~.r-.... r-..... r--.. ,,..
AVF ..J\ ---J\ 4 -A -A A ~
V1
A
Ve "-- I\_ I\_.
"- I\..
HRA
HIS
FIGURE 3-13 • Acceleration-dependent right bundle branch block during atrial pacing at cycle length 360 ms. Note that the first
QRS complex in this tracing represents incomplete right bundle branch block that becomes complete by the third conducted com-
plex. Not shown on this figure are normal QRS complexes that occurred at sllghtly slower-paced rates. As the pacing rate progres-
sively increased, right bundle branch block aberrancy emerged.
sucrose gap model in which a piece of the Purkinje fiber was made progressively inexcitable.
They noted in this model that greater degrees of conduction impairment yielded prolonged
refractoriness, called postrepolarization refractoriness, that extended considerably beyond the
end of the action potential duration. As the rate increased, postrepolarization refractoriness
increased, and this was due mainly to changes in membrane resistance. These observations are
consistent with the clinical findings in humans.
The mechanism for deceleration-dependent block is controversial. Singer et al.40 considered block
due to slow diastolic depolarization during phase four of the action potential that led to inexcit-
ability. Later observations of Antzelevitch et al. 41 suggest that alternative mechanisms exist, and
they showed that slow diastolic depolarization is not a prerequisite for deceleration-dependent
block and in certain circumstances may even facilitate conduction. Although the precise mech-
anism for deceleration-dependent block may differ among patients and may be multifactorial,
Fisch and Miles31 evaluated two patients who demonstrated complete and incomplete LBBB at
variable heart rates; they considered these observations to support the concept of slow diastolic
depolarization as the cause of block.
The development of rate-dependent LBBB can have significant effects on ventricular hemody-
namics and coronary blood flow even in patients with no structural heart disease and normal
coronary arteries. 14•15.42.43 In severe cases, cardiac resynchronization therapy has been shown to
relieve severe dyspnea15 and intractable angina.43
=il:fi~· '"i.... ~l!I! ··~

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... "
•11: •
t••· :::: r:-
.... "' o.'1! •11 ": : I , ..
,, a :"
:
- ..-. '~ t
R -
t
I
'
I I\ ~
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.. l. t
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~-
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.I
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-ill J..
.....,,..
Ii-
~ 3IiL a W$'~.'t.~lli ·ii ~ lit ;J:i'== • ~
'f+ I' 'I'... r ·" r 11 'f': ..t . •''ft 't. L'T' 'I'... r .'I' .'T :T.. ... • 'I' .'T
As I I I I I I I l
s
v. I I I I I I I I I I I I
FIG URE 3-14 • Repetitive bundle branch block aberrancy during atria I tachycardia. {See text for details.) {Reproduced with
permission from Lewis T. The Mechanism and Graphic Registration of the Heart Beat. 3rd ed. London: Shaw and Sons; 1925:256.)
Repetitive Bundle Branch Block Aberrancy

Bundle branch block aberrancy that occurs after a long-short sequence can be repetitive or
persistent, and this has been known for many years.l9 Figure 3-14 is a reproduction of Fig. 251
from Ref. 29 and is a recording of an atrial tachycardia in a child with an atrial rate of290/min.
In this figure, both ECG rhythm strips are displayed on top of a "Lewis" ladder diagram. In
the top strip, the atrial tachycardia undergoes progressive AV conduction delay until the fifth
P wave does not conduct to the ventricle. The subsequent P wave conducts with a relatively
narrow QRS complex, but the next P wave conducts with a wide QRS complex, presumably
because of the preceding relatively long R-R interval closed by a short R-R interval (long-short
sequence). Each subsequent P wave is conducted with a wide QRS complex that is due to bun-
dle branch block aberrancy, and this persists until a P wave fails to conduct to the ventricle.
A similar sequence is noted on the bottom ECG rhythm strip. One needs to explain both the
onset of bundle branch block aberrancy and its persistence. As noted earlier in this chapter, the
long R-R interval produces a prolongation of bundle branch refractoriness due to slowing of
heart rate, and the subsequent atrial complex blocks over one ofthe bundle branches because it
falls within its absolute refractory period. Persistence ofbundle branch block aberrancy may be
explained by 2 different mechanisms (Figure 3-15).
One potential mechanism for persistence of aberrancy is repetitive transseptal retrograde

concealed conduction from the nonblocked bundle into the blocked bundle at a site distal
2 3
Ventricle
2 3 4
PanelA
~ f
400
' 400
2
395
3
390
4
Panel B
FIGURE 3·15 • Potentlal mechanisms for repetitive bundle branch block aberrancy. In the top tracing, the flrst 3 sinus-conducted
complexes demonstrate normal QRS morphology. Rapid atrial pacing was l.tlen Initiated and right bundle branch block aberrancy
occurred for several beats; then normallzatlon of the QRS complex became evident Pan1I A. repetitive transseptal vetrograde con-
cealed conduction. Panel 8, prolongation of action potential duration. (See text for details.)
to anterograde block (Figure 3-ISA-2). In this example, proximal anterograde block occurs
in the right bundle branch and the impulse proceeds to the ventricle over the left bundle
branch system. The impulse then conducts transseptally left to right through the interventric-
ular septum and is able to enter the distal right bundle branch and conduct up to the point of
refractoriness. When this occurs, the right bundle branch refractory period will be prolonged
compared with the left bundle branch because the distal portion of the right bundle branch is
activated later in time than the left bundle branch. Ifthe next anterograde impulse comes soon
enough, it will conduct normally over the left bundle branch but will block once again over
the right bundle branch. This pathophysiologic state can last for long periods of time and is
probably the mechanism in most patients for persistent bundle branch block.aberrancy during
sustained supraventrlcular tachycardia. Transseptal concealed conduction causing repetitive
bundle branch block was demonstrated by Moe and colleagues2:1 in a detailed study of this
phenomenon. Transseptal concealed conduction can also be responsible for persistent LBBB
aberrancy; but in this situation the circuit is reversed, with the initial block occuning in the
proximal left bundle branch.
An alternative mechanism is depicted in Figure 3-lSB. The fust aberrant QRS complex
(number 2) occurs because of the relatively slow heart rate preceding the premature atrial com-
plex, with prolongation of the right bundle branch action potential duration and refractori-
ness. Continued bundle branch block aberrancy is due to persistence of the prolonged action
potential duration. Although we favor transseptal concealed conduction as the cause of sus-
tained bundle branch block aberrancy during supraventricular tachycardia, we think that pro-
longation of action potential duration is the cause of block in those instances in which bundle
branch block aberrancy persists for only several beats. This reasoning is supported by observa-
tions on normalization of QRS conduction:"
The transition from bundle branch block aberrancy to a normal QRS complex due to loss
of transseptal concealed conduction is demonstrated in Figure 3-lSA and supported by the
observations of Moe et al.23 and Wellens and Durrer.45 In this figure, conduction to the ventri-
cle from atrial impulses for QRS complexes 1, 2, 3, and 4 is represented schematically below
the actual ECG tracing. QRS complex 1 is conducted normally, and in this schematic the ven-
tricle is activated over both the right bundle branch and left bundle branch to yield a narrow
QRS complex. Right bundle branch block in QRS complex 2 is caused by a relatively long right
bundle branch refractory period that results from the preceding slow heart rate. The schematic
shows anterograde conduction to the ventricle over the left bundle branch with subsequent
transseptal conduction that penetrates into the distal right bundle branch. This mechanism
persists, resulting in continued RBBB aberrancy. QRS complex 3 is the last one with aberrancy,
and the schematic demonstrates sudden retrograde block into the right bundle branch, which
allows for earlier recovery from refractoriness in the right bundle branch. The next atrial com-
plex can now activate the ventricles over both the right and left bundle branches; therefore, no
bundle branch block aberrancy occurs in QRS complex 4. We do not think this is the mecha-
nism for short runs of bundle branch block aberrancy as noted in V1, but persistent transseptal
concealed conduction as the mechanism for sustained bundle branch block aberrancy is sup-
ported by the observation in Figures 3-16 and 3-17.
Figure 3-16 is an example of atrioventricular reentry with RBBB aberrancy. Note that on the
right ventricular tracing a premature complex (S2) is introduced simultaneously with antero-
grade activation of the His bundle. The next QRS complex is minimally aberrant and the sub-
sequent complexes demonstrate normal QRS conduction, although the heart rate is unchanged.
This observation supports transseptal concealed conduction for the mechanism for aberrancy,
as shown schematically in Figure 3-17. Panel A represents persistent RBBB aberrancy due to
transseptal concealed conduction, with a consequence of continued prolongation of refracto-
riness of the right bundle branch due to late activation of the distal right bundle (b) from ret-
rograde invasion. In Panel B, a premature ventricular complex is introduced after anterograde
block occurs in the right bundle branch but prior to transseptal conduction from the left bun-
dle branch to the distal right bundle branch. In Figure 3-16, the ventricular extrastimulus was
introduced rather late in diastole; therefore, the QRS complex still showed RBBB aberrancy.
In the schematic, an even earlier ventricular extrastimulus is introduced that activates the right
ventricle first with a LBBB morphology, and transseptal activation occurs from the right to left
with even possible retrograde invasion into left bundle branch system (Figure 3-17). Regard-
less, the premature ventricular complex will prevent the transseptal concealed conduction that
would have occurred, and this now allows ample time for recovery of refractoriness in the
right bundle branch. This "peeling" back of the refractoriness of the right bundle branch due to
earlier activation from the right ventricular extrastimulus ends the perpetual sequence of trans-
septal concealed conduction; thus, normalization of subsequent QRS complexes will occur. In
almost all patients in whom a long-short pacing sequence in the electrophysiology laboratory
II
III
V1
V2
v,,
HRA
HBE
RV 290
PCS
DCS
1-200--i
me
FIGURE 3·16 • Termination of transseptal concealed conductton wtth a premature ventrlc:ular ccmplex Introduced during atTlo-
ventrtcular reentrant tachyardla. The first 6 QRS complexes demonstrate right bundle branch .block aberrancy. A premature ven-
tricular complH CS) ls Introduced after activation of the ventricular septum but prior to acthnitlon of the right ventricular apex. This
premature ventricular complex prevents penetration Into the right bundle branch retrogradely from transseptal concealed conduc-
tion and allows for a greater recovery from excltAlblllty of the right bundle branch by the time the next atria! Impulse conducts to
the His bundle. The seventh QRS complex(•) has minimal right bundle branch block abemncy, and the rest of the ORS complexes
are normal. (See Figure 3-17 for a schematic representation of this phenomenon.)
initiates bundle branch block that persists, introduction of 1 or sometimes 2 ventricular extra-
stimuli can normalize the QRS complex, with continuation of tachycardia strongly suggesting
that transseptal concealed conduction is the mechanism in these cases.
Normalization of the QRS complex due to progressive shortening of action potential duration
is illustrated in Figure 3-lSB. QRS complex 2 demonstrates RBBB aberrancy because the atrial
premature complex arrives at the right bundle branch during the absolute refractory period.
A progressive shortening of action potential duration occurs at the newly established faster
heart rate. and there is enough shortening from QRS complex. 3 to QRS complex 4 for the atrial
impulse to conduct over the right bundle branch, normalizing QRS morphology. Evidence
to support progressive shortening of action potential duration as the mechanism for disap-
pearance of aberrancy noted in this figure is shown in Figure 3-18, reproduced from Miles
and Prystowsky.44 In this study. the effect of the duration of the atrial drive train at a new faster
Ventricle
PanelA Pan•IB
FIGURE 3·17 • Schematic representation of a right ventrlcularextrast!mulU$ Introduced during tran$septal concealed conductton
Into right bundle branch retrogradefy that results In '"peeling" back of refractor1ne$$ of the rfght bundle branch with subsequent
ncrmallzatlon cf conductton. In the flgure, tf1e proximal right bundle branch Is represented by•a• and the distal right bundle
branch by•b.• Pan1I A shows anterograde block In "&.:'followed by retrograde activation of the dlstal right bundle noted by•b.•1n
Panel 8, earller activation cf~" occurs with the right ventricular extrastlmulus; therefore, recovery from excltablllty occurs sooner,
resulting in a •peeling•of refractoriness cf the right bundle branch. (See text for details.)
heart rate on right bundle branch refractoriness was studied. Figure 3-18 demonstrates the mean
cumulative shortening of the right bundle branch refractory period at the new faster heart rate.
As can be seen from this figure, the right bundle branch refractory period progressively short-
ened by a mean duration of approximately 15 ms, and one-third of the shortening occurred
within the first 8 complexes at the new heart rate. Thus, it is easy to understand how bundle
15 -
- - -o:7
- 3.5
-
- - -
- 2.9
-
-
-
-
2.9
-
-
-
-
- -
- 5.0
-
-
0
4-8 8 -16 16 - 32 32 - 64 64 - 99
Atrial drive train duration
(number of complexea)
FIGURES·18 • Demonstration of progressive shortening of bundle branch refractoriness over time at a newly estBblrshed faster
heart rate. (See text for details.) (Reproduced with permission from Miies WM et al. arcufatfon. 1986;73:244.}
branch block aberrancy can disappear after several beats at a faster heart rate due to progressive
shortening of the action potential duration in lieu of transseptal concealed conduction suddenly
failing for one complex.
In summary, bundle branch block aberrancy that occurs with a premature interval that follows
a preceding relatively long interval is due to prolonged refractoriness of the blocked bundle
because of the preceding slow heart rate. Sustained aberrant conduction is explained best in
our opinion by transseptal concealed conduction in most instances, whereas normalization
of aberrancy within several complexes at the new faster rate is most likely due to progressive
shortening of action potential duration.
MECHANISMS TO CONVERT WIDE QRS COMPLEX TO NARROW QRS COMPLEX

In most instances, the ECG observation that requires explanation is the mechanism for the
sudden appearance of a wide QRS complex. Just as important, although not as frequently
encountered, is the differential diagnosis for sudden and seemingly unexpected normalization
of the QRS complex in a patient with preceding wide QRS conduction. Table 3-2 lists many of the
mechanisms that explain the sudden transition from wide to narrow QRS complex conduction.
The first 3 mechanisms-change in heart rate, peeling back of refractoriness, and rate-dependent
progressive shortening of bundle branch refractoriness-have been explained in detail in this
chapter; the fourth and fifth mechanisms, dealing with gap phenomenon and supemormality,
are described in Chapter 4.
Intermittent ventricular preexcitation is demonstrated in Figure 3-19. In this patient, during

a constant atrial paced rate, the first and fourth QRS complexes are conducted with a narrow
QRS morphology, but the second, third, and fifth QRS complexes are wide due to conduction
over an accessory pathway. Note in the His bundle lead the easily identifiable His bundle depo-
larization between the atrial and ventricular deflections with narrow QRS complexes, which is
obscured within the ventricular electrogram during conduction over the accessory pathway.
Another mechanism is the occurrence of a premature ventricular complex ipsilateral to the
bundle branch block. This is demonstrated in Figure 3-20 in a patient with right bundle branch
block in whom right ventricular pacing is initiated. The first paced complex results in early
activation of the right ventricle at a time nearly equal to arrival of the sinus complex through
the left bundle branch to activate the left ventricle.
TABLE 3-2 Mechanisms to convert wide QRS complex to narrow QRS.

Change in heart rate
Increase rate (deceleration-dependent block)
Decrease rate (acceleration-dependent block)
•Peel• back refractoriness (transseptal concealed conduction)
Rate-dependent progressive shortening of bundle branch refractoriness
Gap phenomenon
Supemormallty
LDss of preexcitation
Premature ventricular complex ipsilateral to bundle branch block
Equal conduction delay in both bundle branches
I I T 1 I' '1" T '1" I'

1 I
11 1 1 1
I' 1 1 1 1 l l I I I
11 11 11 1 11 11 1
1
11 1
0
1-'"""_...,_..___,. '----"'------:1...---V" "'--- 2000
111------- ___
11---.., ._-._....
v1---"l,.---. ,J_
V2---.A..---
Ve ,..___ __, ~---'""'" _ _ _ _.,,..,_ _ _ ..___ _
CS
FIGURE J·19 • lntermlftent preexdtatton that I$ noted In atrlal paced complexes 2, 3, and 5.The pacing b from the coronary slnU$
(CS). His bundle depolarfz.atlon {H). (See text for details.)
1T'l'l''h I I I 11 I f'r'rm'rm'M'°l f I fim'T'T1 ti f I h rt 1tn11111T1i'T11mr1·111111 I
II
III
V1
HAA "'(I \If
HBE~
RV~~ ''' 00
"' '
0
'
0
J''''' 11111 01 1 ~,& 111111 ~,t, 11111 ~'~
FIGURE 3-20 • Normallzatfon of right bundle branch block morphology with a premature right ventricular stlmulus (S) that acti-
vates the ventTlde almost slmuhaneously with depolarlzatlon of the left ventrlcle by the left bundle branch system. The lest 2 QRS
complexes demonstrate left bundle branch block morphology due to right ventricular apical pacing thilt captures both ventricles.
Thus, the third QRS complex "normalizes" (pseudonormalization), but the mechanism for this
is clearly evident in the last 2 ventricular paced beats that demonstrate a LBBB QRS morphology
consistent with the right ventricular pacing site. Similarly, in a patient with LBBB a left ventric-
ular premature complex critically timed could normalize QRS morphology for that complex.
A more complex mechanism for normalization of the QRS complex, equal conduction delay
in both bundle branches, is illustrated in Figures 3-21and3-22. In Figure 3-21A, a premature
atrial complex (S1S2) is introduced with a coupling interval of 380 ms with a corresponding
H 1H 2 interval of 426 ms, which is the premature interval for the bundle branch system. There
is a very slight alteration of QRS conduction of the premature complex, associated with a min-
imal increase in the His-Purkinje conduction time from a baseline of 44 ms (H 1V1) to 46 ms
(H2V2 ). A closer-coupled premature complex at 340 ms is associated with an H 1H 2 interval of
390 ms and LBBB morphology with marked prolongation of His-Purkinje conduction time
noted by an H 2V 2 interval of 100 ms (Figure 3-21B). The prolonged H 2V 2 interval implies
concomitant conduction delay in the His bundle, right bundle branch, or both. An even more
premature atrial complex of 320 ms conducts with an even shorter H 1H 2 interval of 372 ms,
but the premature complex nearly normalizes (Figure 3-21C). Inspection of the His bundle
electro gram of the premature complex reveals a slightly more prolonged H 2V 2 interval of
102 ms with the emergence of a right bundle potential. The H 2RB2 interval of 68 ms is substan-
tially prolonged, demonstrating conduction delay between the His bundle recording and the
right bundle branch recording. Further, the RB 2V 2 interval of 34 ms is also somewhat delayed.
Thus, normalization of the QRS complex with an even closer-coupled atrial premature interval
is probably due to both gap phenomenon as well as progressive conduction delay in the right
bundle branch, which allows enough time for conduction over the left bundle branch to reach
the ventricle, with resultant normalization of the QRS complex. This concept is illustrated in
Figure 3-22.
In Figure 3-22, a schematic of a premature atrial complex with RBBB is shown in Panel A.
The RBBB could be due to either complete "block" (Panel A-1) over the right bundle branch
or slowing of conduction (Panel A-2) over the right bundle branch with initial activation of
the ventricle from the left bundle branch. It would be impossible to know which mechanism
produced the RBBB pattern on the surface ECG. In Panel B, a premature atrial complex causes
sudden normalization of the QRS complex. In Panel B-1, the mechanism depicted for QRS
normalization is gap caused by proximal slowing of conduction in the His bundle that allows
recovery of excitation in the right bundle branch and subsequent conduction to the ventricles
over both bundle branches with a normal QRS complex. In Panel B-2, the premature atrial
complex conducts without gap to both bundle branches, but marked slowing of conduction
now occurs in the left bundle branch, enabling ventricular activation to occur nearly simulta-
neously over both bundle branches, which results in a narrow QRS complex. In both of these
situations, one would expect a prolonged PR interval, and it would be nearly impossible to
identify whether one or both mechanisms were in part responsible for normalization of the
QRS complex from examination of the ECG only.
In summary, there are many potential mechanisms to explain the sudden and unexpected
normalization of a QRS complex in a patient with a baseline wide QRS complex. However,
knowledge of the potential mechanisms responsible for this phenomenon should allow a cor-
rect diagnosis in most instances.
2000
AVF ......,.._-.11r-----.......-...; i,.._ _,._.....__.,, ,._-~'-----~

V1
H1H2=426
H1V1 =44
H2V2=46
Panel A
0 1000 2000
1 1--~-'1,---~---~- ----...__~~-~------
,....-------------J
11 ..._,,.-._-.1 -~~
Ill ------.J 1.---------------.1 ......._~---'
AVF .......----...;v--------.. . . -J\r---"~-----'

V1 i----'
HBE
Panel B
FIGURE S·Z1 • Normallzatlon of bundle branch block morphology with a very early premature atrlal complex because of equal
conduction delay in both bundle branches and possibly gap physiology. Panel A., atrial premature complex (S) conducu with
nearly normal ORS. Panel 8, atrial premature complex conducts with LB88 morphology. Panel C, earlier atrial premature complex
nearly normal Ires me QRS. (See text for deta!ls.)
0 1000 2000
I ,,..---- /\
II
Ill
AVF
V1
V6
S1 700
HRA
H1H2=372
H2V2= 102
H2RB2=68
RB2V2=34
PanelC
FIGURE3·21 • (Comfnued)
1.
+ 2. 1. 2.
Ventricle
ABB-Block ABB Slowed Gap Equal BB

Conduction Conduction Delay
PlnelA PanelB
FIGURE S-22 • Schematic demonstrating mechanisms for right bundle branch (RBB) blodt as well as nonnallzation of QR5 complex
due to gap or equal bundle branch (88) conduction delay. Panel A, potential mechanisms of RBBB QRS morphology. Panel B,
potential mechilnisms of normalization of ORS morphology. (See text for details.)
REFERENCES
1. Durrer D, van Dam RT, Freud GE, Janse MJ, Meijler FL, Arzbaecher RC. Total excitation of the isolated human
heart. Circulation. 1970;41:899.
2. Willems JL, Robles de Medina EO, Bernard R, et al. Criteria for in~tricular conduction disturbances and pre-
excitation. I Am Coll CardioL 1985;5:1261.
3. Kastor JA, Goldreyer BN, Moore EN, Shelburne JC, Manchester JH. In~tricular conduction in man studied
with an endocardial electrode catheter mapping technique. Circulation. 1975;51:786.
4. Davies MJ, Anderson RH, Becker AE. The Conduction System of the Heart. London: Butterworths; 1983:281.
5. Lev M, Unger PN, Le55er ME, Pick A. Pathology of the conduction system in acquired heart disease: complete
right bundle branch block. Am Heart J. 1961;61 :593.
6. Hiss RG, Lamb LE. Electrocardiographk: findings in 122,043 individuals. Circulation. 1962;25:947.
7. Ericksson P, Hansson PO, Eriksson H, Dellborg M. Bundle-branch block in a general male population: the study
ofmen born 1913. Circulation. 1998;98:2494-2500.
8. Rotman M, Triebwasser JH. A clinical and followup study of right and left bundle branch block. Circulation.
1975;51:477.
9. Fleg JL, Das DN, Lakatta EG. Right bundle branch block: long-term prognosis in apparently healthy men. J Am
Coll CardioL 1983; 1:887.
10. Schneider JF, Thomas HE, Kreger BE, McNamara PM, Sorlie P, Kannel WB. Newly acquired right bundle-branch
block: The Framingham study. Ann Intern Med. 1980;92:37.
11. Xiong Y, Wang L, Liu W, et al The prognostic significance of right bundle branch block: a meta-analysis of pro-
spective cohort studies. Clin Cardiol. 2015;38:604-613.
12. Vassallo JA, Cassidy DM, Marchlinski FE, et al. Endocardial activation of left bundle branch block. Circulation.
1984;69:914.
13. Lev M, Unger PN, Rosen KM, Bharata S. The anatomic substrate of complete left bundle branch block. Circulation.
1974;50:479.
14. Auffret V, Martins RP, Daubert C, et al Idiopathic/iatrogenic left bundle branch block-induced reversible left
ventricular dysfunction. JAm Coll Cardiol. 2018;72:3177-3188.
15. Prystowsky, EN, Padanilam BJ. Cardiac resynchronization therapy reverses severe dyspnea associated with
acceleration-dependent left bundle branch block in a patient with structurally normal heart J Cardiovasc El«troph)'sioL
2019. doi:lO.l ll 1/jce.13840
16. Johnson RP, Messer AL, et al. Prognosis in bundle branch block: II. Factors influencing the survival period in left
bundle branch bloc.k. Am Heart]. 1951;41 :225.
17. Scott RC. Left bundle branch block: a clinical assessment: part I. Am Heart J. 1965;70:535.
18. Schneider JF, Thomas HE, Kreger BE, McNamara PM, Sorlie P, Kannel WB. Newly acquired left bundle-branch
bloc.k: The Framingham Study. Ann Intern Mui. 1979;90:303.
19. Denes P, Dhingra RC, Wu D, Wyndham CR, Amat-y-Leon F, Roaen KM. Sudden death in patients with chronic
bifascicular block. Arch Intern Med. 1977;137:1005.
20. McAnulty JH, Rahimtoola SH, Murphy ES, et al. A prospective study of sudden death in "high risk" bundle-branch
bloc.k. N Engl JMui. l 978;299:209.
21. Rosenbaum MB. The hemiblock.s: diagnostic criteria and clinical significance. Mod Concepts Cardiovasc Dis.
1970;39:141.
22. Mendez C, Gruhzit CC, Moe GK. Influence of cycle length upon refractory period of auricles, ventricles, and A-V
node in the dog. Am JPhysioL 1956;184:287.
branch block. Circ Res. 1965;16:261.
24. Moore EN, Preston JB, Moe GK. Durations of transmembrane action potential and functional refractory periods
of canine false tendon and ventricular myocardium: comparison in single fibers. Circ Res. 1965;17:259.
25. Denes P, Wu D, Dhingra R, Pietra RJ, Rosen KM. The effects of cycle length on cardiac refractory periods in man.
Circulation. 1974;49:32.
26. Prystowsky EN, Pritchett LC, Smith WM, Wallace AG, Sealy WC, Gallagher JJ. Electrophysiologic assessment
of the atrioventricular conduction system after surgical correction of ventricular preexcitation. Circulation.
1979;59:789.
27. Chilson DA, Zipes DP, Heger JJ, Browne KF, Prystowsky EN. Functional bundle branch block: discordant response
of right and left bundle branches to changes in heart rate. Am l CardioL 1984;545:313.
28. Schuilenburg RM, Durrer D. Rate-dependency of functional block in the human His bundle and bundle branch-
Purlcinje system. Circulation. 1973;48:526.
29. Lewis T. The Mechanism and Graphic Registration of the Heart Beat. 3rd ed. London: Shaw and Sons; 1925:256.
30. Gouax: JI., Ashman R. Auricular fibrillation with aberration simulating ventricular paroxysmal tachycardia. Am
Hearl]. 1947;34:366.
31. Denker S, Shenasa M, Gilbert CJ, Akhtar M. Effects of abrupt changes in cycle length on refractoriness of the His-
Purkinje system in man. Circulation. 1983;67:60.
32. Lewis T. Certain physical signs of myocardial involvement. Br Med]. 1913;1:484.
33. Denes P, Wu D, Dhingra RC, Amat-y-leon F, Wyndham C, Rosen KM. Electrophysiological observations in
patients with rate dependent bundle branch block. Circulation. 1975;51 :244.
34. Neuss H, Thormann J, Schlepper M. Blectrophysiological findings in frequency-dependent left bundle-branch
block. Br Heart/. 1974;36:888.
35. Fisch C, Zipes DP, McHenry PL. Rate dependent aberrancy. Circulation. 1973;48:714.
36. Nau GJ, Elizari MY, Rosenbaum MB. Recovery ofimpulse propagation in the bundle branches of the human heart.
The different varieties of phase 3 bundle branch block. In: Rosenbaum MB, Elizari MY, eds. Frontiers of Cardiac
Electrophysiology. Boston: Martinus Nijhoffi 1983:416.
37. Lazzari JO, et al. The "making" ofa bundle branch block. In: Rosenbaum MB, Eliza.ri MV, eds. Frontiers ofCardiac
Electrophysiology. Boston: Martinus Nijhoff, 1983:657.
38. Fisch C, Miles WM. Deceleration-dependent left bundle branch block: a spectrum of bundle branch conduction
delay. Circulation. 1982;65:1029.
39. Davidenko JM, Antzelevitch C. Electrophysiological mechanisms underlying rate-dependent changes of refracto-
riness in normal and segmentally depressed canine Purkinje fibers. Circ Res. 1986;58:257.
40. Singer DH, Lazzara R, Hoffman BF. Inter-relationship between automaticity and conduction in Purkinje fibers.
Gin Res. 1967;21:537.
41. Antzelevitch C, Jalife J, Moe GK. Frequency-dependent alterations of conduction in Purkinje fibers. a model of
phase-4 facilitation and block. In: Rosenbaum MB, Elizari MY, eds. Frontiers ofCardiac Electrophysiology. Boston:
Martinus Nijhoff, 1983:397.
42. Surkova E, Badano LP, Bello R, et al Left bundle branch block: from cardiac mechanics to clinical and diagnostic
challenges. Europace. 2017;19:1251-1271.
43. Czuriga D, Lim PO. Cardiac resynchronization therapy relieves intractable angina due to exercise-induced left
bundle branch block without left ventricular systolic dysfunction: a detailed case study. I Cardiowuc Electrophysiol
2016;27:609-612.
44. Miles WM, Prystowsky EN. Alteration of human right bundle branch refractoriness by changes in duration of the
atrial drive train. Circulation. 1986;73:244.
45. Wellens HJJ, Durrer D. Supraventricular tachycardia with left aberrant conduction due to retrograde invasion into
the left bundle branch. Circulation. 1968;38:474.
Apparent Paradoxical
Conduction
Conduction of premature atrial complexes (PACs) is usually predictable in a patientwith a relatively

constant heart rate. A late (ie., long atrial coupling interval) PAC will conduct to the ventricle and
a relatively early (ie., short atrial coupling interval) PAC often blocks in the atrioventricular (AV)
conduction system. In some instances, however; apparent paradoxical conduction can occur in the
AV conduction system. This happens when a late PAC conducts to the ventricle, an earlier PAC
blocks, but-unexpectedly-a PAC with even a shorter coupling interval again conducts to the
ventricle. Various electrophysiologic phenomena can explain these conduction patterns, but they
are often very difficult to diagnose by surface electrocardiography only. Resumption ofconduction
may occur because of supernormal excitability and conduction, which is probably relatively rare,
but more commonly can be explained by other mechanisms, especially the gap phenomenon. Spe-
cific issues related to the bundle branch conduction system are presented in detail in Chapter 3.
GAP PHENOMENON
Moe and colleagues1 noted in a series of canine experiments that a PAC that did not conduct to
the ventricle could occur .in timing between a later and earlier PAC that did conduct to the ven-
tricle. The unexpected conduction of the earliest PAC was referred to as a gap in AV transmis-
sion. The gap phenomenon was studied by many investigators and several subdivisions of gap
were identified.:i-s However, the basic widerlying electrophysiologic principle for all varieties of
gap is the same and can be described as follows. A relatively late-coupled PAC that conducts
to the ventricle involves transmission through the atria. AV node, His bundle, and all or part
of the bundle branch system (Figure 4-1). When the PAC occurs early enough, it may fail to
conduct to the ventricle due to block either in the AV node or His-Purk.inje system (areas B, C,
and D .in Figure 4-1). In essence, the effective refractory period of the tissue at the site of block
is greater than the functional refractory period of tissue proximal to the site of block. In other
words, an electrical impulse can be conducted through areas proximal to but not distal to the
site of block because of the longer refractory period at that point. Gap occW's when a PAC with
an even earlier premature atrial interval undergoes slowing ofconduction in tissue proximal to
the pmiious area ofblock such that this site of previous block has time to recover excitability and
allow the electrical impulse to conduct to the ventricle.
This seemingly complex electrophysiologic event may be simplified by considering an analogy

that occurs during everyday driving ofan auto.mobile (Figure 4-2). In this figure, the red traffic
Atrium
A AV node
B His
c
FIGURE +1 • Auloventrtc:ular conduc:tton system with levels of potentlal block and conduction delay.
light represents the distal site of block and the automobile the conducting impulse. In the top
panel, as the automobile approaches the red light, there is no decrease in speed, or slowing of
conduction; consequently the car must come to an abrupt stop when it reaches the red light, or
distal site of block. In the bottom panel ofFigure 4-2, the driver of the automobile, recognizing
a red light ahead. slows down so that more time is allowed to elapse before the automobile, or
electrical impulse, reaches the red light. In this instance the car does not need to stop when it
reaches the traffic light, or site of previous blo~ because the slower speed has allowed time for the
light to tum green oi; in electrophysiologic terms, the slower conduction velocity enabled recovery
ofexcitability at the previous distal site of block. Importantly, a PAC may encounter slow conduc-
tion in any tissue proximal to the site of block including atrium, AV node, and His-Purkinje
system, and gap was originally subdivided by the tissue involved in the proximal delay and
FIGURE +z • Amllogy for gap phenomenon. (See text for details.)

CHAPTER 4 • Apparent Paradoxical Conduction 85
1111111111111111111 111111111111i11 1 1; I: :
I /\.._~--- ,~
II II I I I I II I J I I I I I I I I I I I I I I I I I I
I II ~ 11 -~
11 -~~~ Ill -~ 111 -~
111 -~~
V1
V1 ~ v, ~
HRA "S;l~f A1At275

H1H2 305
HRA "S;l~Y,. ._A_"2
, _285___
H1H2 315
. I, A 'llfk _.'\ H
HBE P~l -Y1~
85
.
HBE ~+B~~80 110
PanelB PanelC
FIGURE 4-3 • Gap with dlstal block In the Hls-Purklnje system and proximal delay In the alTlum. (See text for detalls.)
distal block site. In our opinion, differentiation into specific types of gap is artificial, serves no
useful purpose. and belies the underlying fundamental elearophysiologic property common to
all fonns of gap phenomenon.
An example ofgap physiology with proximal conduction delay in the atrium is shown in Figure4-3.
In Panel A, a premature (S1S:i.) stimulus with an interval of 250 ms is introduced into the right atrium
after 8 paced atrial complexes ($1) at 500 ms (120/min). This PAC results in conduction to the ven-
tricle with some conduction delay in the left bundle branch system. Note that although the S1S:i. is
250 ms, there is considerable local atrial conduction delay or latency between the ~ stimulus and
the next atrial electrogram, resulting in an ~A,. interval of 285 ms as measured on the His bundle
lead. In Panel B, the S1S2 interval is shortened by 10 ms with a corresponding ~A,. of275 ms, and
the PAC conducts through the AV node with an atrio-His (AH) interval ofl 10 ms, but block occurs
after the recorded His potential Thus. distal block in this instance is in the His-Purkinje system
(level C or Din Figure 4-1). A further shortening of the premature interval to 230 ms (Pand C of
Figure 4-3) results in resumption ofconduction of the PAC to the ventricle. This apparent paradox-
ical conduction is explained by increased proximal conduction delay from the site ofthe premature
stimulus (SJ to the local atrium and subsequently to the atrial tissue near the AV node (level A in
Figure 4-1). Even though the S1S1 interval is shortened to 230 ms, the resultant A1A,. interval is
285 ms, comparable to that noted in Panel A, and conduction can resume because the proximal
delay ofconduction in the atrium allows recovery ofexcitability in the His-Purkinje system.
Another type of gap is noted in Figure 4-4. In this example, the site of distal block is in the
His-Purkinje system (Figure 4-4A; level C or Din Figure 4-1). The right atrium is paced at a
cycle length of700 ms (86/min) and a PAC is introduced at a coupling interval of360 ms. The
resultant H1H1 interval is 396 ms and block occurs below the recorded His potential (H1).
A closer-coupled PAC with an S1S2 interval of 330 ms conducts to the ventricle (Figure 4-4B).
The H1Ha interval remained the same at 396 ms, but there was a marked delay in His-Purkinje
conduction, with the premature complex, resulting in an~V2 interval of 124 ms (normal
~ 55 ms). As is usually the case in these instances, the QRS complex demonstrates some form
of aberrant conduction, left bundle in this instance. Thus, the site of proximal delay for gap to
occur in this example is somewhere distal to the recorded His potential but still within the His-
Purkinje system Oevel D or lower part of C in Figure 4-1).
The AV node is often the proximal site of conduction delay in gap physiology. Although
subtle changes in vagal tone imposed on the AV node may account for a sudden prolonga-
tion in AV nodal conduction time, as demonstrated by Mazgalev et al.,6 we think this is not
necessary to explain AV nodal gap in most instances. Typical AV nodal behavior is for clos-
er-coupled PACs to engender more AV nodal conduction delay. Thus, if a PAC produced
block in some part of the His-Purkinje system, an earlier PAC would be expected to prolong
AV nodal conduction time; if the resultant slowed conduction was sufficient to allow recov-
ery of excitability in the His-Purkinje system, gap would occur without any alteration in
autonomic tone. Regardless, it is still possible in certain instances for autonomic influences
to play a role in gap physiology. Examples of gap in the AV node are shown in Figures 4-5
and4-6.
Figure 4-SA is taken from a patient with left bundle branch block who underwent pacing of
the right atrium at cycle length 600 ms (100/min). and a premature atrial interval of 350 ms
demonstrates block below the recorded His potential. The H1~ interval is 362 ms. Premature
0 1000 2000
11 r - - - - - - - J
Ill r - - - - - - - . J
AVF r - - - - - - - 1
V8 r - - - - - -........ ~~----...-----..J1....--~~------------1
H1H2396MS
HIS
PlntlA
FIGURE 4-4 • Gap with distal block in the His-Purkinje system and proximal delay also in the His-Purkinje system. (See text f'or
details.)
0 1000 2000
II
Ill
AVF
V1
V6
H1H2396MS
700 330 H2V2124MS
HRA
81 S2
HIS
Panel B
FIGURE+4 • (Conrtnued}
atrial stimuli were initiated at progressively shorter coupling intervals, and at an S1S2 of 310 ms,
conduction of the PAC to the ventricle suddenly reappeared (Figure 4-SB). In this example,
AV nodal conduction delay of the PAC is substantial, with an A,H2 interval of 200 ms and
a subsequent H 1~ interval of 456 ms. This marked increase in AV nodal conduction delay
of the PAC allows for a longer H 1Hl interval, and recovery of excitability has occurred in the
His-Purkinje system Oevel D or lower C in Figure 4-1). Figure 4-6 demonstrates a variant of
this type of gap physiology. In Panel A, the PAC with an A1.A, interval of 280 ms conducts to
the His bundle with an H1~ interval of 310 ms, but block occurs in the right bundle branch.
A closer-coupled PAC with an A1.A, interval of 255 ms (Panel B) produced AV nodal delay,
noted by the increase in~!\ interval and subsequent increase in H1H2 interval to 320 ms. At
this H1fia interval, which is greater than that noted in Panel.A, conduction through the right
bundle branch occurs with normalization of the QRS complex.
Gap phenomena have also been described during retrograde conduction through the ventric-
uloatrial conduction system.' In our experience of introducing premature ventricular com-
plexes as part of the routine electrophfiiologic study of patients, we have rarely encountered
this phenomenon in the absence of pacing the ventricle and introducing extrastimuli. Thus,
although retrograde gap occurs as noted in Figure 4-7, its spontaneous occurrence is probably
rare. In contrast, we have often noted gap physiology during introduction of premature atrial
complexes during sinus rhythm.
0 1000 2000
I
II
Ill
AVF
V1
V6
350
HRA S1 81 $2
H1H2362MS
HBE
Panel A
0 1000 2000
I
II
Ill
AVF
V1
V6
310
HRA 81 S1 S2
H1H2456MS
HBE
PanalB
FIGURE 4-5 • Gap with dlstBI block belOW' the recorded His potentlal and proximal delay In the AV node. (See text for detallsJ
II
Ill
HBE
RV --+~~~~~-t-~~J'-t--~--i11 ~~~
PCS ---4,_,r_,,.i.--~---+-"1'---'Jv+--'li\---11.--~~
DCS ~~~~~~--jr-~-.-~~~~
1-t
200ms
PanelA. Panel B
FIGURE 4-6 • Gap wfd'I dlstal block In the right bundle branch and proxlmal delay In the AV node. (See text for details.)
SUPERNORMAL CONDUCTION
Supernormal conduction has been studied in detail by analysis of action potential characteris-
tics in vitro as well as in some in vivo canine experiments.*"11 These basic investigations demon-
strated a brief time period of improved tissue conduction and excitability that occurs near
V1 -v-v-- ~
~u
HRA
HBE~
600 280 270
RV S
1-200;
s ~ ~
ITl8
PanelA. Panel B PanelC
FIGURE 4-7 • Retrograde gap physiology during right ventTlcular padng and premature stlmulatlon. In Panel A, the right ven-
tricle is paced crt a cycle length of 600 ms and a premature interval of 290 ms yields retrograde conduction to the atTium with a
retrograde His potentlal (H;) followed by an atrial potential CAJ. In Panel 8, shortening of the premature interval to 280 ms results
In retrograde block to the His bundle and attlum. Ashorter premature Interval of270 msec: (Panel C) Is associated with resumption
of conduction to the atrium. careful measurement of the Interval from the premature sUmulus to d'le H1 deflection reveals prolon-
gation of the S2 H2 Interval compared with the S1S1 of290 ms noted In Panel A Because there Is no measurable delay between the
stimulus and local venttlcular recording, this most llkely represents retrograde conduction delay In the Hls-Purkinje system proxi-
mal to the previous site of block. which allows resumption of conduction to the His bundle and subsequendy to the atrium.
the end of the transmembrane action potential repolarization, or phase 3, and the mechanism
appears to be voltage-dependent, occurring when the threshold potential has recovered more
completely than the membrane potential. Such findings cannot be discerned in analyzing elec-
trocardiographic (ECG) tracings or even intracardiac electrograms. Thus, in clinical terms,
supernormal conduction may be defined as propagation ofan electrical impulse at a time when
the tissue would be expected to be refractory to conduction.
The mechanism for supernormal conduction in humans is unclear, and it most likely represents
many possible electrophysiologic events at the basic level. For example, when it has been identi-
fied in His-Purkinje tissue, abnormalities of baseline His-Purkinj e conduction are usually pres-
ent, and it is often demonstrated after long intervals when repolarization of the tissue would
have been expected to be complete.12 Similar observations occur with supernormal conduction
over accessory pathways in patients with Wolff-Parkinson-White syndrome. 0 · 14 In addition to
electrophysiologic events that occur during phase 3 repolarization of an action potential, the
mechanism for supernormal conduction in some individuals might be linked to discontinuous
propagation of an impulse through anisotropic cardiac tissue-that is, muscle in which fiber ori-
entation occurs in more than 1 direction. 15 Importantly; there are many other electrophysiologic
mechanisms in humans that can account for most cases of apparent supernormal conduction-
for example, gap physiology-and these should always be considered when entertaining this
diagnosis. 1.,. 17
An example of supernormal conduction over an accessory pathway is demonstrated in

Figure 4-8. In this patient, the right atrium was paced for 8 beats at cycle length 600 ms
{100/min). In Panel A, a PAC with a coupling interval of 560 ms conducts to the ventricle
over the accessory pathway, which also conducts during the basic pacing drive train. Note that
the QRS complex in the surface ECG leads is wide, and the intracardiac His potential record-
ing occurs after the onset of the surface ECG delta wave. Further, the His bundle electrogram
advances into the QRS complex with the PAC without any change in the interval between the
atrium and QRS complex (A2V). These findings are typical for conduction over an accessory
pathway that connects the atrium and ventricle. As the coupling interval of the premature stim-
ulus is shortened to 540 ms (Panel B), the PAC conducts to the ventricle with block over the
accessory pathway, as can be identified by the narrow QRS complex in the ECG and the His
bundle deflection that now precedes the QRS complex by a normal interval. In Panel C, a
closer-coupled interval continues to block over the accessory pathway; but in Panel D, with a
PAC interval of 430 ms, conduction over the accessory pathway suddenly and unexpectedly
resumes. There is no measurable slowing of proximal conduction as occurs in gap physiology,
and the A2V 2 intervals in Panel A and Panel D are identical. Thus, the most likely explanation
is supernormal conduction, although the exact electrophysiologic mechanism for this cannot
be determined. A graph of conducted and nonconducted atrial impulses over the accessory
pathway is shown in Figure 4-9. Note that all preexcited QRS complexes have an identical~V 2
interval and there is a distinct window of block over the accessory pathway interposed between
earlier and later PACs that conduct over the accessory pathway.
An example of supernormal conduction in the ventricle is demonstrated in Figure 4-10. This is

a patient with an implanted permanent ventricular demand pacemaker that has a sensing mal-
function. During long periods of observation, a repetitious pattern of ventricular capture by the
pacemaker occurred (Figure 4-11). The QT interval in this patient was approximately 480 ms,
1111111 11111111 111111111111 1111111 l I I I 11111111111111111 11111111111111111111 II1
111 - - - -
v, ~\'-..J__f~
HRA "t~r A.. 560
HBE~lrffi~P
Panel A Panela
8tl~,H~7"'F~,
i''"i~
I .
'~tr1t'1t··
~ i
Pa..1c PanelD
FIGURE f f • Supernormi11ainductlon over an i1Ccessory pithwiy. (See text for detallsJ (Reproduced with permission from
Chang MS et i11. NrlJCardio/. 1987;59'.852J
400
300 0
0
100
•
0
·····- ·-·
preeidted
non pramccllBd
FIGURE 4-9 • Graph of1trloventtlcular conduction over
ttte accessory pathway with pl'l!e>edt.aUon or aver ttte normal
conduction system without preexcltatlon. Note ttte constlnt
A,V2 lntrrvals of p~ltrd mmpleiaes. There Is some overlap
300 400 500 600 of supernorm~ conduction wlttt block over the accessory
pathway. (Reproduced with permission from Chang MS et al.
At ~ lnlBrval (ms) Am J Cardlol. 1987;59'.852.)
FIGURE 4-1 O • Possible supernormal excitability and conduction in the ventricle. Note that the sixth and ninth QRS complexes are
ventricular-paced and capture of the ventricle occurs only when the stimulus is positioned near a critical point on the descending
lfmb of the Twave. (See text for further details.)
CID 0 0 0
I I I I I I I I
0 100 200 300 400 500 600 700 800 900
ORS-Stimulus, ms
FIGURE 4-11 • Graph of the relationship of pacemaker capture of the ventricle to the QRS-stimul us interval of the pacemaker
spike. QT= 480. (Key: o, no capture; e, capture.)
and the pacemaker captured the ventricle only during a very distinct QRS to stimulus interval
near the end of the T wave of the QRS complex (Figures 4-10 and 4-11). This portion of the
QRS complex occurs during phase 3 repolarization, and this observation is consistent with
supernormal conduction, although other mechanisms are not totally excluded.
REFERENCES
branch block. Cire Res. l 965;16:261.
2. Wit AL, Damato AN, Weiss MB, Steiner C. Phenomenon of the gap in atrioventricular conduction in the human
heart. Gire Res. 1970;27:679.
3. Akhtar M, Damato AN, Batsford WP, Caracta AR, Vargas G, Lau SH. Unmasking and conversion of gap phenom-
enon in the human heart. Circulation. 1974;49:624.
4. Agha AS, Castellanos AJ, Wells D, Ross M, Befeler B, Myerburg RJ. l)rpe I, type II, and type III gaps in bundle-
branch conduction. Circulation. 1973;47:325.
5. Wu D, Denes P, Dhingra R, Rosen KM. Nature of the gap phenomenon in man. Circ Res. 1974;34:682.
6. Mazgalev T, Dreifus LS, Michelson EL. A new mechanism for atrioventricular nodal gap-Vagal modulation of
conduction. Circulation. 1989;79:417.
7. Akhtar M, Damato AN, Caracta AR, Batsford WP, Lau SH. The gap phenomena during retrograde conduction in
man. Circulation. 1974;49:811.
8. Weidmann S. Effects of calcium ions and local anesthetics on electrical properties of Purkinje fibers. f Physiol
(London). 1955;129:568.
9. Dominguez G, Fozzard HA. Influence of extracellular K+ concentration on cable properties and excitability of
sheep cardiac Purkinje fibers. Circ Res. 1970;26:556.
10. Spear JF, Moore EN. Supernormal excitability and conduction in the His Purkinje system of the dog. Gire Res.
1974;35:782.
11. Childers RW. Merideth J, Moe GK. Supemormality of Bachmann's bundle: an in vitro and in vivo study in the dog.
Circ Res. 1968;22:363.
12. Levi RJ, Salerno JA, Nau GJ, Elizari MV, Rosenbaum MB. A reappraisal of supernormal conduction. In:
Rosenbaum MB, Elizari MV, eds. Frontiers of Cardiac Electrophysiology. Boston: Martinus Nijhoff; 1982:427.
13. Chang MS, Miles WM, Prystowsky EN. Supernormal conduction in accessory atrioventricular connections. Am l
CardioL 1987;59:852.
14. Przybylski J, Chiale PA, Sanchez RA, et al. Supernormal conduction in the accessory pathway of patients with
overt or concealed ventricular preexcitation. J Am Coll CardioL 1987;9: 1269.
15. Spach MS, Dolber PC. The relation between discontinuous propagation in anisotropic cardiac muscle and the
"vulnerable period• of reentry. In: Zipes DP, Jalife J, eds. Cardiac Elec1rophysiology and Arrhythmias. Orlando,
Florida: Grune 8r Stratton; 1985:241.
16. Moe GK, Childers RW, Merideth J. An appraisal of "supernormal" AV conduction. Circulation. 1966;38:5.
17. Gallagher JJ, Damato AN, Varghese PJ, Caracta AR, Josephson ME, Lau SH. Alternative mechanisms of apparent
supernormal atrioventricular conduction. Am l CardioL 1973;3 l :362.
Mechanisms of Tachycardia
George J. Klein, MD
The basic scientist is able to explore mechanisms experimentally in a controlled and rigorous
fashion that can never be duplicated by the clinical electrophY5iologist. On the other hand, the
clinician is dealing with the actu.al pathologic entity and does not have to be concerned with the
clinical relevance of the model. Basic and clinical information are complementary to the stu-
dent of arrhythmias. The following will attempt to summarize basic tachycardia mechanisms,
emphasizing highlights of interest to clinicians.
CLASSIFICATION OF TACHYCARDIA MECHANISMS

Tachycardia mechanisms have been traditionally classified as due to disorders of impulse for-
mation, impulse conduction, or combinations of the two {Table 5-1).1
Abnonnal Impulse Fonnation

Normal automotfclry.'
All impulse formation results from loc:alized changes in ionic currents that traverse cell mem-
branes. The natural pacemaker cells exhibit a ph.asic, spontaneous depolarization during diastole
(phase 4), which results in an action potential when threshold potential is reached (Figure 5-1).
These cells are found in the sinus node. parts of the atria, the atrioventricular (AV) junctional
region, and the His-Purkinje system. In the normal heart. the sinus node is the dominant pace-
maker, because it depolarizes most rapidly and remains dominant due to "overdrive suppression"
of the subsidiary pacemaktrs.4 Subsidiary pacemakers may become dominant under certain
conditions, such as sympathetic stimulation or ischemia. Digitalis may enhance the automaticity
ofsubsidiary pacemakers by inhibiting extracellular Na+ transport that promotes ea2+entry into
cells. By definition, automaticity can neither be initiated nor terminated by pacing techniques.
Abnormal automat/clty
Normal working muscle remains at a high negative resting membrane potential in the range
of -90 mV. depolarizing only when stimulated. Under certain conditions (such as electrolyte
imbalance or ischemia), the action potential is transformed to one with a reduced membrane
potential (range of-60 mV), resembling a "slow response" action potential typical of natural
pacemaktr cells (Figure 5-2). Such cells may exhibit spontaneous phase 4 depolarization5 and
have been demonstrated experimentally such as with canine Purkinje fibers surviving myocar-
dial infarction. Like normal automaticity, abnormal automaticity cannot be induced by pro-
grammed stimulation. In contrast to normal automaticity, abnormal automaticity does not tend
Normal automaticity Reentry Conduction and automaticity (e.g ~ parasystole)

Abnormal automaticity Reflection
Triggered activity
to be suppressed by overdrive stimulation, and this provides a useful clinical distinction of

the 2 mechanisms. This may be related to the fact that abnormal automaticity tends to involve
more Ca2+-dependent action potentials not affected by activation of the Na+ /K+ pump felt to be
causative in overdrive suppression of normal automaticity.6
+20
0
0
-20 0
-20
-40
--40 0
--60
-60
-80
-80 4 PanelB
-100
Panel A 100 ms
1--------i
0
-20
-40
+20 -60
0 -80
100 ms
-20 1--------i
0
--40
0
-20
-60
-40
-80 4
-60
-100
PanelC PanelD
FIGURE 5-1 • Action potentials from typical ventrlcu lar (Panel A), slnoatrlal node (Panel BJ, and atria I (Panel q cells. Cells with
Intrinsic automatfclty show clear spontaneous depolarization during phase 4, typlcal of the SA node. Panel D Is a representation of
the major mechanisms responsible for changes in frequency of depolarization of a fiber with normal automaticity. A decrease in the
slope of phase 4 (a to b) in the upper trace reduces frequency. A lowering (less negative) of threshold potential, TP-1 to TP-2, in the
lower trace also prolongs cycle length, as does an increase in resting potential from a to d. (Reproduced with permission from
Hoffman BF, Cranefleld PF. ElectrophysiologyoftheHeart. Mount Klsco, New York: Futura; 1976.)
CHAPTER 5 • Mechanisms of Tachycardia 97
T20
..._j mV
50ms
T10
..._Jmv
SOO ms
Panel A PanalB
FIGURE 5·2 • Abnormal automatlclty In an atrlal fibre. Panel A shows an actlon potentlal and the first derivative (dv/dt) from a
normal atrial flber. It has a high (--80 mV) resting potential and no spontaneous depolarization. Panel Bis a record from diseased
human atrium. Spontaneous diastolic depolarization is occurring from an abnormally low (-40 mV) resting potential. (Reproduced
with permission from Rosen MR et al. Am Heart J. 1975;89:665. e Elsevier.)
Triggered activity-early after-depolarizations (EADs)

Triggered activity is defined as pacemaker activity that requires at least 1 preceding impulse or
action potential.7 Triggered activity is caused by after-depolarizations-subthreshold depolar-
izations occurring during repolarization (early after-depolarization [EAD]) or after repolariza-
tion is complete (delayed after-depolarization [DAD]).
EADs occur during repolarization of action potentials from a normal resting membrane
potential (approximately-90 mV).3•4 They appear as a positive deflection during repolarization
(Figure 5-3). They may reach threshold potential for activation of the slow inward current
and result in a second action potential. Repetitive rhythmic activity may occur, continuing
until repolarization is completed to a point where the initiating action potential is nearer to
' ' ' \
Panel A PanelB
FIGURE 5-3 • Early after-depolarizations in canine Purkinje fibers exposed to 4 mM K+Tyrode's solution. Panel A shows a second
upstroke arising from an EAD (unfilled arrow) and a second EAD during repolarization (solid arrow) after a brief exposure to norepi-
nephrlne. Panel B shows another preparation where the EAD gives rlse to repetitive rhythmic activity from a low membrane poten-
tlal. The maximum dlastollc potentlal was -84 mV In Panel A and --87 mV In Panel B. Time lines occur every second. (Reproduced
with permission from Zipes DP et al, eds. The Slow Inward Current and Cardiac Arrhythmias. Springer Netherlands; 1980;437.)
its normal resting potential. Thus, single ("fixed coupled"), repetitive, or sustained activity can
occur. A variety of experimental conditions including hypoxia, mechanical injury, ischemia,
hypokalemia, aconitine, cesium, catecholamines, and antiarrhythmic drugs (sotalol, quinidine,
N-acetyl procainamide) have been associated with EAD. The unifying theme in many of these
experimental preparations is the increase in the time course of repolarization, which favors
occurrence of EAD.
It is difficult to prove EADs as a mechanism in clinical arrhythmias. They may be suspected

in arrhythmias associated with prolonged repolarization (long QT), especially if they are
bradycardia-dependent.8 Pacing at more rapid rates should diminish or abolish BAD-dependent
arrhythmias, since this usually decreases action potential duration. Arrhythmias resulting from
EAD would be expected to exhibit slowing of the heart rate prior to spontaneous termination,
because this is usually observed in experimental preparations. There is some evidence that the
syndrome of QT prolongation and polymorphic ventricular tachycardia (torsades de pointes)
initially described by Francois Dessertenne is related to EADs, especially the bradycardia-
dependent variety associated with many antiarrhythmic agents, such as quinidine.9 Arrhythmias
associated with this syndrome "fit" the experimental model in their behavior, and potentials
resembling EAD have been recorded by monophasic action potentials in individuals. 10
Triggered activity-delayed after-depolarizations (DADs)
Delayed after-depolarizations (DADs) are oscillatory depolarizations that are dependent on a
preceding action potential and occur after completion of repolarization,4. 11•12 Triggered activity
may be seen in atrial, ventricular, or Purk.inje cells. A unifying mechanism in experimental
models is a build-up and oscillation of intracellular calcium concentration (for example, dig-
italis toxicity, potassium-free environment, or high-catecholamine environment). DADs have
also been recorded in disease models such as human atrial myocardium and surviving Purk.inje
fibers in infarcted canine myocardium.4 DADs may be subthreshold and initiate a triggered
impulse only when their amplitude reaches threshold.
The response of DADs to stimulation techniques is variable, but a few generalizations can be
made.13•14 Increasing the rate of stimulation or the prematurity of extrastimuli will increase the
amplitude of DADs, increasing the probability of inducing tachycardia (Figure 5-4). The time
to the emergence of the first triggered response decreases as the cycle length of the drive short-
ens (faster drive, earlier coupling of first tachycardia beat). The cycle length of the first triggered
beat after an extrastimulus is, in contrast, more variable. In some preparations, the cycle length
of tachycardia rate varies directly with the cycle length of the inducing drive.
Triggered rhythms will terminate reproducibly with overdrive pacing at a sufficiently rapid rate
but will frequently persist for several cycles after cessation of pacing. DADs have been impli-
cated though not proven in clinical arrhythmias due to digitalis toxicity, 15 torsade de pointes
associated with adrenergic-dependent QT syndrome, and some types of idiopathic VT in
patients with "normal" hearts, especially "right ventricular outflow" VT induced by exercise. 16. 17
Abnormal Conduction
Classical reentry
Normally, a cardiac impulse is transmitted from the sinus node to its final destination, leaving
a wake of refractoriness, and is then extinguished. Under specific circumstances, the propagat-
ing impulse may detour from its destined path and return to a previously depolarized area to
J
Panel A
:1 c
PanelB
1000 ms
FIGURE 5-4 • Effect of prematurity on after-depolarization amplitude. The preparation is canine coronary sinus super fused with
Tyrode's solution containing norepinephrine. Panels A to C show progressive prematurity of an extrastimulus after a drive. Progres-
sive prematu rlty results In Increasing amplltude of the after-depolarlzatlon (delayed) untll repetitive activity ls triggered ln Panel C.
(Reproduced with permlsslon from Wit AL et al. Clrc Res. 1977;41 (4):434-445.)
re excite it (reenter) if it has recovered excitability. An autonomous rhythm can then result if this
sequence is repetitive.
It is useful to classify reentry into two categories. The first is classical reentry as described by
Mines; 18 it is also called ordered reentry by Hoffman and Rosen19 or reentry utilizing an ana-
tomic obstacle. The second category is reentry without a clear and constant anatomical circuit
where the circuit is variable from beat to beat and may be influenced by anatomic obstacles
and facilitating factors but is complex with multiple waves, some variable and some apparently
fixed. 19.20
Reentry may be initiated or sustained by rapid foci such as from pulmonary veins. This is
exemplified by atrial and ventricular fibrillation. It is fair to say that the mechanism of such
arrhythmias remains very controversial with the role of random reentry, leading circle reentry,
spiral waves, or rotors 21-23 still remaining to be verified.
Classical reentry involves a relatively constant anatomic pathway, a concept described lucidly
by Mines18 in studying isolated strips of cardiac muscle cut into rings. The frequently repro-
duced hypothetical circuit (Figure 5-5) illustrates the fundamental features. Establishment of
reentry in this model requires unidirectional block, slow conduction in an alternate pathway,
and return of the impulse to the original pathway after it has recovered excitability. The estab-
lished circuit may be thought of as a revolving wave with an advancing "head" and a "tail"
with relatively refractory and absolutely refractory portions. A "gap" (excitable gap) between
Panel A PanelB PanelC PanelD
FIGURE 5-5 • Traditional model of classic reentry with an anatomic obstacle. The impulse passes through a hypothetical conduit
via 2 pathways, a and ~.which meet at a common exit point (Panel A). Because a and ~ have different refractory properties, a hypo-
thetical extrasystole could be blocked In~ pathway (unidirectional block), conduct slowly over a pathway, and •reenter• ~pathway
retrogradely (Panel B).This could resu It in sustained circus movement (Panel C). In Panel D, you will note that the entrance and exit
from the circuit are anatomically distinct, i.e., there is no "upper common pathway.•
the head and tail reflects a "margin of safety" for the circuit that would be extinguished if the
head collided with the tail. Thus, stability of the circuit is promoted by slowing conduction
vdocity, shortening refractoriness, or increasing the anatomic dimensions of the circuit. Anti-
arrhythmic medications may cause "incessant" tachycardia by shortening refractoriness (very
unusual), slowing conduction, or both, thereby stabilizing a potential circuit. The anatomic
pathway length must accommodate the "wavdength" of the circuit. It is clear that the pathway
length must exceed the average conduction vdocity (CV) and refractory period (RP) of the
circuit to sustain reentry (anatomic length> CV x RP). Ultimate proof of reentry in such a
circuit is the demonstration that interrupting any obligatory part of the circuit terminates
tachycardia.
Slow conduction is possible in normal and diseased myocardium. It is physiologic in the AV

node, which is largely dependent on "slow channel" conduction. Acute ischemia:u and other
pathologic states may slow conduction by decreasing resting membrane potential, by impairing
cell-to-cell conduction by fibrosis, or by causing conduction along the transverse axis of cells
(anisotropic conduction).25 Early coupled ectopic beats may slow conduction if they encounter
tissue prior to full repolarization. In Figure 5-5, Panels A to C illustrate a model with both an
upper and lower "common" pathway. If this were a model of AVNRT, it would suggest that
tachycardia could carry on without the participation of either the muscle above (atrium) or the
structure below (His bundle). Panel D changes the model where there is no upper common
pathway, i.e., entrance and exit sites from the circuit to the atrium are distinct. This would mean
that at least part of the circuit resides in atrial tissue or a border zone of "atrio-nodal" tissue.
This is probably the best model for most AVNRT, still not perfectly understood but probably
eclectic and not of exactly uniform mechanism.
A macro reentrant circuit might also be envisaged where the impulse enters a slow conduction
area superiorly, exits inferiorly, and then returns to the entrance with part of the circuit being
outside of the core slow conduction area (Figure 5-6, Panel A). Although this is illustrated in
1 plane in the figure, it is obviously 3-dimensional. This latter modd probably fits VT related
to infarct scar where the macro reentrant circuit would include in its simplest iteration an
CHAPTERS • Mechanisms of Tachycardia 101
P x n:romic
~ve
Panel A PanelB PanelC

FIGURE 5-6 • Reset and fusion in a classical model of reentry. This is a 2-dimensional depiction for clarity. The circuit in Panel A con-
sists of a slow conduction mne {gn!en) with an advancing wave In red and an "excitable gap"ln the drrult ahead ofthe arrow. It Is noted
that the slow conduction has a separate entrance and exit A paced impulse (Panel B) timed to get into the excitable gap is shown in
blue. The pacing wavefront provides a component that is against the direction of the arrhythmia circuit (antidromic) and a component
that is in the direction of the circuit (orthodromic). One can see that this impulse can generate a"fusect• activation pattern while at the
same time It can reset (usually advance) the next wave. If one considers a point source or focal arrhythmia, It Is evident that the paced
Impulse can fuse with the arrhythmia wave front but cannot reach the source to reset It, which Is surrounded by refractoriness after the
wave leaves. On the other hand, it can reach the point source to alter its timing (reset) but then it cannot contribute to the wave front
of the paced complex that reaches it. Simultaneous reset and fusion is invariably seen only with reentry with rare exceptions when the
point source of tachycardia can be reached from a different direction than its output. i.e., has a separate entrance and exit.
entrance area into the scar, a route through the scar, an exit from the scar, and a return to the
original site via muscle around the core scar.
Many experimental models have been used that fit classic reentry in both atrium and ventri-
cle. These are frequently validated by determining the activation sequence of the arrhythmia,
demonstrating the need for slow conduction, and showing that interruption of any obligatory
link terminates tachycardia. Coronary occlusion models have revealed both the classic single-
circuit loop and more complicated loops, including "figure of 8." An interesting variant of reen-
try has been termed reflection.2.6 In this in vitro model, there is only a single fiber and no circuit
per se. The impulse is slowed in a depressed zone and the impulse returns along the same
pathway electronically to reexcite the proximal portion of the fiber.
Reentry has been convincingly demonstrated to be the mechanism of most of the recurrent
paroxysmal tachycardias observed clinically, including atrial flutter, AV node reentry, atrio-
ventricular reentry involving accessory pathways, and VT associated with chronic myocardial
infarction or other scarring. Validation of reentry is carried out in the clinical electrophysiology
laboratory when possible, using principally the following criteria:
1. Reproducible initiation and termination of tachycardia using extrastimuli within a range
of coupling intervals. When a series of programmed premature beats initiates tachycardia,
an inverse relationship between the inducing coupling interval and the interval to the first
tachycardia beat is typical of reentry. That is , the shorter the coupling interval of the induc-
ing beat, the longer the interval to the first beat of tachycardia.
2. Demonstration of a slow conduction zone within the proposed circuit.
3. Demonstration of unidirectional block required to initiate tachycardia. This is readily
demonstratable in AV node reentry or AV reentry but more difficult where the circuit com-
ponents are more cryptic such as in the confines of a large infarction scar. One interesting
exception to this rule is induction of AV node reentry with a 2-for-1 response.
4. Demonstration that the tachycardia circuit has an "excitable gap." This is done using a single
extrastimulus ("reset") phenomenon27•28 as demonstrated in Figure 5-6 or overdrive pacing,
i.e., entrainment211-3 • of the rhythm with repetitive reset. Of course , the fundamental phe-
nomenon is the same and one can consider reset with an extrastirnulus as "entrainment" for
1 beat and conversely consider entrainment as repetitive "reset."
If the cycle following the extrastirnulus is "reset; it indicates that the critical part of the mecha-
nism has been reached to alter (advance, delay, or terminate) the timing. This might be the excit-
able gap of a reentrant circuit or an automatic focus. The difference is illustrated in Figure 5-6.
Because the critical slow conduction zone of the circuit has an anatomically separate entrance
and exit site, it is possible to reset via the "back door" so to speak via an orthodromic wave (the
component of the paced beat going in the same direction as the circuit) while the antidromic
wave collides with the orthodrornic wave corning from the exit of the slow conduction zone
to create "fusion" or a composite activation pattern, if you will. This may be demonstrated by
the ECG or by intracardiac electrograrns. It may not always be demonstrable if the collision of
the antidromic and orthodrornic occurs in a very slow conduction zone with the signals fall-
ing below the limits of our resolution as occurs in a myocardial infarction scar ("concealed").
Panel C of Figure 5-6 represents a hypothetical "focal" or point source tachycardia. Because the
entrance and exit to the point are not distinct, it can be reset only if entirely penetrated. Fusion
cannot happen because any component of depolarization coming out of the focus would prevent
the reset. Thus, it either fuses or resets but cannot do both simultaneously. With very few excep-
tions, fusion and reset means macro reentry. Keep Figure 5-6 in mind as we move to a couple of
clinical examples in the electrophysiology laboratory (Figures 5-7 and 5-8).
"Entrainment" is a related phenomenon whereby the pacing rate is gradually accelerated during
tachycardia until the pacing rate exceeds the tachycardia rate. The ability to accelerate the tachy-
cardia rate to the paced rate without terminating it is referred to as entrainment. Entrainment
depends on the presence of an excitable gap through which the reentrant wave can be driven
faster than its natural rate (Figure 5-9). Entrainment is basically repetitive "fusion and reset."
The stimulus provides an antidromic wave that results in fusion while concurrently accelerating
the tachycardia via an orthodromic wave. This is evident from a single extrastimulus demon-
strating reset and fusion or from entrainment when each beat of the drive provides a fused
complex (such as in Figure 5-9) while concurrently accelerating the subsequent cycle. Thus,
during stable entrainment, each beat is both fused while resetfrom the previous beat. After the last
paced beat, the subsequent cycle is NOT fused but reset to the cycle length of pacing as the last
paced beat comes full circle but there is no further pacing to fuse with it. Figure 5-9 illustrated
a major criterion for entrainment, namely constant fusion at a given paced cycle length with
constant fusion at a more rapid rate but with a different morphology (in this instance, QRS
morphology) due to a larger component driven by the antidromic wave. With continued pacing
rate acceleration, the paced morphology at a critical rate replaces the fused morphology and
the antidromic wave penetrates the slow conduction zone. At this point, the tachycardia is no
longer evident when pacing is terminated. The reader is encouraged to read one of the original
papers by Waldo describing this in more detail. 29.lo The diagnostic value of entrainment in the
various tachycardias is illustrated further in the chapters dealing with specific arrhythmias.
One must differentiate overdrive pacing from entrainment. The former occurs when the under-
lying tachycardia is replaced by more rapid pacing, at least during the duration of tachycardia.
However, the criteria for entrainment as described above can't be demonstrated.
II
V1
HRAp
HISd
HISp
CS7,8 •
CSS,6
CS3,4
•
534
RVad
8:S:40AM
FIGURE 5·7 • Re.set and fusion In atrloventricular re entry, a cla55lcal model of reentry. A PVC programmed in the cardiac cycle
when the His is refractory ("His refractory PVC") advances the next atrial electrogram, proving the presence of an accessory path·
way. This ls actually a demonstration offusion ••• the QRS morphology (F) ls lnte1medlate between the paced QRS and the tachy-
cardia QRS. An ea rifer coupled PVC (not shown) more closely resembled the pure paced QRS. The following beat Is not fused but Is
advanced (E).The postpadng Interval PPI at the RV electrogram Is approxlmatety 60 mllllseconds. short enough (<115) for this RV
site to be considered within the drcult.
The Inset Indicates the paced complex {P) generating an antldromlc wave (grffll arrow) and an orthodromlc wave {blllft a1TOw) dur-
ing ongoing AV reentry.
I, II, and V1 are surface ECG leads, respectively. CS 9-10 to CS 3-4 are bipolar electro grams from a coronary sinus catheter, from
proximal to distal, respectively. E=entrained complex. F =fused complex. H=His bundle electrogram. PPI =post pacing interval.
Rvad represents a right ventricular apical electrogram. The numbers indicate the interval in milliseconds.
The related concepts of fusion and reset and entrainment are very valuable mechanistic
observations In dlnl"1 electrophyalology.
This type of mechanism is invoked for the grossly irregularly tachycardias, notably atrial and
ventricular fibrillation. Basic scientists have invoked various models potentially explaining the
apparently chaotic wavefronts that are observed that are determined by the physical and func-
tional boundaries to advancing wavefronts. The clinician may choose to think of all of these as
variants of reentry in 3 dimensions, complex impulse propagation with the seeking of nonrefrac-
to.rytissue bythe advancing waves (~5-10). The arrhythmia may be initiated or sustained by
rapid focal automaticity or reentry or ·drivers"' as observed in the role of the pulmonary veins in
atrial fibrillation. The clinician interested in ablation wishes to uncover patterns ofactivation in
the apparent chaos that signal tissues necessary for the continuation of fibrillatory conductions.
This is the practical end ofthe issue, regardless ofwhether the major basic mechanism is '"leading
circle" (Allessie)20 reentry (whereby a reentrant wave circles a functional obstacle at the center,
I I I I I I I I I I I I I I I I I I I I lfTTll
l '
IIIIIIIIIIIII
' :
220 I 220 !
CS3 --,_,.--,,,., ,,----....,. _..-_,...... ,.-----.---........,.....-,---.,...---.....,.. , . . . - - " " " ' - -
CS2
CS1 _....,___,, . r - - - " " - - - " _,,-----""--4..i i

I ,v ~-
11111111111111111111l lLLI1111111111111
FIGURE 5·8 • Ruet and fu1lon In atrlal flutter, another d11111lcal model of reentry. This patient had typical "'Isthmus-dependent"
counterdockwise atrial flutter. An atTial extrasystele is delivered into the cardiac cycle. Although the surface Pwave can't be seen
with clartty, the lntracardlac electrograms dearly Indicate fusion. The RA electrogram Is early but the CS electrograms are not;
hence, the atrium has at least 2 concurrent waves. The follow1ng atrial cycle Is advanced (entrained) but not fused. The right atrtal
electrogram after the early paced one has a postpadng Interval of220 ms, l.e~ the PPI Indicates thatthls electrogram ls'"ln"the dr·
cult. This could not happen with a point source.
whichiskeptrefractorybythedrculatingwave).or"random"orchaoticreentrythatcanbethought
afas multiple wavelets of excitation, all darting about seeking nonrefractory tlssue in constantly
changing directions. Most recent interest has been in the concept of atrial fibrillation driven
by rotors21 or a tomadolike activation that may be relatively fu:ed to provide an ablation target.
The physics and mathematics of the rotors are very complex. and, it is fair to say, still theoretical.
The clinician looking at a high-resolution activation map will see a complex activation pattern
where rotational 6.ud elements may be visible but more probably require considerable process-
ing to uncover the patterns. The burden af proof would the:n be on demonstrating that these
elements contribute to the tachycardia by eliminating tachycardia when ablated. Regardless of
the mechanism, the ultimate clinical objective is to find tissue that is important to sustaining
the arrhythmia be it a relatively 6.ud rotor or an anatomical juncture that facilitates random
or leading circle reentry. This will likely require a high-density mapping system in addition to
signal processing as the patterns will surely not be readily evident upon simple inspection in the
majority of instances.
Mechanisms of Tachycardia: Clinician's Viewpoint

Basic scientists using controlled experimental conditions and sophisticated cellular and sub-
cellular techniques have provided a comprehensive framework for understanding the many
potential mechanisms resulting in arrhythmia. The clinical eleci:rophysiologist faces the for-
midable challenge af relating these concepts to clinical settings. The clinician dealing with
·natural,. arrhythmias in patients is constrained by logistic and technical limitations and must
PanelA
PanelB
FIGURE 5·9 • Entrainmetrt of ventriadar tachyc.antia. Ventricular tachyardia {VT} in this patient was stable with a cycle length
of 300 ms. In Panel A, rtght ventrtcular apical pacing ls lnltlall!d at a sllghtly shorter cycle length than the VT cycle length (280 ms).
By the ninth paced beat (astetls/c), a stJtble fusion pattern has been embllshed and the tachycardia has been accelerated to the
paced rate (cycle length, 280 ms). After padng Is discontinued (red a"ow), the flrst nonpaced cycle Is entrained and the subsequent
cycle ls again at the VT cycle length. In Panel B, ventricular pacing Is Initiated at a sl!ghtly shorter cycle length (250 ms). By the fifth
paced beat (asterisk} a stable fusion pattem has been established and the tachyr.ardia rate has been accelerall!d to the paced rate.
The fusion pattem is progressive {i.e., greater contribution from ventricular pacing than VT} as compared to Panel A. The first non·
paced cycle after cessation of pacing {green alfOW) occurs at cycle length 250 ms. which Is the cycle length of pacing. This Indicates
dearly that this flrst nonpaced cycle has been entrained. That Is, the excitable gap was clearly penetrated by the last paced stlmu·
lus, resulting In accelefation of the next cycle to the paced rate.
depend heavily on inference. Even different experimental models of a given mechanism can
differ sufficiently to complicate the exercise of applying the experimental template to a clinical
arrhythmia. For these reasons, a clinician proclaiming a "mechanism" for an unknown arrhyth-
mia does so with appropriate reservations and humility. The following discussion is intended to
facilitate a mental framework for approximating an arrhythmia mechanism in a clinical setting,
PllnelA Panel B
FIGURE 5·10 • R411ntrywlthout a fbClld drcultand anirtDmk:lll obstacle. Graphic representation of"ordered' or dasslcal reentry
(Pan1I A) and 'random" reentry (Pan1I B). Ordered reentry has a relatively fl:xed anatomic route with an excitable gep {G). In random
reentry without an anatomic obstacle, the pilthways are fluid, with the adYancing ci!Ulit constantly seeking ncmrefractory tissue.
Initiation by No No Enhanced by Enhanced by Enhanced by increase in

basic drive decrease in increase in drive drive rate; usually highly
drive rate rate reproduclble
Initiation by No No No Enhanced by Range of critical
extrastimulus shorter coupling coupling intervals;
interval; less highly reproducible
reproducible
Sustained tachycardia May•warm up• May•warm up" Variable Often Initial Usually stable but may
"warmup• and oscillate or slow down
terminal before termination
"slowdown•
Response of No termination; No termination; No Terminates with Terminates with
tachycardia to overdrive may accelerate; termination critical rate; critlca I rate;
overdrive suppression no overdrive reproducible entrainment
suppression demonstrable
Response of No termination No termination Unlikely Unlikely ter- Terminates within a
tachycardia to termination mination; not defined range; may
single extrastimulus reproducible "reset• (stimulus
must penetrate
excitable gap)
appreciating that the generalizations to follow can always be challenged in specific circum-
stances (Tables 5-2 and 5-3).
Electrocardiographic observation ofspontaneous arrhythmias

Mechanism can be elucidated when the arrhythmia occurs frequently and one is fortunate
enough to record a particularly illuminating episode. Autonomic and pharmacologic maneuvers
during a sustained arrhythmia may cause changes in arrhythmia upon which specific hypotheses
TABLE 5-3 Clinical algorithm for arrhythmia mechanism.

Initiated by usual pacing techniques
No Yes
Highly reproducible initiation and

termination; reset, entrainment
demonstrable
I
OVerdrive to No overdrive suppression; Bradycardia-dependent;
suppression overdrive acceleration prolonged repolarization
Yes No
Normal automaticity Abnormal automaticity Early after-depolarization Reentry Consider DAD

Ill
Ill
Ill
FIGURE 5-11 • Detennlnlng mechanlim by deductive analysl5 of surface ECG recordings. This early record from the collection
of Pick and Langendorf illustrates analysis by picking the best hypothesis to fit the ECG data. The proposed mechanism of the
observed tachycardia (as shown In the •1addergram"} Is AV JuncUonal reentry utlllzlng a retrograde pathway with rate-dependent
conduction. The tachycardia Is lnldated by premature ventricular contractions that ccnduct retrogradely to the atrium with a
prolonged conduction time. Self-termination occurs with a retrograde Wenckebach pattern. This analysis Is remarkably lnslghtfut
although we currently know that the substrate for the observed tachycardia could be a retrogradely conducting accessory AV
pathway with decremental properties. (Reproduced with permission from Pick A. Langendorf R. Interpretation ofCompleK.Arrhythmias.
Philadelphia: Lea & Febiger; 1979.)
regarding mechanism can be formulated. Early electrocardiographers created an impressive

body of knowledge using deductive reasoning and these simple techniques (Figure 5-11).~1
These methods have obvious limitations in arriving at a specific mechanism. The record
obtained may be brief. or multiple hypotheses may fit the observations. The effect of certain
drugs and autonomic maneuvers can be useful, but none is absolutely specific for a given mech-
anism. Facilitation or induction with catecholamines is compatible with multiple mechanisms.
Termination of a supraventricular tachycardia with the Ca2+ blocker verapamil usually suggests
that the AV node is a critical part ofa reentrant circuit causing tachycardia. However, idiopathic
LV VT can be terminated by verapamil, as part of the reentrant circuit includes a slow conduc-
tion "'AV node-like,. zone (Figure 5-12).n
Effet:t ofprogrammed stimulation

Clinical e1ectrophysiologica1 testing (programmed stimulation and intracardiac record-
ing) is arguably the most useful technique for determining mechanisms of clinical arrhyth-
mias as illustrated in subsequent chapters. Failure to induce a specific ECG-documented
tachycardia with a rigorous protocol of stimulation including isoproterenol may imply the
arrhythmia may not be due to classic reentry with a stable substrate. However, exceptions
can occur, for example, in some patients with AV node reentry the tachycardia may not be
rn:t I aVR V1 V4
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l • i µ.,:' ;rt_
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.
iJJ. II! ++ -+++ ~VF
:r•Lj3:-r-:.__t "
-r I
. V3-T- ~::(.. .
-rt-;-t
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-~
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-j-+~ r~ +
•tt·
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T - .. .,~
ON
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'" -
'" · 1111-.
.,
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4-1: lf=t
.
Panel A PanelB
FIGURE 5·12 • "Verapamil-sensitive"'ventric:ulartachyc.ardia. This is t.ne most common form of this type of tachycardia, with
rtght bundle branch block, left axis morphology (Panel A). After verapaml~ s mg, the cycle length gradually prolongs and the
tachycardia stops (Panel B).The tJlchyardla Is frequently misdiagnosed as•supraventrfcular' and It Is easy to see why. In this case,
there Is a retrograde P wave on the heel of each QRS, reinforcing tne mistaken Impression that this Is SVT.
able to be initiated at electrophysiologic study even in the presence ofdrugs such as atropine,
isoproterenol, and epinephrine. Not uncommonly, the arrhythmia is induced with ease at
electrophysiology study on a different day. It is possible that conditions at that time of spon-
taneous arrhythmia (such as acute ischemia or heart failure) provided a reentrant substrate
no longer present at the time of study. One should also consider that the observed tachycar-
dia was due to alternate mechanisms, such as abnormal automaticity, enhanced ·normal"
automaticity, or after-depolarizations. Arrhythmias due to EADs would be expected to occur
in conditions resulting in prolonged repolarization and relative bradycardia.
Arrhythmias inducible by programmed stimulation may be considered to be either reentrant or

triggered (DADs). The features of triggered activity vary according to the experimental prep-
aration but those of classic reentry are relatively more constant and independent of a specific
preparation. Thus, it may be useful to consider how closely the given arrhythmia resembles
typical reentry and to consider triggered activity as an alternative possibility when such is not
the case. Features favoring reentry include highly reproducible (in an individual) initiation and
tennination by extrastimuli within a given range, an inverse relationship between prematurity
ofan initiating extrastimulus and the first beat of tachycardia, the demonstration ofan excitable
gap using entrainment or e:rtrastimuli (reset), the requirement ofslow conduction in the circuit,
the presence of a relatively stable rate independent of induction mode, and sudden termination
of the tachycardia with programmed stimulation. Triggered activity would be more likdy to
be induced by rapid pacing (rather than e:rtrastimuli), would not be as consistent in mode of
onset, and may have a more variable tachycardia rate dependent on mode ofinduction. In gen-
eral, a faster initiating drive results in an earlier first beat of tachycardia and one expects a direct
CHAPTERS • Mechanisms of Tachycardia 109
relationship between the first tachycardia cycle and prematurity of an extrastimulus initiating
the tachycardia. It must again be emphasized that the characteristics of triggered activity vary
considerably with different experimental preparations and conditions. It is impossible to be
definitive in ascribing any clinical arrhythmia to triggered activity using these generalizations.
Even if mechanism cannot be definitively stated, the issue of "inducibility" is critical to the clin-
ical electrophysiologisl Inducibility provides a means of studying the arrhythmia and assessing
potential pharmacologic and nonpharmacologic therapies objectively.
Activation sequence mapping

Activation sequence for a tachycardia was traditionally determined during electrophysiology studies
by examining individual electrograms on catheters and this is still easily done for the more common
tachycardias. More recently, mapping systems are widely available that analyze multiple electro-
grams obtained in sequence or simultaneously and provide an activation or a voltage map. A rhythm
may have a focal pattern with the waves emanating from a point source. A larger circuit pattern with
a slow conduction zone will usually be reentrant but this needs to be demonstrated independently
by entrainment or extrastimuli with fusion and reset A point source may follow a larger circuitlike
pattern with the correct anatomical boundaries and this may mimic a macro reentrant circuit
REFERENCES
1. Hoffman BF, Cranefield PF. The physiological basis of cardiac arrhythmias. Am l Mell. 1964;37(5):670-684.
2. Hoffman BF, Cranefield PF. Electrophysiology ofthe Heart. Mount Kisco, New York: Futura; 1976.
3. Zipes, DP. Genesis of cardiac arrhythmias: electrophysiological considerations. In: Heart Disease: A Textbook of
Cardiovascular Medicine. Saunders; 1988:581-620.
4. Wit AL, Rosen MR. Cellular electrophysiology of cardiac arrhythmias. In: Tachycardias: Mechanisms, Diagnosis,
'.ITeatment. Philadelphia: Lea & Febiger; 1984:51-127.
5. Rosen MR, Wit AL, Hoffman BF. Electrophysiology and pharmacology of cardiac arrhythmias. VI. Cardiac effects
of verapamil. Am Heart J. 1975;89(5):665-673. doi:l0.1016/0002-8703(75)90514-1
6. Vassalle M. The relationship among cardiac pacemakers. Overdrive suppression. Circ Res. 1977;41(3):269-277.
7. Cranefield PF. Action potentials, afterpotentials, and arrhythmias. Circ Res. 1977;41(4):415-423. doi:l0.1161/01.
RES.41.4.415
8. Shah SR, Park K, Alweis R. Long QT syndrome: a comprehensive review of the literature and current evidence.
Curr Probl Cardiol. 2019;44(3):92-106. doi:l0.1016/j.cpcardiol2018.04.002
9. Roden DM, Thompson KA, Hoffman BF, Woosley RL. Clinical features and basic mechanisms of quinidine-
induced arrhythmias. JAm Coll Cardio/.1986;8(1 Suppl A):73A-78A.
10. Schartz P, Crotti L. Long and short QT syndromes. In: Cardiac Electrophysiology: From Cell to Bedside. 6th ed.
Philadelphia: ELSEVIER, Saunders; 2014:935-947.
11. Moak JP, Rosen MR. Induction and termination of triggered activity by pacing in isolated canine Purkinje fibers.
Circulation. 1984;69(1):149-162.
12. Wit AL, Cranefield PF. Triggered and automatic activity in the canine coronary sinus. Circ Res. 1977;41 (4):434-445.
13. Rosen MR, Gelband H, Merker C, Hoffman BF. Mechanisms of digitalis toxicity: effects of ouabain on phase four
of canine Purkinje fiber transmembrane potentials. Circulation. 1973;47{4):681-689.
14. Johnson NJ, Rosen MR. The distinction between triggered activity and other cardiac arrhythmias. In: Cardiac
Arrhythmias: Where to Go from Here?. Mount Kisco, New York: Futura; 1987:129-145.
15. Ferrier GR. Digitalis arrhythmias: role of oscillatory afterpotentials. Prog Cardiovasc Dis. 1977;19(6):459-474.
16. Zipes DP, Foster PR, Troup PJ, Pedersen DH. Atrial induction of ventricular tachycardia: reentry versus triggered
autornaticity. Am J Cardiol. 1979;44(1):1-8.
17. Wu D, Kou H, Hung J. Exercise-triggered paroxysmal ventricular tachycardia: a repetitive rhythmic activity possi-
bly related to afterdepolarization. Ann Intern Med. 1981;95(4):410-414.
18. Mines GR. On circulating excitations in heart muscle and their possible relation to tachycardia and fibrillation.
Trans R Sac Can. 1914;8:43-52.
19. Hoffman BF, Rosen MR. Cellular mechanisms for cardiac arrhythmias. Circ Res. 1981;49(1):1-15. doi:l0.1161/01.
RES.49.1.1
11 O CARDIAC ARRHYTHMIAS: INTERPRETATION, DIAGNOSIS, AND TREATMENT
20. Allessie MA, Bonke FI, Schopman FJ. Circus movement in rabbit atrial muscle as a mechanism of tachycardia. III.
The "leading circle~ concept: a new model of circus movement in cardiac tissue without the involvement of an
anatomical obstacle. Circ Res. 1977;41(1):9-18.
21. Zaman JunaidAB, Peters NS. The rotor revolution. CircArrhythm Electrophysiol. 2014;7(6):1230-1236. doi: 10.1161/
CIRCEP.114.002201
22. Nattel S. New ideas about atrial fibrillation 50 years on. Nature. 2002;415(6868):219.
23. Gray RA, Jalife J, Panfilov AV, et al Mechanisms of cardiac fibrillation. Science. http://link.galegroup.com/apps/
doc/Al 7817372/AONE?sid=googlescholar. Published November 17, 1995. Accessed June 3, 2019.
24. El-SherifN, Mehra R, Gough WB, Zeiler RH. Ventricular activation patteI11$ of spontaneous and induced ventric-
ular rhythms in canine one-day-old myocardial infarction. Evidence for focal and reentrant mechanisms. Circ Res.
1982;51(2):152-166.
25. Spach MS, Dolber PC, Heidlage JF. Influence of the passive anisotropic properties on directional differences in
propagation following modification of the sodium conductance in human atrial muscle. A model of reentry based
on anisotropic discontinuous propagation. Circ Res. 1988;62(4):811-832.
26. Antzelevitch C, Jalife J, Moe GK. Characteristics of reflection as a mechanism of reentrant arrhythmias and its
relationship to parasystole. Circulation. 1980;61(1):182-191.
27. Rosenthal ME, Stamato NJ, Almendral JM, Gottlieb CD, Josephson ME. Resetting ofventricular tachycardia with
electrocardiographic f\uion: incidence and significance. Circulation. 1988;77(3):581-588.
28. Gilliam FR, Fanazapir L, Irwin JM, Greer GS, German LD, Prystowski EN. Characterization and differentiation of
reset response curves in automaticity and reentry. J Am Coll Cardiol. 1988;11:115A.
29. Waldo AL, Plumb VJ, Arciniegas JG, et al. Transient entrainment and interruption of the atrioventricular bypass
pathway type of paroxysmal atrial tachycardia. A model for understanding and identifying reentrant arrhythmias.
Circuliition. 1983;67(1):73-83.
30. Waldo AL, Henthorn RW, Plumb VJ, Maclean WA. Demonstration of the mechanism of transient entrainment
and interruption of ventricular tachycardia with rapid atrial pacing./ Am Coll Cardiol. 1984;3(2 Pt 1):422-430.
31. Brugada P, Wellens HJ. Entrainment as an electrophysiologic phenomenon. /Am Coll Cardiol. 1984;3(2 Pt 1):
451-454.
32. Pick A, Langendorf R. Interpretation of Complex Arrhythmias. lst US- lst Printing edition. Philadelphia: Lea &
Febiger; 1979.
33. Belhassen B, Rotmensch HH, Laniado S. Response of recurrent sustained ventricular tachycardia to verapamil.
Br Heart/. 1981;46(6):679-682. doi:lO.l 136/hrt.46.6.679
34. Wit AL, Cranefield PF, Gadsby DC. 'IJiggered activity. In: Zipes DP, Bailey JC, Elharrar V, eds. The Slow Inward
Current and Cardiac Arrhythmias. Developments in Cardiovascular Medicine. Dordrecht: Springer Netherlands;
1980:437-454. doi: 10.10071978-94-009-8890-3_20
PART
Arrhythmias
Chapter6 SupraventricularTachycardia
Chapter7 Preexcitation Syndromes
Chapters Ventricular Tachycardia
Chapter9 Atrial Fibrillation
Chapter 10 Bradycardia: Causes of Pauses
Su praventricu la r Tachycardia
George J. Klein, MD
CLASSIFICATION
Supraventricular tac:b.ycardia may be defined as tachycardia in which the atrium o.r atrioventric-
ular (AV) junction is the source or a vital link of the arrhythmia mechanism. Specific tachycardia
entities have been traditionally cataloged descriptively using criteria such as atrial rate. P-wave
contour, regularity of ventricular response, response to vagal stimulation, and mechanism.1
We have proposed a simple and clinically useful working classification that divides the
supraventricular tachycardias into the "'atrial" and "junctional" tachycardias (Table 6-1). The
atrial tachycardias originate in the atria and are not affected by conduction over the AV node
('"AV node-independent") (Flgute6-l).
Junctional tachycardias (Figure 6-2) require the AV node as a critical component of the tachy-
cardia mechanism c·Av node-dependent"). The distinction can often be made clinically using
vagal maneuvers or adenosine, observing the effect of AV node slowing or temporary block on
the tachycardia. Adenosine may terminate some atrial tachycardias, possibly due to triggered
activity. but termination may be preceded by a brief period of AV block in these cases. The AV
reentrant tachycardias are considered in detail in Chapter 7.
Sinus Tachycardia
Sinus tachycardia is associated with a variety of physiologic and pathologic states resulting in
increased sympathetic and decreased vagal stimulation of the sinus node. These are numer-
ous and include exercise, anxiety, hypovolemia, hypoxia, fever, hyperthyroidism, and anemia.
Agents such as alcohol and nicotine and many drugs with atropine-lilre or sympathomimetic
effects cause sinus tachycardia. The heart rate is greater than 100/min (by definition) and can
be 200/min or greater, although the muimal rate decreases with age. Sinus tac:b.ycardia is •non
paroxysmal." with a graduated onset and offset It may be slowed transiently by carotid massage
or other vagotonic manoeuvres. A shift in the site of the dominant pacemaker within the sinus
node may cause slight changes in rate and P-wave morphology. Sinus tachycardia is managed
by dealing with the primary cause. Occasionally, ifit is not compensatory related to cardiac or
respiratory failure. sinus tachycardia may be treated with beta blockers for symptomatic relief.
Sinus node re-entry and •inappropriate" sinus tachycardia are not related to the usual physio-
logic stimuli causing sinus tachycardia but are considered here because the site of impulse fo.r-
mation is in the sinus node region and they resemble sinus tac:b.ycardia electrocardiognphically.
• Sinus tachycardia • AV node reentry

• Sinus node reentry • AV reent.ry
• •cttronlc"sinus tllchycardla • Nonparoxylmal junctlonal tachycardia
• Atriill tachyurdia
• Atriill flutter
• Atr1al flbrlllrtlon
Sinus Node Reentry

The sinus node consists ofa central zone with densely packed cells and a transitional zone merg-
ing into atrial tissue. Conduction in this region can be sufficiently slow to allow reentry, and
sinus node reentry has been demonstrated in animal studies.2 A clinical diagnosis of sinus node
reentry is less precise and cannot entirely exclude reentry in atrial tissue near the sinus node.3
Sinus node reentry is more prevalent in older patients of either sex with organic heart disease.
It is an uncommon cause of problematic supraventrlcular tachycardia referred for electrophys-
iologic testing, although. its prevalence as an asymptomatic arrhythmia is probably higher. In
contrast to physiologic tachycardia, the onset and offset are paroxysmal. The tachycardia rate is
often less than 130/min and the P waves during tachycardia are identical or nearly so to those
seen in sinus rhythm. At electrophysiologic testing. tachycardia can be induced and terminated
with single atrial extrastimuli. Intra-atrial conduction delay is not necessary for initiation. Ear-
liest atrial activation during tachycardia is in the sinus node region, and the atrial activation
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FIGURE.,, • The major diagnostic hallmarttof an atrial tachycardia is continuation during AV block as seen in
U,Js example of spontaneous te1mlnatlon of AT with 2-to-1 AV block.
CHAPTER 6 • Supraventrlcular Tachycardia 115
L1
t t
FIGURE 6-2 • Spontaneous termination of AVNRT frequently observed In slmllar fashion In this lndlvldual. The last event at the
break Is atrial activation (arrow) and lnfonns that tachycardia could not continue after block In the AV node. That Is, the AV node
is a critical part of the circuit. A fortuitous block in the AV node at the time of AT termination would be very unlikely especially if
observed consistently.
sequence is "high to low." Carotid sinus massage and other vagal maneuvers typically slow and
terminate tachycardia, because increased vagal tone prolongs sinus nodal refractoriness but
shortens atrial refractoriness. This observation supports the involvement of sinus node tissue
as part of the reentrant circuit.
Treatment, rarely necessary, is empirical and beta blockers or calcium antagonists seem
reasonable.
"lnappropriatew Sinus Tachycardia

An ill-defined '"syndrome" of chronic, nonparoxymial, apparently inappropriate sinus tachy-
cardia has been described.• The heart rate is variable but frequently in the range of greater than
80/min. at rest or during sleep.5 The tachycardia is indistinguishable from sinus tachycardia
electroc.ardiographically and electrophysiologically except that the •resting" rate seems to be
reset higher than normal. During24-hour Holter monitoring the classic pattern is one ofhigher
than expected sinus rate during the awake hours but slower during sleep. The rate during sleep
is often faster than expected but still slower than during the awake hours. Atrial tachycardias do
not have such a pronounced awake/sleep heart rate difference and are thus typically excluded
when this pattem exists. There is often an exaggerated acceleration with upright posture or
exercise, suggesting some potential overlap with postural tachycardia syndrome (POTS). It has
been suggested that the fundamental abnormality is altered autonomic modulation, although
this is not well-established. Treatment with beta blockers is often initiated emp:lrlcally with very
little success in the experience of the authors. Ivabradine is an If blocker, a mixed Na+ and K+
inward current highly expressed in the sinus node. It slows sinus pacemaker activity relatively
selectively with promising clinical results. Sinus node ablative therapy has been suggested for
refractory patients with variable success and is generally not appropriate.
In the experience of the authors, such patients are often younger women, not infrequently
health care workers. Abuse of adrenergic or atropinic compounds may be suspected in some
patients, but others appear psychologically stable and no evidence of substance abuse is found.
At this point. it is unclear whether this is a homogeneous pathologic entity or if some of these
patients have a primary cause of sinus tachycardia that remains elusive.
ATRIAL TACHYCARDIA
Atrial tachycardia (AT) may be broadly deflned1 as tachycardia originating in atrial muscle. Atrial
flutter and fibrillation are •atrial" by this definition but are sufficiently unique to be described sep-
arately. The nomenclature for this tachycardia is not uniform. We have used the tenn atrial tachy-
cardia in lieu ofectopic atrial tachycardia and consider the descriptor ectopic to be redundant.
AT affects fewer than 10% of patients with a paroxysmal supraventricular tachycardia presen-
tation.6 These are usually "focal• tachycardias, often adenosine sensitive. A different category
of AT occurs in the context of diffuse atrial disease such as after cardiac surgery for congenital
or valvular heart disease or after ablation of atrial fibrillation.7 The latter can be •focal" but
is generally macro reentrant and dependent on atrial conduction delays. During tachycardia,
P waves dissimilar from sinus P waves are usually discernible, with rates between 100 and
240/min. The essence of diagnosis is observing that AT continues during AV node block occur-
ring spontaneously or induced byvagalmaneuvers or adenosine (Figure 6-3). An important diag-
nostic clue to differentiate AT from the AV node-dependent tachycardias is seen in Figure 6-4.
One observes slight variation in the RP interval with a relatively constant AV interval with the
slight variations in the AT cycle length mirrored in the subsequent QRS appearing as a variable
VA interval. In other words, the AA interval predicts the VV interval. This would be expected
in an atrial tachycardia but unusual for an AV node-dependent tachycardia. Finally, the absence
of retrograde conduction at electrophysiologic study in a patient with documented supraven-
tricular tachycardia (SVT), especially after the administration of atropine or isoproterenol, is
very suggestive of atrial tachycardia.
FIGURE 6-3 • With adenoslne, termination occurs with sllght prtor prolongation of the PR Interval before complete AV block
during tachycardia. The AV node effect persists after termination wtth a couple of sinus beats showing no conduction to the wn-
trlcle. The AV node effect has a different time course than the effect on the atria Itachycardia. allowing us to see that the SVT Is NOT
AV node-dependent In this young lndMdual wtth no heart disease. One would not generally expect termination In patients with
macro reentrant AT.
···-- -- -:.--------~---····-.:. .......... .:..........:. .........:............:,. ________:, .........:..........:..........:. ..........:,.........:..........:.
FIGURE H • Numbet's represent lntl!rvals (P to P upper and QRS to QRS IO'W'ef} In mllllseconds. {See text for dmlls.)
AT is often associated with cardiac or puhnonary disease, although. it can occur in isolation,
especially in the pediatric population. Patients usually present with paroxysmal or nonparox-
ysmal tachycardia but c:an present with dyspnea and heart failure secondary to incessant tachy-
cardia.s The latter is dependent on the duration and rate of tachycardia although considerable
individual variation to susceptibility exists, most likcly genetically determined. Left ventricular
dysfunction secondary to tachycardia-induced myopathy is generally reversible to some extent
after the tachycardia is suppressed unless the tachycardia has been very long-standing.
The mechanism of AT may be difficult to establish unequivocally even with elearophysiologic

testing.' The essential feature of intra-atrial reentrant tachycardia is induction (and termination)
by atrial extrastimuli within a consistently defined range of prematurity (Figure 6-5). Induction
occurs with closely coupled extrast:imuli and onset of tachycardia is dependent on intra-atrial
conduction delay.10 Entrainment and reset may be demonstrated if the tachycardia rate is not
excessive. Resting abnormalities of atrial conduction and refractoriness are often observed, not
surprisingly because the atrial substrate of scarring and slow conduction has been established
by heart disease and enlarged atria. AT frequently coexists with atrial flutter or fibrillation, espe-
cially after AF ablation. The atrial rate is not affected by adenosine in these individuals.
The mechanism is postulated to be abnonnal automaticitywhen the tachycardia is not induced

or terminated by pacing techniques. Triggered activity may be suggested when atrial tachy-
cardia is induced by rapid atrial pacing without the other features associated with classical
reentry and may be terminated by verapamil or adenosine. The latter mechanisms (abnormal
automaticity, triggered activity) are more frequent in children without other heart disease.
They may also be implicated in AT associated with pulmonary disease and digitalis toxicity.
Medical therapy for AT generally requires a drug to prolong AV node refractoriness and limit
the ventricular response (verapamil, digitalis, beta blocker) and a second membrane-active
drug (class la, le, or 3) to maintain sinus rhythm. Drugs su.ch as sotalol and amiodarone are
II
aVF - - - " " ,..-....---"--" ,_______,
V1 - - - - . . . r----.. . r----.. ,_____ ~-~ ,__--..__ ,...---...._

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RV ~
l,
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PanelA
II
aVF
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RV~~~~~t~~~'~~~~i----~~(r---
200
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Panel B
FIGURE 6-5 • Induction of tachycardia In Panel Ashows an ArV-A Initiation that ls compatlble with AVRT or AVNRT but does
not rule out AT. However, a repetition as per Panel B now results In block to the ventricle with no change In the Interval from the
A'J. to the first tachycardia A O.e~ now an A-A-V response) that exposes tflls clearly <IS an <ttr!al tachycardia with a long conduction
time between the A'J. and the fi~t tachycardia beat II, aVF, V,, RA. HB~ RV= leads 2, aVF, His bundle. right atTium, right ventTicles,
respecttvely.
used as monotherapy, because they prolong AV node refractoriness in addition to providing

membrane stabilization. Catheter ablation is generally preferred for patients who are drug
intolerant or refractory or who have a preference not to take medication.
Multifocal Atrial Tachycardia

This AT is traditionally defined electroc:ardiographically bya heart rate greater than 100/min, 3 or
more different ectopic P-wave morphologies, and an irregular ventricular response (Figure 6-6).
It is observed in critically ill patients with diabetes mellitus, hypoxia, respiratory failure, acidosis,
and electrolyte imbalance as concomitant features but may be found in ambulatory patients with
no apparent heart disease.11 The tachycardia usually resolves with improvement of the patient's
general condition. Robust drug trials to establish efficacy are not available but beta-blocking agents
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or calcium antagoniBts such as diltiazem may be useful for rate control as in atrial fibrillation.1 2
Slowing of the atrial rate after verapamil has been observed suggesting that the mechanism may
be triggered activity at least in some cases.
ATRIAL FIBRILLATION13
Atrial fibrillation (AF) is a unique atrial tachycardia and one of the first encountered by a nov-
ice medical student It is sufficiently unique and clinically important that it is given specific
consideration in Chapter 9. Nonetheless, it is useful for us to consider the overlap between
AF and the other SVT mechanisms.14 Of course, more than 1 tachycardia may be present in
an individual but SVT may trigger AF (rarely the reverse) (Figure 6-7). This may be related
to atrial stretch or hemodynamic stress in the individual more vulnerable to develop AF. SVT
V1
RV -
HRA
HB
\
esp
CSd
FIGURE &-7 • AVN reentranttachycardiil in an individu;il presenting with <itrial fibrillation. AVNRTwas readily induced in the EP
laboratory Oeft part of p;inel) and transition to AF (orrow) observed several times.
FIGURE 6'-1 • AV reentrant tachyc;ardla In a young lndlvldual presenting with preexdted atrfal flbrtlla'don. AVfrr
was reproduclbly Induced (left part of panel} and degenerated to AF on several occasions durtng the study. The
AVIU conducted ovef a left lateral AP (dlstal CS, earllest) and It Is Interesting that AVIU continued for sevefal
more cycles after onset of flbrlllatory activity In the right atrium (arrow).
may be the only trigger for AF with the result that ablation of the primary svr
may be all that
is needed clinically. This is especially true for younger patients presenting with preexcited AF
where only ablation of the accessory pathway is necessary (Figure 6-8).
ATRIAL FLUTTER
Atrial flutter was recognized as a clinical arrhythmia as early as 1910.1s.i6 It is characterized
electroc:ardiographically as a supraventricular tachycardia with atrial rate between 250 and
350/min and with atrial rates as low as 200/min. in the presence of membrane-active drugs.
"Typical" atrial flutter has a •sawtooth" pattern of flutter waves with a continuously undulating
baseline usually best appreciated in the inferior leads 2, 3, and AVF. The ventricular response is
frequently one-half of the flutter rate (150/min). but higher degrees of AV block are also seen.
There may be variable Wenckebach patterns, producing an •trregularly irregular" ventricular
rate. One of the flutter waves may be obscured by the QRS and not readily apparent with 2:1 AV
conduction. This may be exposed by carotid sinus massage or adenosine (Figure 6-9).
Atrial flutter has been traditionally defined electrocardiographic:ally by rate, generally atrial
rate between 250 and 350/min. Two categories of atrial flutter are recognized electroc:ardio-
graphic:ally. Typical ("common" or ~e l ") flutter is characterized by predominantly initial
negative flutter waves ("sawtooth") recorded in the inferior limb leads and upright P wave in
Vl (Figure 6-10). The "uncommon" flutters are those that have a similar rate but are not elec-
trocardiographically "typical." While typical flutter is probably mechanistically unifonu (see
below), the others are more mechanistically eclectic, including a variety of atrial tachycardias
that share these rates. We recall that the definition of"flutter" has been largely based historically
on a specific: rate range and that an atrial tachycardia of rate 250-350/min (flutter by definition)
will undoubtedly have varying mechanisms.
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FIGURE 6-9 • This tachycardia has 1 obvious P wave although a second obscured by the ORS might be .suspected midway
between the 2 evident ones (anow.s). Adenosine readily e>eposes flutter during transient AV block.
Mechanisms
The mechanism ofatrial flutter, long debated.'·17 was elucidated in the era ofoperative arrhythmia
ablation18 followed by the era ofcatheter ablation.19 The ECG pattern oftypical flutter is associated
with a macro reentrant right atrial circuit that conforms to classic reent.rr°'21 with an excitable gap
FIGURE 6-10 • Twelve-lead ECG oftypic;il atrial fluttet'. (See text for details.)
SVC
IVC
FIGURE 6-11 • The circuit for typical atrial flutter is shown in blue. The tricuspid caval isthmus is an obligatory
part of the circuit. The crlsta termlnalls functions as a line of block providing a long •track• with a non-excitable
central area. CT, crista terminalls; HB, His bundle; CS, coronary sinus; FO, foramen ovale; IVC, inferior vena cava;
LA, left atrium; SVC, superior vena cava; TCI, tricuspid caval isthmus; TI, tendon ofTodaro.
(Figure 6-11). The excitable gap can be demonstrated using single atrial extrastimuli or entrain-
ment by incremental atrial pacing (Figure 6-11). Mapping of the circuit demonstrates a low-to-
high sequence up the anterior and septal walls, with a high-to-low sequence down the lateral and
posterior walls (Figure 6-12). A corridor ofblock characterized by "double spike" potentials can
be demonstrated during endocardial mapping during flutter and largely corresponds to the crista
terminalis as a line of block.22 A relative slow conduction zone of the circuit is in the region of the
isthmus between the inferior vena cava orifice and the inferior tricuspid ring, with the impulse
emerging from this zone near the orifice of the coronary sinus. The tricuspid caval isthmus (TCI)
is the narrowest part of the circuit and serves as a convenient target for catheter ablation.
Atrial flutter that is electrocardiographically atypical has eclectic mechanisms that depend on
context (post AF ablation, associated with congenital heart disease, etc.), but the most common
remains RA macro reentry as per Figure 6-11 with the circuit reversed, i.e., clockwise. The tar-
get of ablation remains the narrowest part of the circuit as per typical flutter, the TCI.
Clinical Presentation
Atrial flutter is observed in patients of any age with common risk factors similar to those for atrial
fibrillation, namely organic heart disease, hypertension, obesity, diabetes, alcohol, and others.
The clinical setting overlaps considerably with that of atrial fibrillation with both arrhyth-
mias observed in the same individual relatively frequently. Atrial flutter may be paroxysmal
CHAPTER 6 • Supraventricular Tachycardia 123
(self-terminating) or persistent. TCI-dependent flutter terminates in less than a few minutes

very infrequently, and other mechanisms should be sought if that occurs. It usually presents as
palpitations but can present with syncope, hypotension, and even cardiac arrest in individuals
capable of one-to-one AV conduction during flutter. Importantly, asymptomatic or minimally
symptomatic patients may present with effort intolerance, dyspnea, or congestive heart failure.
Acute Therapy23
The "traditional" strategy in managing any atrial arrhythmia is control of the ventricular rate
using AV node blocking drugs. Subsequent consideration is then made to reversion to sinus
rhythm using membrane-active agents, such as propafenone with cardioversion considered if
the former is not adequate or hemodynamic compromise occurs. This "classic" approach is
frequently difficult to apply in atrial flutter. Control of the ventricular rate is difficult to achieve
and abrupt transitions from too fast to too slow can occur. Membrane-active drugs, especially
the le agents propafenone and Flecainide, are very effective at prolonging the flutter cycle
length but less effective at terminating flutter with the drug ibutilide24 more successful at con-
version at the cost of a small risk of proarrhythmia. For these reasons, it is appropriate to con-
sider cardioversion as an early strategy. Atrial pacing techniques may be useful if an implanted
device has such capability or an atrial lead is present for another reason such as after cardiac
surgery. Atrial pacing by the esophageal route is preferred by some, although it can be painful
and not widely used. An abrupt change in flutter-wave morphology indicates termination of
flutter with incremental atrial pacing (Figure 6-12). The critical rate required to terminate
type 1 flutter is usually between 115% and 125% of the flutter rate. Attempts at pace termina-
tion of atrial flutter may result in induction of atrial fibrillation, which is frequently self-ter-
minating in the patient without a history of atrial fibrillation.
Chronic Management
Pharmacologic prophylactic therapy for atrial flutter is empirical with efficacy determined by
trial and error. Dual therapy with both an AV node blocking drug and a membrane-active drug
is recommended except for drugs such as sotalol and amiodarone, which have both properties.
The use of membrane-active drugs alone may slow the atrial rate sufficiently to allow one-
to-one AV conduction in some patients and are thus potentially "proarrhythmic" when used
alone (Figure 6-13). Thus, a drug to prolong AV node refractoriness such as a beta blocker,
verapamil, or Cardizem is usually recommended to accompany membrane-active drugs such
as propafenone.
It is fair to say that chronic pharmacological management of atrial flutter has largely been sup-
planted by catheter ablation (Chapter 17).25.211
AV NODE REENTRY
Gordon Moe and coworkers27 originally demonstrated AV node reentry in the dog and intro-
duced the concept of dual pathways in the AV junctional region as the substrate for this arrhyth-
mia. This concept was supported in human studies by Kistin,28 who observed 2 populations of
PR intervals in selected patients during electrocardiographic recording, with short PR inter-
vals postulated to be over the "fast pathway" and long PR intervals postulated to be over the
"slow pathway." Schuilenburg and Durrer29 first demonstrated dual-pathway curves in humans
utilizing the extrastimulus technique, relating inter atrial interval (A1-A2) to prematurity of a
ventricular extrastimulus. Finally, Rosen,:ro Denes,'1 Wu,32 and others proposed the connection
between paroxysmal supraventricular tach.ycardia in humans and dual-pathway physiology
demonstrated by the extrastimulus tec.hnique.
Clinical Presentation and Electrocardiographic Recognition

AV node reentry accounts for the majority of cases of paroxysmal supraventricular tachycardia
referred to an electrophysiology laboratory.» It can occur in any age group but most frequently
presents in young to middle-aged adults, being slightly more prevalent in women than in men.
After presentation, further episodes will vary in frequency and duration but will usually persist
for years. Once tachycardia has established a pattern, recunence is the rule. There are generally
no precipitating factors, although some patients will report a consistent relationship to exer-
cise, posture, or gastrointestinal symptoms with initiation of tachycardia. The onset is typically
A II
B II
C II
PanelA
FIGURE 6-12 • Entrainment during atrial flutter. Panel A illustrates atrial pacing at progressively more rapid rates, with acceleration
of the flumr cycle length to me paced rate. A Is the control strip and the paced rate Is progresslvely Increased frcm strip Bto strip
D. The pacing has not altefed the flutter-wave morphology, and the arrhythmia resumes at Its fonnef rate after cessation of pacing
In each strip. Panel B Illustrates the effect offurther aa:eleratlon of the padng rate. At the first astmsk In stl'lp A. there Is a sudden
change In the flutter-wave mOfphology, signifying the transition from entrainment of me drcult to cessation of reentry. Sinus rhythm
ensues after discontinuation of peeing In strip Bend continues In slTip C. S denotes stimulus artefact. (Reproduced with pennlsslon
from Wildo AL. Carlson MO, Biblo LA. Henthom RW. The role c:K transient entrainment in atrial fluttet'. In: Touboul P, waldo AL eds.
AtriofAtrllytflmios: C.Urrerit Concept$ and Management. St Lcuis. MO: Mosby Year Book; 1990:21 o. Copyright c Elsevier.)
- 18 -
B II
* =Samebeal
c *
Panel B
FIGURE 6-11 • (Continued)
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431529
CONTROL
~~~.~r~~
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PanelA
FIGURE 6-U • Propafenone In at?tal flutter. The records are fn:lm a patient treated wtth prapafertone as monotherapy for praphyla)ds
of atrial flutcer. The patient retumed wtth wide QRS tachycardia necessttaUng cardlove1'$1on. Electrophyslologlcal tesUng In 1tie absence
of drug n!ll'l!lled Inducible atrial flutter (Panel A) at an atrial cycle length of 220 ms. The adcllUon of pmpafenone (Panel B) 140 mg
Intravenously resulted In pralongatton ofthe flutter cycle length ccruidenlbly, to 320 ms. At this point. upright ttlt {Panll C) resulted. In
aslfght shortl!nlng of cydelength to 285 ms with the occurrence of 1:1 AV conduction wlthaberrancy and reproductfonof thepattl!fTB
dtnk:ill tadlyca!dla. One-to-one AV-node conduction during tllt was related to tllt-indU<l!d autonomic dlanges. namely, vagolysls <1nd
enhanced sympathetic tone. This"proantiythmia"would have been prevented by addition of an agent to provide AV node blockade.
r"""l"'"'l'a.,l..,...,.l'"r''T"Dlj•.,...,....,.,....r-,.....,....,."'1•j,•..,...'Jll"IJDllllJ"',,_,.ll.,.ll'l"'lllrlll,..b,.,___,- i-i-
431529
PROPAFENONE 140
II 0.._ I~
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431529
PROPAFENONE, TILT
FIGURE6-13 • (Continued)
sudden and termination occurs abruptly, i.e., paroxysmal However, spontaneous termination
is frequently perceived by the patient as gradual, possibly related to the occurrence of sinus
tachycardia after abrupt termination of AV node reen1l'y tachycardia in some individuals.
Symptoms are not specific, the most common being palpitation or the sensation of a rapid
heartbeat. This may be accompanied by light-headedness, dyspnea, or chest pain. A sensation
of throbbing in the neck is common. Syncope may occur and usually does so either at the onset
of tachycardia or well into the tachycardia episode. Syncope is usually related more to impaired
vasomotor adaptation to tachycardia than to a prohibitively rapid rate.33 Occasionally, syncope
may be the presenting symptom, with the patient not having any awareness ofa rapid heartbeat.
The signs are similarly nonspecific, with most patients presenting with a diminished, regular
pulse. Cannon A waves may be seen if carefully sought. The prognosis is generally excellent in
the absence of concomitant heart disease.
II
FIGURE 6-14 • Typical AV node reentry. A tefmlnal deflection after the QRS seen best In lnf'erior leads In this lndMdual Is a retro-
grade Pwave.
Electrocardiographically,34 a regular supraventricular tachycardia is observed with rates rang-

ing from 120 to 220/min (Figure 6-14). Minor oscillations in cycle length. may be observed and
QRS alternans of QRS amplitude may be present with more rapid tachycardia. Functional bwi-
dle branch block does not affect the rate of tachycardia, because the bundle branches are not
part ofthe reentrant circuit. The P wave is invariably simultaneous with a QRS complex or may
be seen slightly before or after the QRS complex (Figure 6-15). AV node reentry not fitting the
above most common pattem is •atypical:' It is often atypical by having a longer ventriculo-atrial
interval (RP> PR) (Figure 6-16), also referred to as "short-long.. by some. P-wave locations
intermediate between the 2 described are also noted. ST depression of considerable magni-
tude is frequently observed and is a nonspecific phenomenon generally not related to coronary
artery disease. The onset of tachycardia, when observed electrocardiographically, is often her-
alded by a premature atrial depolarization, which results in a sudden prolongation of the PR
interval, marking the onset of tachycardia. When spontaneous termination is observed and the
P wave can be identified, the last QRS of the tachycardia is usually associated with a P wave,
because reentry usually stops by block in the anterograde limb (PR) of the circuit. Consistent
termination of tachycardia with a P wave not followed by a QRS (ie., block in the AV node) is a
major clue to an AV node-dependent tachycardia, either AV or AV node r~try (Chapter 12).
Electrophysiologic Features
The fundamental concept for the substrate of AV node reentry is duality of AV nodal pathways
with disparate electrophysiologic properties. Classically, one pathway has a shorter conduction
time and a longer refractory period (the fast pathway), while the other has a longer conduc-
tion time and a shorter refractory period (the slow pathway). Unidirectional block in one of
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Panel B
FIGURE 6-15 • Finding the P In AV node reentTy. The rettograde P Is more subUe here U'lan that In Figure 6-14. Panel Ashows AV
node re entrant tachycardia In lead V,. The P wave Is observed. as a tiny hump (rprime) at the end of the QRS complex (a!TOWhead);
this ls best appreciated by comparing the QRS complex to that In sinus rhythm side by side (Panel B).
V5
FIGURE 6-16 • ECG during atyplcal AV node reentry. The RP lnteMil ls longer than the PR lnteMil In this example (•short-long"}
and the Pwave Is charactertstk:ally negative In leads 2, 3, and AVF. Mechanlstlcally, the dlfl'erentlal diagnosis for such a tracing
Includes atrial tachycardia and atrloventrlcular reentTy with retrograde conduction over a slowly conducting accessory pathway.
the pathways allows conduction over the alternate route, with retrograde conduction over the
previously blocked pathway allowing for reentry. This basic concept is well-established and no
longer a subject of debate, although the specific anatomic correlates underlying the physio-
logic phenomena are probably more eclectic and surely more complicated,35-n Typical AV node
reentry is by far the most prevalent and is associated with ·slow" anterograde conduction and
"fast" retrograde conduction. The RP interval is short (<90 ms) and the retrograde activation
sequence as measured by intracardiac recordings usually demonstrates earliest atrial activity
at the standard His catheter recording site, a "'superior" ei:it site. Atypical AVNRT is observed
probably in fewer than 5% of patients presenting with supraventricular tachyc:ardia.4D..tl The
most common of these "atypical" AVNRTs has a long RP interval (RP > PR) with retrograde
conduction occurring over a '"slow" pathway. Earliest retrograde atrial activation as assessed by
electrophysiologic testing occurs near or at the orifice of the coronary sinus, at some distance
from the recorded His electrogram. More infrequently. patients will experience a non reentrant
tachycardiau related to "2-for-1" conduction, in which each sinus impulse produces 2 ventric-
ular activations, 1 over the fast pathway and 1 over the slow pathway (Figure 6-17). This type
of tachycardia is facilitated by an absence ofconnection from the anterograde AVN pathway to
the retrograde AVN pathway and consequently, a patient will generally have AVN reentry or
non-reentrant AVN reentry. but rarely both.
The essential features of AV node reentrant tachycardia are enumerated in Table 6-2. The
diagnosis is usually made on the basis of multiple criteria. The essence of proving AVN
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PanelA
1 ~-~~~.f'...~~--f'-.....-~~~..r.....~~~~r-...~~~-f'....--~~-r...--~~----
PanelB
FIGURE 6-17 • SupraventTlcular tachycardia due to '"2..for-r conduction In sinus tachycardia. Panel A shows lead 2 of the ECG
with the cycle length altemlltlng between long and short coupling lnteMlls. There Is one P wave {b/u~ dots) preceding each of
the fast and slow AV node pathways with distinct PR Intervals {rrdarrows). The electrophyslologlc basis for this Is demon mated In
Pa Ml 8, where It Is dear thBt a single alTlal depolarimtlon results In 2 QRS complexes, one OVl!f the fast pathway (AH 60) and one =
slmuhaneously over the slow pathway {AH'= 400 ms). This was treated by catheter ilblatlon of the slow pathway. It Is noted that
the differential diagnosis for such a piittern would include sinus rhythm with ii bigeminal piittem due to ectopy.
reentry can be thought of as disproving AV reentry and atrial tachycardia. Neither the atria
nor the ventricles are obligatory parts of the circuit and neither the atria nor the ventricles are
"inn the circuit when assessed by programmed stimulation or entrainment. Preex<:itation of
the atria by a programmed premature ventricular depolarization introduced into the cardiac
cycle during tachycardia when the His bundle is refractory can NOT occur with AVN reentry in
the absence ofaccessory pathways. A noncentral atrial activation sequence indicates either atrial
tachycardia or AV reentry, although earliest activation can occur in the proximal to mid CS in
atypical AVNRT. Dual-pathway physiology is present in more than two-thirds of patients. It is
TABLE 6-2 Electrophysiologic features of AV node reentry.

• Dual-pathway physiology is usually demonstrable.
• The retrograde atrial activation sequence during tachycardia is •central: with earliest activation recorded at the His bundle site
(typical AV node reentry) or the orifice of the coronary sinus (atypical AV node reentry). There are rare exceptions to this.
• The ventrlculoatrlal Interval measured at the His bundle electrogram Is usually <60 ms (typical type).
• Premature ventrlcu lar depolarizations programmed Into the cardiac cycle during reciprocating tachycardia cannot preexclte
the atrium when delivered at a time that the His bundle is refractory. Very early coupled premature ventricular depolarizations
may preexcite the atrium.
• Entrainment from the RV apex will result in ventricular return cycle (PPI) greater than 115 ms. This respo nse generally differen-
tiates AV node reentry from AV reentry over a septal accessory pathway but ls not entlrely specific and may be observed with
accessory pathways with decremental retrograde conduction.
• There is generally a 1:1 atrioventricular relationship. This is not obligatory and AV node reentry may continue in t he face of AV
dissociation due to ventriculoatrial block or atrioventricu lar block (both above and below the recorded His bundle).
• Onset of reciprocating tachycardia by atrial extrastimuli requires a critical AH delay, and achievement of this delay usually coin-
cides with the•echo zone"for return cycles. It must be remembered that AV reentry Induced In a slmllar fashion also requires a
critical atrioventricular delay.
best demonstrated during atrial extrastimulus testing, with the usual diagnostic criterion being
a "jump" of at least 50 ms in the AH interval when atrial extrastimuli are decremented by 10 ms
(Figures 6-18 and 6-19). Failure to demonstrate dual pathways may occur if conduction times
over the fast and slow pathways are similar, if the effective refractory period of the fast pathway
is similar to that of the slow pathway, if the effective refractory period of the fast pathway is
not obtainable due to atrial refractoriness, or, finally, if either pathway exhibits unidirectional
350
00
300
0
00
250
0
Is 200
::c:"'
..[ 150 • 0 0
•• i 0
100
• • • 0 0 0
0
50
o~~~~~~~~~~~~~~~~~~~~~~~~
200 250 300 350 400 450 500 550 600

A 1 ~(msec)
FIGURE 6-18 • Dual-pathway physiology. The curve relates prematurity of an atrial extrastimu lus (A,, A) on the x-axis to the AH
interval on the y-axis in a patient with AV node reentrant tachycardia. At an A,. A, interval of approximately 350 ms (open cirdes),
there is an abrupt increase in the AH interval coinciding with the onset of tachycardia. There is frequently some minor variability of
the coupling Interval produclng this transition. The filled squares are obtained after ablation ofthe slow pathway region, showing
a frequently observed slight shortening of the ERP of the fast pathway and absence of the slow pathway portion of the curve. This
sequence firmly validates the theory.
H H
HBEd
FIGURE 6·19 • Onset of typlcal AV node reentry. ~Is premature and follows a drfve of 8 paced bNt5 {51) from the high right atTfum,
the last of which ls shown. There ls abrupt prolongation of the AH Interval reflectfng the•jump•from the fast to the slOW' AVN pathway.
The cycle Is completed when there Is conduction biick to the atrium (A) via the retTograde fast AVN pathway. The atriill electrogram
at the His site HBE is not seen but is probably the earliest retrograde A (central activation} but obscured within the ORS.
conduction (i.e., anterograde conduction occurs exclusively over the slow pathway and ret-
rograde conduction exclusively over the fast pathway). The demonstration of retrograde
dual-pathway physiology is less frequent
It is useful to appreciate that dual-pathway physiology is frequently present in patients without

supraventricular tachycardia and has been reported in up to 4696 of patients undergoing elec-
trophysiologic studies for reasons other than supraventricular tachyc:ardia..u.44 Finally, the pres-
ence of dual pathways does NOT exclude atrial tachycardia or AV reentry as the mechanism of
SVT because AT may conduct over a slow pathway and present with a long PR interval and the
slow pathway may be the anterograde limb ofan AV reentrant circuit.
Acute Therapy
The treatment options for atrioventricular nodal reentrant tachycardia are not dissimilar from
those for atrioventrkular reentry. Cardioversion is indicated at any time in the event of serious
hemody:namk decompensation, although this should rarely be necessary. Vagotonic maneu-
vers such as carotid sinus massage, use of edrophonium (Tensilon) or the Valsalva maneuver
are time-honored and may be very effective in some patients but probably rarely invoked today.
Patients may find self-administered vagal maneuvers such as Valsava effective. Anterograde
conduction is more responsive to traditional "AV node blocking" drugs such as digoxin, ver-
apamil, and adenosine than retrograde conduction. The latter is, in general. more responsive
to the membrane-active antlarrhythmic drugs, namely c:lass la (quinidine, disopyramide, pro-
cainamide) and le (Flecainide, propafeno.ne) agents. The latter are not commonly used today
for acute therapy.
This said, adenosine is the most widely utilized drug, well-tolerated with rare failure to ter-
minate. Intravenous verapamil or diltiazem are reasonable second-line agents for those with
contraindication to adenosine such as severe asthma or when adenosine works but SVT recurs
repeatedly.
Chronic Management
Patients with relatively infrequent and better-tolerated episodes may choose to deal with them
on an as-required basis, seeking medical help when needed. Some patients may also be suc-
cessful at learning vagotonic maneuvers that may terminate tachycardia, such as the Valsalva
maneuver, carotid sinus massage, and facial ice-water immersion. The mainstay of chronic pro-
phylactic therapy in the past has been pharmacologic, largely on a trial-and-error (empirical)
basis. Drug therapy may be directed at the anterograde limb ofthe circuit (calcium blocker, beta
blocker, digoxin) or the retrograde limb (flecainide, propafenone) or both (sotalol amiodarone).
Combination therapy or drugs that combine more than 1 mode of action (for example, sotalol
with class 3 and beta-blocking effect) may be used in difficult cases.
It is fair to say that curative slow pathway ablation, radiofrequency or cryothermic, has become
the prevalent management for problematic AVN reentry and first-line (see Chapter 17). The
very high success rate and safety of the procedure frequently done on an outpatient basis make
it the preferred approach in most patients.4 S.46
Anatomic Considerations
There remains very little dispute about the functional validity of the dual-pathway physiology
concept to explain AV node reentry. The anatomic correlates of the constituents of the circuit
are not as well-established. Electrophysiologic data support the view that the entire circuit in
AV node reentry is in the AV "junctional" area. This is most evident from the following obser-
vations during tachycardia:
1. The ventricles are not required for maintenance of tachycardia. Block below the recorded
His electrogram does not affect tachycardia'7- 49 (Figure 6-20).
2. The His bundle is not essential to perpetuation of tachycardia. Tachycardia can continue
with block above the recorded His,48 and AV node reentry is inducible in the face of ventric-
ular atrial block at the AV node level.50
3. Atrial activity as measured by electrode catheters is not necessary for perpetuation of
tachycardia.38•51
Observations after operative and ablative therapy ofAV node reentry have also provided insights
into AV node function. It is clear that either the fast pathway or the slow pathway can be ablated
rather selectively, the fast pathway generally being posterior and inferior to the recorded His
bundle site and the slow pathway generally at the "base" of Koch's triangle between the orifice of
the coronary sinus and the tricuspid leaflet. In addition, there may be multiple slow pathways.
The anterograde fast pathway and retrograde fast pathway may be ablated together but not
necessarily, suggesting that they may be anatomically distinct. 52 One must also remember that
"fast" and "slow" refer to conduction time and not necessarily to breakout site into the atrium
and these pathways are best described by both conduction time and breakout site.
Whether or not fast and slow pathways are "extra nodal" or "intra nodal" may be a moot
issue. The AV junctional area in its entirety is situated at the base of the atrial septum on the
II
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PllMIB
FIGURE 6-20 • AV node reenuy wld'I block below the His. Panel A shows supraverrcrlcular tachycaltlla with a Pwave dlscemlble
precisely at mld·dlastole. AP wave Is also dlscemlble In the termlnal portion of the QRS In many leads. APVC converts the tachy-
cardia to a faster ventricular, namely AVNRT with 1·to·1 conduction. Alttiough I.tits Is undoubtedly related to concealed conduction
from the PVC, d'le exact mechanism cannot be determined. Of note, the 1·to·1 tachycardia has longer cycle length than d'le atrial
cycle length during 2·to·1 block and this Is accounted for by AV prolongiltlon.The PVC must have penetrated d'le actual circuit to
change the a, perhaps causing a switch to another antet'ograde slow AV node pathway. Panel 8 shows electrophysiologic testing
demonstrating typlcal AV nodal reentry with dual.pathway physlology. Two-to-one block below I.tie recorded His bundle elec:m>-
gram was observed lntermlttently. (Abbreviations as In previous flgul'ff.)
Transitional cell zone

A) Posterior
B) Deep Penetrating bundle

Tendon of todaro
Compact node
Origin of tricuspid valve
FIGURE 6-21 • Schematic representation of the anatomy of the AV node. The AV node ls seen as an Irregular structure with multl-
ple atrial inputs. It is tempting to hypothesize that the so-called slow pathway is the posterior protuberance of the AV node toward
the coronary sinus as depicted in this diagram. (Reproduced with permission from Becker AE, Anderson RH. Morphology of the
human atrioventricular junctional area. In: Wellens H, Lie K. Janse M, eds. The Conduction System ofthe Heart. Springer; 1978;263-286.)
right atrial aspect of the central fibrous body. The boundary between atrium and AV node
is indistinct and irregular, both anatomically36 and physiologically. 37 It is probable that the
slow and fast pathways are in the "transitional zone" as described by Becker and Anderson
(Figure 6-21), with the slow pathway corresponding to the crista terminalis "extension" of the
AV node. Transitional cells at the "boundary" of the AV node and atrium have rapid upstroke
action potentials but transitional morphology when examined histologically. The transitional
zone is thought to account for the normal delay in AV nodal conduction, whereas the compact
AV node is thought to account for most of the delay during Wenckebach periodicity. Because
the transition between AV node and atrium is not a clear boundary, this issue may never be
resolved for the purist.
JUNCTIONAL TACHYCARDIA
Junctional tachycardia not related to reentry or intra-Hisian re-reentry is relatively uncommon,
especially as a chronic or recurrent arrhythmia.53.54 Fascicular foci or nodofascicular pathways55
may form the substrate for narrow QRS tachycardia that can be confused with pure junctional
tachycardia or AVNRT junctional tachycardia may be observed in infants less than 6 months old
and as a perioperative arrhythmia in children undergoing cardiac surgery. It generally occurs
within 12 h of cardiac surgery and gradually dissipates over the subsequent hours to days if the
patient survives the perioperative period. Pediatric patients may present with congestive heart
failure and tachycardia-induced myopathy. The QRS during tachycardia has supraventricular
morphology and a widely variable rate. The tachycardia rate and regularity may be more vari-
able within a patient than that seen in AV node reentry. Although the mechanism of junctional
tachycardia is frequently quoted as "automatic," large, systematic studies using intracardiac
recording techniques are not available.
Nonparoxysmal junctional tachycardia may be seen in adults but is infrequent. The descrip-
tor nonparoxysmal refers to the onset, which shows more gradual acceleration rather than an
abrupt onset with immediate reversion to the tachycardia rate. Clinical settings can include
the acute phase of myocardial infarction, the postoperative phase of cardiac surgery (espe-
cially valve surgery), digitalis intoxication, and acute myocarditis.56 Electrocardiographically,
the QRS morphology is supraventricular and the rate is generally between 70 and 130/min,
although it can be as high as 200/min or greater. The rate is frequently variable and the tachy-
cardia may be irregular. AV dissociation is frequently observed, potentially creating an impres-
sion of ventricular tachycardia, especially if bundle branch block aberration is present.
The tachycardia rate increases with exercise and isoproterenol and decreases with beta block-
ers. Evidence supporting a mechanism is sparse but nonparoxysmal junctional tachycardia in
adults is generally thought to be a triggered rhythm due to delayed after-depolarizations or
enhanced automaticity.
Therapy for nonparoxysmal junctional tachycardia in adults is guided by trial and error when
necessary. Beta blockers will slow the rate but controlled systematic drug studies with other
agents are not available. Tachycardia generally resolves with resolution of the primary asso-
ciated problem. Atrial pacing greater than the spontaneous tachycardia rate may occasionally
be helpful in instances where tachycardia is hemodynamically problematic and AV synchrony
would help in spite of a slightly higher pacing rate. Experience with other antiarrhythmic agents
is largely anecdotal. Catheter ablation would be reasonable in problematic instances but the
incidence of heart block is substantial.
REFERENCES
1. Klein GJ, Sharma AD, Yee R, Guiraudon GM. Classification of supraventricular tachycardias. Am J CardioL
1987;60(6):27-31. doi:l0.1016/0002-9149(87)90705-3
2. Bonke FI, Bou.man LN, Schopman FJ. Effect of an early atrial premature beat on activity of the sinoatrial node and
atrial rhythm in the rabbit. Circ Res. 1971:29(6):704-712.
3. Narula OS. Sinus node re-entry: a mechanism for supraventricular tachycardia. Circu/ation. 1974;50(6):1114-1128.
4. Bauernfeind RA. Chronic nonparoxysmal sinus tachycardia in otherwise healthy persons. Ann Intern Med.
1979;91 (5):702. doi: 10.7326/0003-4819-91-5-702
5. Olshansky B, Sullivan RM. Inappropriate sinus tachycardia. I Am Coll Cardiol. 2013;61(8):793-801. doi:l0.1016/j.
jacc.2012.07.074
6. Josephson ME, Seides SF. Supraventricular Tachycardias. In: Clinical Cardiac Electrophysiology: Techniques and
Interpretations. Lea & Febiger; 1979:147-190.
7. Llu CF, Cheung Jw. Ip JE, et al. Unifying algorithm for mechanistic diagnosis of atrial tachycardia. Circ Arrhythm
Electrophysiol. 2016;9(8):e004028.
8. Packer DL, Bardy GH, Worley SJ, et al. Tachycardia-induced cardiomyopathy: a reversible form ofleft ventricular
dysfunction. Am J Cardiol. 1986;57(8):563-570.
9. Akhtar M. Mechanisms of supraventricular tachycardia originating in the atria. In: Atrial Arrhythmia. St Louis,
MO: Mosby Year Book; 1990:270-281.
10. Haines DE, DiMarco JP. Sustained intraatrial reentrant tachycardia: clinical, electrocardiographic and electrophys-
iologic characteristics and long-term follow-up. J Am Coll Cardiol. 1990;15(6):1345-1354.
11. Habibzadeh MA. Multifocal atrial tachycardia: a 66 month follow-up of50 patients. Heart Lung. 1980;9(2):328-335.
12. Levine JH, Michael JR. Guarnieri T. Treatment of multifocal atrial tachycardia with verapamil. N Engl J Med.
l 985;312(1):21-25.
13. Lewis T. Report CXIX. Auricular fibrillation: a common clinical condition. BMJ. 1909;2(2552):1528.
14. Hurwitz JL, German LD, Packer DL, et al. Occurrence of atrial fibrillation in patients with paroxysmal supraven-
tricular tachycardia due to atrioventricular nodal reentry. Pacing Clin Electrophysiol. 1990;13(6):705-710.
15. Jolly WA, Ritchie WJ. Auricular flutter and fibrillation. Heiirt. 1910;2:177.
16. Lee KW. Yang Y, Scheinman MM. Atrial flutter: a review of its history, mechanisms, clinical features, and current
therapy. Curr Probl Cardiol. 2005;30(3):121-167.
17. Rosenblueth A, Ramos JG. Studies on flutter and fibrillation: II. The influence of artificial obstacles on experimen-
tal auricular flutter. Am Hearl J. 1947;33(5):677-684.
18. Klein GJ, Guiraudon GM, Sharma AD, Milstein S. Demonstration of macroreentry and feasibility of operative
therapy in the co=on type of atrial flutter. Am l Cardiol. 1986;57(8):587-591.
19. Cosio FG, L6pez-Gil M, Goicolea A, Arribas F, Barroso J. Radiofrequency ablation of the inferior vena
cava-tricuspid valve isthmus in common atrial flutter. Am J Cardio/.1993;71(8):705-709.
20. Waldo AL, Carlson MD, Biblo LA, Henthorn RW. The role of transient entrainment in atrial flutter. In: Atrial
Arrhythmias: Current Concepts and Management. St Louis, MO: Mosby Year Book; 1990:210.
21. Waldo AL, Carlson MD, Henthorn RW. Atrial flutter: transient entrainment and related phenomena. In: Cardiac
Electrophy$iology: From Cell to Bedside. Philadelphia, PA: WB Saunders; 1990:530-536.
22. Olshansky B, Okumura K, Henthorn RW, Waldo AL. Characterization ofdouble potentials in human atrial flutter:
studies during transient entrainment./ Am Coll Cardiol. 1990;15(4):833-841.
23. Page RL, Jogl.ar JA, Caldwell MA, et al. 2015 ACC/ AHA/HRS guideline for the management of adult patients with
supraventricular tachycardia: a report of the American College of Cardiology/American Heart Association Task
Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll CardioL 2016;67(13):e27-e115.
24. Ellenbogen KA, Stambler BS, Wood MA, et al. Efficacy of intravenous ibutilide for rapid termination of atrial
fibrillation and atrial flutter: a dose-response study./ Am Coll Cardiol. 1996;28(1):130-136.
25. Feld GK, Fleck RP, Chen PS, et al. Radiofrequency catheter ablation for the treatment of human type 1 atrial
flutter. Identification of a critical zone in the reentrant circuit by endocardial mapping techniques. Circulation.
1992;86(4):1233-1240.
26. Saoudi N, Atallah G, Kirkorian G, Touboul P. Catheter ablation of the atrial myocardium in human type I atrial
flutter. Circulation. 1990;81(3):762-771.
27. Moe GK, Preston JB, Burlington H. Physiologic evidence for a dual AV transmission system. Circ Res.
1956;4(4):357-375.
28. Kistin AD. Multiple pathways of conduction and reciprocal rhythm with interpolated ventricular premature sys-
toles. Am Heart J. 1963;65(2):162-179.
29. Schuilenburg RM, Durrer D. Atrial echo beats in the human heart elicited by induced atrial premature beats.
Circulation. 1968;37(5):680-693.
30. Rosen KM, Mehta A, Miller RA. Demonstration of dual atrioventricular nodal pathways in man. Am J Cardiol.
1974;33(2):291-294.
31. Denes P, Wu D, Dhingra RC, Chuquimia R, Rosen KM. Demonstration of dual AV nodal pathways in patients with
paroxysmal supraventricular tachycardia. Circulation. 1973;48(3 ):549-555.
32. Wu D. Dual atrioventricular nodal pathways: a reappraisal. Pacing Clin ElectrophysioL 1982;5(1):72-89.
33. Leitch JW, Klein GJ, Yee R, Leather RA, Kim YH. Syncope associated with supraventricular tachycardia. An
expression of tachycardia rate or vasomotor response? Circulation. 1992;85(3):1064-1071.
34. Kay GN, Pressley JC, Packer DL, Pritchett EL, German LD, Gilbert MR. Value of the 12-lead electrocardiogram in
discriminating atrioventricular nodal reciprocating tachycardia from circus movement atrioventricular tachycar-
dia utilizing a retrograde accessory pathway. Am J CardioL 1987;59(4):296-300.
35. linuma H, Dreifus LS, Mazgalev T, Price R, Michelson EL. Role of the perinodal region in atrioventricular nodal
reentry: evidence in an isolated rabbit heart preparation./ Am Coll Cardiol. 1983;2(3):465-473.
36. Becker AE, Anderson RH. Morphology of the human atrioventricular junctional area. In: The Conduction System
ofthe Heart. Springer; 1978:263-286.
37. Janse MJ, Van Capelle FJ, Anderson RH, Touboul P, Billette J. Electrophysiology and structure of the atrioventric-
ular node of the isolated rabbit heart. In: The Conduction System of the Heart. Springer; 1978:296-315.
38. Josephson ME, Miller JM. Atrioventricular node reentry tachycardias. Is the atrium a necessary link. In: Atrial
Arrhythmia: Current Concepts and Management. St. Louis, MO: Mosby Year Book; 1990:331-339.
39. Schuger CD, Steinman RT, Lehmann MH. The excitable gap in atrioventricular nodal reentrant tachycardia.
Characterization with ventricular extrastimuli and pharmacologic intervention. Circulation. 1989;80(2):
324-334.
40. Sung RJ, Styperek JL, Myerburg RJ, Castellanos A. Initiation of two distinct forms of atrioventricular nodal
reentrant tachycardia during programmed ventricular stimulation in man. Am J Cardiol. 1978;42(3):404-415.
41. Wu D, Denes P, Amat-Y-Leon F, Wyndham CR, Dhingra R, Rosen KM. An unusual variety of atrioventricular
nodal re-entry due to retrograde dual atrioventricular nodal pathways. Circulation. 1977;56(1 ):50-59.
42. Wang NC. Dual atrioventricular nodal nonreentrant tachycardia: a systematic review. Pacing Clin Electrophysiol.
2011;34(12):1671-1681.
43. Casta A, Wolff GS, Mehta AV, et al. Dual atrioventricular nodal pathways: a benign finding in arrhythmia-free
children with heart disease. Am l Cardiol. 1980;46(6):1013-1018.
44. Akhtar M. Supraventricular tachycardias: electrophysiologic mechanism$, diagnosis, and pharmacologic therapy.
In: Tachycardias: Mec:hanisms, Diagnosis, Treatment. 1984:121-147.
45. Katritsis DG, Zografos T, Katritsis GD, et al. Catheter ablation vs. antiarrhythmic drug therapy in patients
with symptomatic atrioventricular nodal re-entrant tachycardia: a randomized, controlled trial. Europace.
2016;19(4):602-606.
46. Scheinman M. Supraventricular tachyarrhythmias: drug therapy versus catheter ablation. Clin Cardiol.
1994;17(S2):11-11.
47. Wellens HJ, Wesdorp JC, Diiren DR, Lle Kl. Second degree block during reciprocal atrioventricular nodal tachy-
cardia. Circulation. 1976;53(4):595-599.
48. D!Marco JP, Sellers ID, Belardinelli L. Paroxysmal supraventricular tachycardia with Wenckebach block: evidence
for reentry within the upper portion of the atrioventricular node. JAm Coll Cardiol. 1984;3(6):1551-1555.
49. Schmitt C, Miller JM, Josephson MB. Atrioventricular nodal supraventricular tachycardia with 2: 1 block above
the bundle of His. Pacing Clin Electrophysiol. l 988;11(7):1018-1023.
50. Molina RZ, Fujimura 0, Sharma AD, Yee R, Klein GJ. Atrioventricular nodal tachycardia in the absence of retro-
grade conduction. Can J Cardiol. 1989;5(3):143-146.
51. Bauernfeind RA, Wu D, Denes PO, Rosen KM. Retrograde block during dual pathway atrioventricular nodal
reentrant paroxysmal tachycardia. Am J Cardiol. 1978;42(3):499-505.
52. Fujimura 0, Guiraudon GM, Yee R, Sharma AD, Klein GJ. Operative therapy of atrioventricular node reentry and
results of an anatomically guided procedure. Am J Cardiol. 1989;64(19):1327-1332.
53. Ruder MA, Davis JC, Eldar M, et al. Clinical and electrophysiologic characterization of automatic junctional
tachycardia in adults. Circulation. 1986;73(5):930-937.
54. Scheinman MM, Gonzalez RP, Cooper MW, Lesh MD, Lee RJ, Epstein LM. Clinical and electrophysiologic fea-
tures and role of catheter ablation techniques in adult patients with automatic atrioventricular junctional tachy-
cardia. Am J Cardiol. 1994;74(6):565-572.
55. Chung R, Wazni 0, Dresing T, et al. Clinical presentation ofventricular-Hisian and ventricular-nodal accessory
pathways. Heart Rhythm. 2019;16(3):369-377. doi:l0.1016/j.hrthm.2018.08.006
56. Rosen KM. Junctional tachycardia. Mechanisms, diagnosis, differential diagnoaia, and management. Circulation.
1973;47(3):654-664.
Preexcitation Syndromes
Eric N. Prystowsk:y, MD
HISTORICAL PERSPECTIVE
There has been a fascination with the preexcitation syndromes that has spanned decades and
led to a rich history of discovery (Figure 7-1). Over a century ago investigators began looking
into the mechanism of how an atrial impulse activated the ventricle.1 Stanley Kent reported
on an atri.oventricular (AV) connection in mammalian hearts. This nodelike structure most
likely does not represent the AV muscle connection more typically described by anatomists
in patients with preexcitation, and Sir Thomas Lewis dismissed this alternative theory of AV
conduction. However, Mines was more visionary and postulated the use of this AV connection
in a reentrant circuit using the main AV bundle for anterograde activation and the accessory
pathway (AP) for retrograde conduction. Electrocardiographic (ECG) evidence of preexcita-
tion was reported by Cohn and Fraser, as well as Wilson. who also demonstrated intennittent
preexcitation in one of the figures. The mechanism for the delta wave of preexcitation had
several postulates including mechanical, chemical, and electrical Holzmann and Scherf. and
Wolferth and Wood suggested that the abnormal ventricular depolarization was due to conduc-
tion over the anomalous AV connection.
Wolff. Parkinson, and White in 1930 reported on a "combination of bundle-branch block.

abnormally short P-R interval, and paroxysms of tachycardia ... in young, healthy patients
with normal hearts" as a distinctive entity. Years later they published a follow-up of the original
series of patients and made some key observations: congestive heart failure could rarely occur
from uncontrolled tachycardia (now referred to as tachycardia-induced cardiomyopathy); the
delta wave disappeared in many patients; and digitalis ineffectively controlled the ventricular
rate in a patient with atrial fibrillation (now it is .know that digitalis can also increase the risk of
sudden death in some patients with preexcitation).
Anatomic confirmation of typical APs was reported separately by both Wood and Ohnell, and
Mahaim described accessory nodoventricular and fasciculoventricular connections (NOT attio-
fascicular connections that are often incorrectly called Mahaim fibers). Lev and Brechenmacb.er
made additional anatomic findings of preexcitation, including ones that connect the atria with
the His bundle (atri.o-Hisian tract). The clear demonstration of an AP as the cause of pre-
excltation was shown by several investigators: Durrer, Burchell, and Wallace, and Wellens in
FIGURE 7-1 • History of the preexcltlrtlon syndromes. (See text for detallsJ
Amsterdam and Gallagher at Duke contributed many observations to our understanding ofthe
preexcitation syndrome. The decades of research led to possibly the most important event in
nonpharmacologic therapy fo.r cardiac arrhythmias-the first successful surgical disse<:tion of
an AP with the cure of the patient by D.r. Will C. Sealy at Duke University.
GENERAL OVERVIEW
Under usual circumstances, an impulse originating in the atrium conducts over the normal AV
node-His-Purkinje system to activate the ventricles. When an accessory pathway is present, the
opportunity exists to bypass some or all ofthe normal conducting system. The term ventricular
preexcitation denotes that an atrial impulse activates at least some part of the ventricular muscle
earlier than anticipated, assuming conduction had occurred over the normal AV conduction
system.1 Several anatomic forms of APs have been identified (Figure 7-2).1.i However, an acces-
sory AV muscle connection is the cause of preexdtation in more than 90% of patients.
Recent data have clarified certain pathway characteristics. For example, a slowly conducting
AV connection that is ordinarily used only for retrograde conduction in a specific type of
tachycardia termed the permanent form ofjunctional reciprocating tachycardia (PJRT) can also
be used for anterograde conduction.' In addition, a form of reentrant preexcited tachycardia
previously thought to use a nodoventricular or nodofascicular fiher for anterograde conduc-
tion in most cases actually conducts over an atrlofasci.cular tract (atrium to right bundle)
(Figure 7-2).H
CHAPTER 7 • Preexcltatton Syndromes 141
AV Connection Atrlofascicular Tract

Atrium-+His Atrium -+RB
Mahalm flbers
Fasclculoventricular Nodoventricular
FIGURE 7·2 • Classlflcation cf the preexcltatlon syndromes. The European Study Group for Preexdtatlon suggem!d an anatomic
dasslficatton for accessory pathways {APs) with use of tract to designate APs that Insert Into speclallzed conduction ttssue and
connection when they terminate Into working myocardium. Four generallzed types of preexcltatton syndromes are demonstrated
Recent data suggest variations ofsome of these broad categories, as detailed in the text. AVN, atrioventricular node; RB, right bun-
dle; LB, left bundle. (Reproduced with pennission from Prystcwsky EN, et al. Med Clin North Am. 1984;68:831.)
The preexcitation syndrome is commonly referred to as Wolff-Parkinson-White (WPW) syn-

drome but the WPW syndrome more properly defines patients with accessory AV connections
that have tacbyarrhythmias.7 Ventricular preexcitation should be used to identify the presence
of a delta wave on the ECG and does not imply symptoms.
Electrophysiologic studies over the past 2 decades have enabled investigators from around
the world to define more precisely mechanisms of preexcitation and the reentrant circuits
involved in tachycardia. The study of patients with this disorder involves the placement of
several catheters in multiple areas of the heart. Cardiac pacing and recording of electrograms
from these various sites are done to identify pathway location and mechanisms of tachycardia.
In general, we perform electrophf5iologic studies o.n almost all patients with WPW syndrome,
typically followed by catheter ablation of the accessory pathway(s) during the same session. The
approach to the asymptomatic patient with ventricular preexcitation is more controversialHo
Patients can have atrial fibrillation with a rapid preexcited ventricular response (Figure 7-3)
that can rarely degenerate into ventricular fibrillation and cause sudden cardiac death.1"'11-15
Since the risk for sudden death is exceedingly small in the asymptomatic patient, we do not
favor routine testing of all these individuals. Our current approach is detailed later in the
chapter.
FIGURE 7-S • Atrlal fibrillation with a rapid preexdted ventricular response.
MECHANISMS OF PREEXCITATION
A typical ECG pattern from a patient with an AV connection is noted in Figure 7-4.. The PR inter-
val is short (<0.12 s); the early portion of the QRS complex has a slurred upstro.ke (delta wave);
and the QRS complex is prolonged (0.12 s or more). In most patients the preexcited complex is
present constantly, but in some, intermittent pree:xdtation is present (Figure 7-S). Intermittent
pree:xdtation bnplies a poor margin of safety of conduction over the accessory pathway; rapid
pree:xclted ventricular responses during atrial fibrillation are extremely uncommon in this situa-
tion. Although relatively rare in our experience, pree:xdtation may become manifest only during
situations resembling supernormal conduction over the accessory pathway (Figure 7-6).141s
The preexcited QRS complex represents fusion of a supraventricular impulse depolarizing

ventricular myocardium over the normal AV conduction system and the accessory pathway
(Figure 7-7). In Panel A, a QRS complex with a late premature atrial beat is recorded. The red
portion of the ventricular myocardium represents that area of the ventricle that is activated
over the accessory pathway and forms the delta wave, which is red in ECG lead I. Note that
conduction over the AV node and His-Purkinje system occurs with similar timing to activation
of the ventricle over the AP; therefore, minimal preexcltation is present. Panel B represents
conduction ofan early premature atrial complex. As expected, AV nodal delay occurs, as repre-
sented by increased conduction time through the AV node on the bottom schematic. However,
conduction time over the AP usually remains the same even with premature atrial complexes;
~ -
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FIGURE 7-4 • Preexdted QRS complexes In a patient with WPW syndrome.
therefore. more of the ventricle can be activated over the accessory pathway (in red). which
results in a widened QRS complex. The His bundle deflection is no longer identified. A prema-
ture atrial complex that occurs early enough when the accessory pathway is still refractory will
block over the AP (Panel C).Then AV node conduction will be delayed and the QRS complex
will normalize, because ventricular activation (green) results entirely by the normal AV con-
duction system. Thus, the PR interval prolongs but a delta wave is now absent
Ventricular preexcitation is a classic case offusion, and the resultant QRS complex depends on
several factors. These include the relative conduction times over the AP and normal conduc-
tion system and the relationship of the origin of the atrial impulse to the location of the AP. For
example, minimal pree.i:citation often occurs in a patient with a left lateral free-wall accessory
pathway with relatively short AV nodal-His-Purkinje activation time (Figure 7-8). This figure
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FIGURE 7·5 • lntermittl!nt preexcltation. During normal sinus rhythm, preexcltatlon occurs In complexes 1, 3, S, and 7 and a nar-
raw QRS morphology representing normal conduction from the atrium to ventricle is present in complexes 2, 4, 6, and 8 to 10.
1 11 1111111111111111 11 11111 111 1111 1 1 1111 1 1111 I I I I I I I I I I I I

AA-3
FIGURE 7-6 • Supemormal conductfon over an AP. Tracings from top to bottom are ECG leads I, II, Ill,v,, and V6 and Intra cardiac
electrcgrams from the high right atrium (HRA), His bundle area (HBE), and right ventricle (RV). A premature atrfal stlmulus (S) Is
Initiated In die high right atTlum and results ln ventricular preexcitation. Note that the QRS complex widens and die Hls bundle
electrogram moves into die ventricular electrogram. In this patient ventricular preexcitation was noted only during slow sinus rates
and with very early atrial premature complexes.This suggests supemonnal conduction over the accessory padiway.
demoll8trates ventricular preexcitation during normal sinus rhythm. Note that atrial activation
near the AV node occurs 60 ms after the Oll8et of the P wave, whereas activation of the base of
the lateral left atrium occurs at 100 ms. Preexcitation is minimal because the accessory pathway
is located in the left atriwn relatively far from the origin of the sinus impulse. If this patient had
very short AV conduction times over the nonnal system, preexcitation might not be apparent on
the standard ECG. This concept is explored further in Figure 7-9. This patient has a left lateral
accessory pathway. and minimal preexcitation is present during sinus rhythm (Figure 7-9A);
note the often observed characteristic feature of this location of the QS configuration in aVL
with an R:S :<?1.0 in V1• Pacing from the right atrium produced AV nodal delay and ventricular
preexcitation is more marked (Figure 7-9B). However, pacing from the coronary sinus near the
atrial origin of the accessory pathway at the same heart rate dramatically increases ventricular
preexcitation, as is most evident in the precordial leads (Figure 7-9C). Since the pacing site is
near the AP, conduction proceeds quickly from the atrium to the ventricle over this structure
and the QRS complex is maximally pr~xcited. The differential effect of site of origin of the
atrial impulse and activation time over the normal conduction system is useful in identifying
pathway locations, and data suggest that in the presence of preexcitation a left free-wall acces-
sory pathway is almost alwa}'5 present if the PR interval is >0.12 s.16
1-----"-
FIGURE 7·7 • Mechanism of preexclta'don with AV connection. From top to bottom, tradngs are ECG lead ~HI$ bundle electro-
gram, and a schemattc of AV conduction that can occur over the AP ldenUfled on the left side of the figure or the normal AV node-
Hls.Purklnje system seen In the center. (See text for deta!lsJ
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u
35
0
HRA
60
HBE
!i_.'V-V
' "h
PCS
100
DCS I ~ ~
RV
f 1
FIGURE 7·1 • Activation times from the right and left atria during sinus rhythm. PCS, proximal coronary sinus; DCS, dlstal coro-
nary sinus. (See text for details.) (Reproduced with permission from Pry.stowsky EN, et al. Med Qin North Am. 1984;68:831.}
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FIGURE 7-9 • (Continued}
MECHANISM OF ATRIOVENTRICULAR REENTRANTTACHYCARDIA

Atrioventricular reentrant tachycardia (AVRT) is the paradigm of reentry. Reentrant excitation
can occur when at least 2 functionally distinct path.ways of conduction are present. Unidirec-
tional block is initiated in one pathway; and the ensuing conduction time is slow enough over
the nonblocked pathway to allow recovery of excitability in the blocked pathway. This permits
retrograde conduction over the previously blocked pathway and completion of the reentrant
circuit (Figure 7-10).
Reentrant AV tachycardia is defined as either ortbodromic or antidromic. Orthodromic refers to

propagation of an impulse in the normal direction. In AV reentry. this occurs when conduction
proceeds in the anterograd.e direction from the atrium over the normal conduction system to the
ventricle and retrogradely backto the atrium over the AP. Antidromic reentry designates retrograde
conduction over the normal AV node-His-Purkinje syiitem with anterograde conduction over an
AP (see later; Figure 7-27). With ortbodromic reentry, the QRS is narrow unless bundle branch
block is present
Premature atrial or ventricular complexes can initiate orthodromic AV reentry.1•17 Figure 7-11
demonstrates induction of AV reentry with a premature atrial complex. In Panel A. the high
right atrium is paced at a cycle length of 600 ms and a premature atrial complex is introduced
AVN
His
Pan•IA PaMIB Pantle
FIGURE 7·1 o • Schematic l'el)resentation of induction of AV reentrant tachyardia. Panel A. Conduction of an atrial impulse over
1he AV node (AVN) and Hls-PurklnJe system {HIS} as well as over the accessory pathway (AP). Panel B. Apremature atrlal complex
blocks antercgradely over the accessory pathway and conducts slowly enough over the normal system to allow retrcgrade con-
duction over the AP. Panel C. Retrograde conduction proceeds over the AP with ensuing anterograde conduction, thus ccmpletlng
the tachycardia drcult. (Reproduced with permission from Prystowsky EN. Diagnosis and management of the preexcltatlon syn-
dromes. Cutr Probl Cardlol. 1988;13:225.)
II
Ill
v,
HBE
DCS -t--------1,_-'""'""_ _ __
CS4
CS3
CS2
cs,
PanalA Panel B
FIGURE 7·11 • lnltlattcn of AV reenuy with a premature atTlal complex. cs. through CS, are unipolar recordings from the proximal
pole to the dlstal pole of a quadrfpolar catheter In the coronary sinus (CS). (See text for details.)
CHAPTER 7 • Preexcitation Syndromes 149
at an interval of 300 ms. The premature complex blocks anterogradely over the accessory
pathway and conducts tluough the AV node, as demonstrated by the His depolarization (H2).
However, tachycardia is not initiated because the impulse does not conduct to the ventricle,
which is a requisite part of the AV reentrant tachycardia circuit. In fact, this is very important
to remember, because this is the only form of supraventricular tachycardia in which ventricu-
lar activation is necessary for initiation and maintenance of the arrhythmia. Panel B demon-
strates a premature atrial complex introduced with an earlier coupling interval of 280 ms. The
accessory pathway is blocked again and conduction through the AV node is accomplished.
In this instance, however, conduction proceeds slowly tluough the His-Purkinje system and
reaches the ventricle with a His to ventricle (H2 - V2) interval of 70 ms. Note that the QRS
complex is no longer preexcited, although right bundle branch block morphology is pres-
ent. Conduction occurs retrogradely over the accessory pathway, which in this case is
in the left atrium, as demonstrated by earliest retrograde activation at the distal coronary
sinus electrogram (DCS and CS 1). Tachycardia starts as anterograde conduction occurs
again over the normal system. Note that the HV interval shortens after a few complexes-a
common occurrence-and the HV interval is now 40 ms. If the interval from the His bundle
electrogram to a constant atrial electrogram is measured, the His-to-atrial interval will be
found to shorten as the HV interval shortens. This critical observation demonstrates that
the His-Purkinje system is part of the tachycardia circuit, which is specific for AV reentry.
In summary, initiation of orthodromic AV reentry with a premature atrial complex requires
block over the accessory pathway, conduction to the ventricle over the normal system, and
retrograde activation of the atrium over the accessory pathway, with subsequent conduction
over the normal conducting system.
Atrioventricular reentry can also occur in a patient with a concealed accessory pathway. A
concealed accessory pathway is one that is incapable of anterograde conduction but can con-
duct in the retrograde direction. 18-22 In this situation, tachycardia is initiated with a premature
atrial complex that provides sufficient anterograde delay to allow retrograde conduction to
occur over the accessory pathway (Figure 7-12). Although manifest or overt preexcitation is
not present in these patients, it is possible that total anterograde block in the AP is not always
present and that, for induction of tachycardia, the premature atrial complex is required to
provide this block in addition to AV nodal conduction delay. Some patients with left-sided
accessory pathways capable of anterograde conduction have rapid conduction over the nor-
mal AV conduction system and demonstrate no ventricular preexcitation in sinus rhythm.
These are not concealed accessory pathways, because preexcitation can become manifest
when AV nodal delay occurs-for example, with premature atrial complexes or during ade-
nosine administration.
Premature ventricular complexes can also induce AV reentry (Figure 7-13). The same concepts
of reentry apply in this situation except that the PVC blocks retrogradely in the normal con-
ducting system and progresses over the accessory pathway for tachycardia induction. Panel A
of Figure 7-13 shows a relatively late PVC conducting over both the accessory pathway and the
normal ventriculoatrial conduction system. In Panel B, an earlier PVC blocks retrogradely in
the His-Purkinje system and progresses over the accessory pathway, with subsequent antero-
grade penetration into the normal conducting system. Panel C shows completion of the reen-
trant circuit. Initiation of AV reentry during programmed ventricular stimulation is shown
in Figure 7-14. In Panel A, the right ventricle is paced at 500 ms (120/min) and 2 PVCs are
II
Ill
v,
HAA
RV _._.....-"'1~.............,.....,rlll"-----...ri1~--..-flf'im....-.~~----""""1
111~nL1~11~11~11,1ul111J111J111~u~11~11~11Lu~u~u~11J.1~n~11~11~11 11~11~111111'11' ~11~11~11J111~11 11l•1J1111l1111l111J11111111i11l111l11
FIGURE 7·12 • Induction of AV reentry with a concealed left-sided AP. Note that during high right atrial pacing {S,), a premature
attlal complex (S;) Increases AV nodal conduc.1fon time. This Is followed by retiograde conduction ever a left free.wall AP Identified
by earliest retJOgrade attlal activation In the dlstal coronary sinus lead. (See text for details.)
introduced. The first PVC (S2) never initiated tachycardia; this is explained by the presence of
a retrograde His bundle depolarization (HJ, indicating that retrograde conduction proceeded
into the AV node.13 Thus, unidirectional AV nodal block was never present However, a second
premature complex (SJ demonstrates no retrograde His depolarization but still conducts
over a left-sided accessory pathway, noted by earliest retrograde atrial activation recorded in
the distal coronary sinus electrogram. Tachycardia occurs with anterograde AV node con-
duction, with left bundle branch block aberrancy yielding a wide QRS tachycardia. In Panel B,
the left bundle branch block aberrancy disappears and a narrow QRS complex tachycardia
is now present. Note that the cycle length of the tachycardia shortens from 350 to 300 ms
with disappearance of left bundle branch block. This important observation is diagnostic of
AV reentry and identifies the site of the accessory pathway to the ipsilateral site of bundle
branch block. The primary reason for a shortening in tachycardia cycle length is a decrease
of ventriculoatrial conduction time from 160 to 70 ms as measured on the distal coronary
AVN
AP
His
PanelA PanelB PanelC
FIGURE 7-13 • Initiation of AV reentTywlth a premature ventricular complex. {See text for detalls.)
sinus lead.l4-.u The reentrant tachycardia circuit is represented schematically for this situation
in Figure 7-15.
The length of the AV reentry cycle depends on the total time through all tissues involved
in the tachycardia circuit. In reality, variation among patients in conduction characteristics
of the accessory pathway, His-Purkinje system, and atria and ventricles are usually minimal
II
Ill
v1
v,,
HRA
HBE
RV
PCS
DCS
PantlA
FIGURE 7-14 • Initiation of AV reentry after 2 premal'Ure ventricular complexes. (See text for details.)
PaMIB
and the major difference occurs because of AV nodal conduction properties. This is also the
reason that patients may sometimes have faster tachycardia rates during exercise than at rest.
Figure 7-16 shows the effects, demonstrated at the time of electrophysiologic study, of intra-
venous isoproterenol and atropine on the rate of AV reentry in one patient. The heart rate is
approximately 150/min during control; but the tachycardia rate increased to 230/min with
isoproterenol at a dose of I µlmin (middle panel). Adequate time was allowed for washout of
isoproterenol; then atropine 0.4 mg was given and tachycardia reinitiated. The tachycardia
rate again increased to approximately 230/min (right-hand panel). In both instances the accel-
eration of the tachycardia rate resulted directly from a shortening of AV nodal conduction
time. Please note also that during the more rapid rates with either isoproterenol or atropine,
QRS amplitude alternans is present and noted particularly in ECG leads V2 and V,. This has
been suggested by some as relatively diagnostic for AV reentry,27 although in our experience
it can occur in any form of supraventricular tachycardia with a fast enough rate, as has been
shown by others.la.l9 An unusual cause of alteration in tachycardia cycle length can be seen in
patients who have dual AV nodal pathways (Figure 7-17).'°
Atrium Atrium AVN
I I
4 4
I I
I I
... __, , , ,,
I I
··················· ···• · '

Narrow ORS LeftBBB
Tachycardia CL= Tachycardia CL=

AH+HV+VA AH+ HV + '!_~(!"':~t. .
FIGURE 7·15 • Schematic of the effect of Ipsi lateral bundle branch block cm the AV reentrant tllchyardla circuit. During narrow
QRS complex tachycardia, conduction proceeds over the normal H~.Purkinje systl!m to the ven111cle and retrogradely over the AP In
this example, located in the left free.wall position. During left bundle branch block (888), the excitation wavefront proceeds over the
right bundle branch and then transseptallyto get to the left ventricle. This anatomical change in the tachycardia circuit prolongs the
ventrlc:\lloattlal CVN Interval and typlcalty prolongs the tachycardia c:yde length (Qj unless total compensa'don occurs In am:erograde
conduction with a shortening of the atrfo-Hls (AH) Interval.lt:, transseptal conduction.
Control lsoproterenol 1 tJg/min iv Atropine 0.4 mg iv
v1T l l m
V2 ~
V3
FIGURE 7·16 • Effect of alterations In autonomic tone with lsoproterenol and atropine on AV reentrant tachycardia rate. (See text
for details.) (Reproduced with permission from Prystowsky EN. Diagnosis and management of the preexcitrtion syndromes. Curr
Pt0b/C4rdiol. 1988;13:225.)
SLO'N AVN PATHWAY FAST AVN PATHWAY
Ill __/I " " !\__
v, -"~~
Lat.RA
Vs _J._-~L--_J~
HBEi
I 41
RV ~~1r--+-~~~~---~~--1r---.~~~1..-+-
I
DCS
~
200ms
Panel A Panel B
FIGURE 7·17 • Rate of atrloventrtcular reentry with conduction over the slow and fast AV nodal pathways. Panel A demonstrates
AV reentry wl1fl conduction over the slow AV nodal pathway (long AH Interval on HBE) In a paUent with dual AV nodal physlology.
Note that the earllest retrograde atrlal actlvBt!on occurs In the lateral right atrium (Lat. RA). In Panel 8, tachycardia was reInitiated,
but this time conduction occurred OVl!f the nonnal, fast AV nodal pathway (short AH lnterwl on HBE), with conUnued retrograde
amduction over the right free-wall AP. The tachycardia rate is considerably faster when AV nodal conduction prcxeeds over the fast
conducting pathway.
ATRIOVENTRICULAR RECIPROCATING TACHYCARDIA

Clinical Diagnosis
Patients with AVRT usually present with ECG evidence of a regular narrow QRS tachycardia
and no evidence of associated heart disease. Although tachycardia can start at any time in life,
it is very common to get a history of childhood arrhythmias that progress in severity as the
patient ages. In fact, if a patient presents with paroxysmal supraventricular tachycardia that
began in childhood, the diagnosis is AVRT until proven otherwise, regardless of the presence or
absence of overt preexcitation on the ECG. When associated heart disease is present. it is most
commonly Ebstein's anomaly, which is usually associated with posteroseptal and right free-wall
accessory pathways,n alone or in combination. There may also be an increased incidence of
WPW syndrome in patients with mitral valve prolapse or idiopathic hypertrophic subaortic
stenosis, although. the data are less compelling with these conditions.
Palpitations are the usual symptoms associated with AVRT, although individuals can have pre-
syncope and syncope. With rates approaching 200/min or more, it is not uncommon for the
patient to experience a retrostemal chest pressure even in the absence of coronary artery dis-
ease. ECG evidence of ST segment depression and T-wave changes commonly appears dur-
ing tachycardia and has no prognostic significance. Whether these events are due to a relative
ischemic state is not known, but these patients typically have rapid AVRT induced at electro-
physiologic study. Patients with AVRT can also have atrial fibrillation with a rapid preexcited
ventricular response; if this arrhythmia degenerates to ventricular fibrillation, cardiac arrest

can occur. Although this is a relatively rare presentation of this syndrome, it has been well-
documented.1·11-13 In our experience, most patients do not give a history of onset of tachycardia
with a consistent initiating event-for example, exercise. The usual situation is a tachyarrhyth-
mia that can occur with rest or exercise, and, uncommonly, can even awaken the patient from
sleep. If an etiologic factor is predominant, this is important in the therapeutic approach to the
patient (e.g., beta-adrenergic blockade to prevent episodes of exercise-induced AVRT).
Laboratory Data
Electrocardiographic observations
Atrioventricular reciprocating tachycardia is usually a narrow QRS tachycardia unless bundle
branch block is present (see Chapter 12). In many patients, a retrograde P wave is evident in the
early ST segment, but this is often not discernible, especially when tachycardia rates are >180/min.
If a retrograde P wave is present and the RP interval is less than half of the RR interval, AVRT
is a likely diagnosis. If a P wave is not evident on the surface ECG during tachycardia, an
esophageal lead may be inserted through the nares. If the resulting VA interval is <95 ms, it is
against the diagnosis of AVRT; whereas a VA interval of >95 ms suggests but does not prove
this diagnosis.1 The most helpful clue is the transition from bundle branch block to narrow
QRS tachycardia with a change in the tachycardia cycle length24-u; (Figure 7-14). Acceleration
of tachycardia with loss of bundle branch block conduction identifies an accessory pathway as
part of the retrograde limb of the tachycardia circuit, and the accessory pathway is anatomically
ipsilateral to the blocked bundle branch; the relatively rare situation of two separate tachycar-
dias in this situation must always be considered. In our opinion, this is the only absolute ECG
observation that identifies an accessory pathway as part of the retrograde tachycardia circuit.
Practically, if the 12-lead ECG in sinus rhythm demonstrates preexcitation, the most likely
diagnosis of tachycardia is AVRT, even though other forms of tachycardia can occur in such a
patient with an accessory pathway.
Electrophysiologic study
In a patient with AVRT, electrophysiologic investigation is undertaken for several reasons and
can identify the presence and location of the accessory pathways (APs) as well as document the
participation of the AP in multiple types of arrhythmias.32 The location ofthe AP can be identi-
fied by several methods that are listed in Table 7-1. A complete description of all of these elec-
trophysiologic methods is discussed in detail elsewhere.1 Regarding ECG criteria for accessory
pathway location, the following general rules are helpful. 1•7•16.33 During maximal preexcitation, a
positive initial (first 40 ms) delta wave in ECG lead V1 identifies a left-sided AP; negative delta
TABLE 7-1 Anatomic location of accessory pathway.

Delta wave morphology
Differential atrial pacing
Retrograde atrial activation sequence
Ventriculoatrial prolongation with ipsilateral bundle branch block
Preexcltatlon Index
Number of PVCs needed for preexcltatlon
Earliest ventricular contraction
Q or isoelectric .6. in U, aVL, or V6
YES NO
LBBB * Q or isoelectric .6.in two of l2, l3, or aVF
YES NO
Rs or RS in Vl, V2 or VJ
NO NO
Rs or RS in Vl orV2
• + QRS~90 msec in ll
and rS in Vl and V2
FIGURE 7·18 • Algorithm to locallze acc:e.ssory pathway. l:i, delta wave;+, positive; RAS, right anteroseptal; LL. left lateral; PS,
posterosepta~ RI.., right lateral. (Reproduced with permission from Milstein S, et al. An algorithm fur the electrocardiographic local-
lzatton ofaccessory pathways In the Wolff-Parklnson-Whl'te syndrome. PACE. 1987;1 &.SSS.)
waves in ECG leads II, III, and aVF locate pathways on the posterior portion of the ventricles;
a positive delta wave in V2 through V,, with a negative or isoelectric delta wave in V1 strongly
suggests a posteroseptal location; positive delta waves in leads II, III, and aVF suggests that the
pathway is located on the anterior portion of the heart; the presence of isoelectric to negative
delta waves in V1 through V,. represents an anteroseptal or anterior location. As V2 through V,.
become positive, the AP on the right side of the heart is located in a progressively more pos-
terior direction around the tricu.spid ring. Figure 7-18 is an ECG algorithm to provide a first
approximation to AP locations.
Differential atrial pacing consists of stimulating different areas of the right and left atria to
determine the shortest stimulus to delta-wave interval, which occurs when the pacing site is
near the atrial insertion of the accessory pathway. An example of differential pacing is noted
in Figure 7-9B and C, taken from a patient with a left-sided AP in which a shorter stimu-
lus to delta wave occurs during coronary sinus pacing (Figure 7-9C). The retrograde atrial
activation sequence is a very important method for locating the AP. Analysis of Figures 7-14
and 7-17 demonstrates the earliest retrograde atrial activation during AVRT to be in the left
atrium, defined by an early coronary sinus atrial electrogram, and in the right atriwn, noted
by an early right atrial electrogram, respectively. in these 2 patients with a left-sided and right-
sided AP.
The concept ofintroducing PVCs during AVRTto cause retrograde preexcitation is represented
in Figures 7-19 and 7-20. Figure 7-19 shows the AVRT tachycardia circuit schematically.
During AVRT, retrograde atrial activation occurs over the AP and anterograde conduction is
over the normal AV conduction system. In this figure, the tachycardia cycle length is identified
as X and a premature ventricular stimulus (St) is introduced during tachycardia. This PVC
conducts retrogradely over the AP to the atrium at a time when anterograde conduction from
AVN
HPS
v St
FIGURE 7·1 t • Schematic representation of atrial preextitation. A. atrium; AVN, AV node; HPS, His-Purkinje system;
V, ventricle; H, His; AP, accessory pathway; St.. stimulus. (See text for details.) (Reproduced with permission from
PrystOWSky EN, Heger JJ, Zlpes OP. The Wolff-Parkinson-White syndrome-diagnosis and treatment Heart Lung.
1981;10:465.)
the previous tachycardia beat has activated the His bundle. This results in shortening of the
tachycardia cycle length and is represented by X minus N (X - N). Since the His bundle has
been anterogradely activated from the prior tachycardia beat, conduction can proceed to the
atrium only by an alternative route, that is, over an AP. Although this confirms the existence of
II
Ill
V1
Ve
LAT.RA
HBE
RV
PCS
DCS
t-i
200ms
FIGURE 7·20 • Atrtal preexcltatlon during AVRT.A PVC CSJ lnltlall!d late In diastole preexcltes ttie atrium with
an Identical retrograde atria I activation sequence as that which first activated the latefal right atrium (IJrt. RA).
The preexcltatlon Index {PO Is 35 ms. {See text f'or detalls.)
an AP that functions in a retrograde direction, it does not confirm that the AP is involved in
the tachycardia. It is also important that the retrograde atrial activation sequence during tachy-
cardia and following the PVC are identical.
Preexcitation of the atrium during AVRTcan be used to locate the AP. One method, the pre-
excitation index, is based on the principle that during right ventricular pacing, a PVC intro-
duced relatively late in diastole can preexcite the atrium in a patient with a right free-wall or
septal AP location, whereas a much earlier PVC is necessary to do this for a left free-wall AP
location.34 In Figure 7-20, AVRT is present and utilizes a right free-wall AP for retrograde
conduction. Note that a relatively late PVC (S2) preexcites the atrium (atrial cycle length
shortens from 460 to 425 ms) and the preexcitation index equals 35 ms. This index is derived
by subtracting the first premature ventricular interval that initiates preexcitation from the
baseline tachycardia cycle length (V1V 1 - V1V2). 34 In patients with left-sided APs, the ability
of one PVC to preexcite the atrium suggests a more posterior AP location, compared with 2 PVCs
required for atrial preexcitation. Two PVCs are more commonly needed if the AP is in a more
lateral position.35 Accessory pathways can also be localized by a variety of methods that iden-
tify ventricular excitation sequences. These techniques localize the earliest area of activation
of the ventricle and represent the site of the AP's insertion into the ventricle. 36.37
Evidence for accessory pathway participation in tachycardia

Several methods that are discussed in detail elsewhere1 can be used at electrophysiologic inves-
tigation to confirm the participation of the AP in AVRT. These are (1) ventriculoatrial (VA)
prolongation with ipsilateral bundle branch block (Figures 7-14 and 7-15); (2) His-atrial prolon-
gation with increase in HV interval (Figure 7-11 ); (3) termination of tachycardia with a PVC that
does not conduct to the atria and occurs when the His bundle is refractory (Figure 7-21); and
prolongation ofthe AA interval with a PVC that is introduced when the His bundle is refractory.
Atrial preexcitation with a PVC introduced when the His bundle is refractory (Figure 7-20) suggests
but does not prove that the AP is involved in the tachycardia circuit
Therapy
The approach to the patient with AVRT involves acute therapy to terminate the arrhythmia and
an approach to chronic suppression of further recurrences. Chronic therapy for these individ-
uals depends on several factors, including the frequency of arrhythmic episodes, the severity
of symptoms associated with the arrhythmia, as well as the patient's age and state of myo-
cardial function. No therapy may be necessary for an arrhythmia that occurs infrequently, is
not sustained, and is associated with only minimal symptoms. In contrast, an arrhythmia that
produces substantial hemodynamic compromise such as syncope needs aggressive suppressive
therapy even if it occurs infrequently.
Chronic therapy can be pharmacologic or nonpharmacologic. Prior to catheter ablation, sur-

gical therapy was often suggested to treat patients who (1) have a history of atrial fibrillation
with rapid preexcited ventricular response; (2) are young and face decades of pharmacologic
treatment; (3) have AVRT as the primary arrhythmia but associated with marked hemody-
namic consequences such as syncope; and (4) are young women of childbearing age who may
face the difficult decision of whether to continue pharmacologic therapy, with its potential
danger to the developing fetus during pregnancies or risk recurrent episodes of tachyarrhyth-
mias that may also cause harm to mother or child. Data from Duke University demonstrated
that the quality of life after surgery was excellent and supported nonpharmacologic treatment
A-4
FIGURE 7·21 • Evidence that an AP Is pan of the tachycardia circuit. An Induced PVC occurs when the His ls refractory and ter-
minates tachycardia without acttvatlng the atria. Stmultaneous recordings from ECG leads I, II, Ill, and Vl; high-right atrium (HRA);
His bundle area (HBE); proxlmal (P), mid (M) and distal (0) CS; and right ventricle (RV).
as first-line therapy in many instances." However, endoc.ardial catheter ablation has eliminated
the need for surgery in ahnost all patients, and it is our usual treatment of choice if chronic
therapy is needed (Chapter 17).sHS In fact. in ce.nters with expertise in ablation of APs, it is typ-
ically recommended for any patient with documented AVRT or who may be at risk for sudden
cardiac death (see later section on Risk Stratification).
Phannacologic therapy is directed toward the AV nodal limb of the tachycardia circuit, the
accessory pathway, or both ('lable 7-2).1 A proposed schema for the acute therapy of WPW
Olgltalls Qulnldlne Flecalnlde

Beta·adrenergfc blockers Proatnamlde Propafenone
Slow channel blockers Dlsopyramlde Sota fol
Purines Lldoc:alne Amlodarone
Mexlletfne
lbutlllde
Hamodynamic Stability
Stable Unstable
Narrow QRS (AVR"D DC cardioversion

WideQRS
1. Vagal maneuvers
2. IV adenosine IV procainamide
3. IV verapamil: diltiazem
4. Repeat vagal maneuvers
Persistent Tachycardia
•
•
I
1-+·-I
IV adenosine
IV verapamil; diltiazem
I
Observe
•Atrial pacing (except AF)
• DC cardioversion
Observe
CONTRAINDICATED
• IV procainamide
• Atrial pacing •Digitalis
• DC cardioversion •Verapamil
FIGURE 7-22 • Approach to acute therapy for tachyarrhythmlas Involving an accessory pathway. {See text for details.)
tachyarrhythmias is demonstrated in Figure 7-22. In a patient in whom AVRT is hemody-

namically unstable, DC cardioversion is the initial treatment of choice. This is a relatively rare
situation; most patients can undergo acute drug therapy or maneuvers to increase vagal tone.
If carotid sinus massage or the Valsalva maneuver does not terminate tachycardia, intravenous
adenosine (6 to 12 mg), verapamil (5 to 10 mg), or diltiazem (15 to 20 mg) is recommended.
If tachycardia still has not terminated, which would be rare, vagal maneuvers can be repeated.
Persistent AVRT can be treated with additional intravenous adenosine, verapamil, or diltiazem.
Alternatively, procainamide given as 50 mg/min intravenously to a total dosage of I 0 mg/kg
with constant recording of the blood pressure can be used. Maneuvers such as atrial pacing-
using either a catheter inserted into the atrium or an esophageal lead-can also be employed,
as can DC cardioversion. One may also opt for an observation period if the patient is stable
and the tachycardia has slowed. With continued rest, it is not uncommon for the arrhythmia to
terminate. If pharmacologic therapy is chosen for chronic suppression of the arrhythmia, drugs
that affect the AV node or APs may be chosen. In our experience, efficacy can be achieved
with many of these agents. It is recommended that digitalis not be used unless the electrophys-
iologic properties of the AP are known, since this agent can shorten AP refractoriness and
might increase the chance for the development of ventricular fibrillation.« If a rapid preexcited
ventricular response is demonstrated during atrial fibrillation at electrophysiologic study, it is
recommended that drugs that affect the AP be given either alone or in combination with agents
that affect the AV node.
Ablation ofaccessory pathways

It is possible to position the tip of an electrode catheter near either the atrial or ventricular inser-
tion site of an accessory pathway on the right, septa!, or left side ofthe heart and cause destruction
of the accessory pathway apparatus typically with radiofrequency energy. Two approaches are
used to ablate left-sided acussory pathways. The retrograde aortic catheterization technique
involves introducing the ablation catheter into a femoral artery and advancing it under flu-
oroscopic guidance across the aortic valve into the left ventricular cavity, or one can use the
transseptal catheterization approach. The site of the accessory pathway is mapped using subtle
movements of the ablation catheter to an area that reoords an accessory pathway potential, early
ventricular activation preceding the surface ECG delta wave in manifest preexcitation, or both
(Figure 7-23). Introduction of energy at such a site will eliminate conduction over the AP.
Mapping of concealed accessory pathways with retrograde conduction only is done during AV
reentry or ventricular pacing. The ablation catheter is positioned at the AV groove to record
adequate atrial and ventricular electrograms. Success occurs at sites that demonstrate the ear-
liest VA intervals for a give.n patient and continuous electrical activity bridging the ventricular
and atrial electrograms, with or without the presence of a discrete accessory pathway potential.
Figure 7-24 shows mapping and ablation of a concealed left free-wall AP.
It is not always dear why a particular lesion causes loss of conduction over the accessory
pathway. As demons1rated in Figure 7-25, which is a schematic representation of the poten-
tial mechanism for sucussful catheter ablation of accessory pathways, the accessory pathway
"apparatus" includes the atrial and ventricular insertion sites and the accessory pathway itself.
In Figure 7-25, a catheter is positioned near the AV ring, where an early ventricular activation
point has been recorded. Radiofrequency energy presumably destroys atrial and ventricular
tissue in this region but might also directly ablate the accessory pathway. Regardless, complete
disruption of any part of the accessory pathway apparatus should result in lack of conduction
over the pathway from the atriwn to the ventricle. It is theoretically possible that in some
RAO LAO
PanelA
FIGURE 7·23 • Ablatton of a rlghtfree.:wall accessory pathway. Panel A. Radlograph ofthe abla'don catheter
position (mlddle catheter) In the right (RAO) and left (LAO) obllque views. The upper and lower catheters are In
the high right atrium and right ventrlcular apex,, respecttvely. Panel B. Right atrial pacing to maximize ventrlcu-
lar preexdtatlon. The electro gram on the ablatlon catheter shows an lnltlal large atriaI deflection followed by a
probable AP potential and ventricular acttvity preceding the onset of the delta wave (vertical line}. Panel C. Initia-
tion of radlofrequency current Instantaneously abolishes conduction over the AP. as noted by the nonnalfiatlon
of the fifth ORS complex. AMP, amperes.
0 500 1000
ABLATION SfTE
lli.----~-----
lllr - - - - - -
VI
V2
V6;1---- - -- - - '
Rv~-----'-~""'----------'----""------,
Panel B
I 'I
0 1000 2000 3000
RF ABLATION
II
Ill
VI
V2
V6
HRA
ABLATION
RV
O.SAMP
Current1 - - - - - - - - -=
o
PanelC
FIGURE 7·23 • (Contfnutd)

patients the ac~sory pathway remains unharmed by this technique but conducts into a blind
alley of dead ventricular or atrial tissue. In fact, in some of our patients a~sory pathway
potentials have been recorded before and after successful catheter ablation. although ventric-
ular preexcitation is lost (see Chapter 17 for more details).
PRE EXCITED TACHYCARDIA

Clinical Diagnosis
Preexcited tachycardias present as a wide QRS complex arrhythmia. A differential diagno-
sis is supraventricular tachycardia with anterograde conduction over an accessory pathway,
supraventricular tachycardia with bundle branch block aberrancy; and ventricular tachycardia
(Chapter 13). In most instances, the patients have a history and physical examination similar
to those of patients who present with AVRT, and the 2 arrhythmias often occur in the same
patient. The 1 exception may be the marked hemodynamic compromise that can occur during
atrial fibrillation with a rapid ventricular response due to conduction over an accessory path-
way (Figure 7-3).
0 500 1000
ABLATION SITE
II
A
DCS - - - . - .
S1 S1
PanelA
FIGURE 7·24 • Ablation of concealed left free-wall accessory pathway. Panel A. Right ventricular pacing shows eccentric retro-
grade atrlal activation sequence wtth CS preceding HBE atrium (A}. Earliest AactMty Is on the ablatlon catheter (ABL) In the left
ventricle on the mhral annulus. with a probable AP potential between the lnltlal ventricular and atria! deflection. Panel 8. During
radlofrequency current delivefy, there Is a sudden change In the retrograde atrial activation sequence on the third beat Note the
VA Increase In the CS leads. e.g., 158 to 220 ms on the mid-CS electro gram. Retrograde conduction ls now concentric over the nor-
mal conducting system with the eartrest Aon the HBE lead. The constant VA Interval on the HBE lead confirms that during ventricu-
lar pacing, the atrial septum is activated over the nonnal conduction system and not via the left-sided AP.
0 2000
II
V1
HBE
ABL
PCS
A 220MS
A 158MS
MCS
A A 22SMS
166MS
DCS
RV
CURRENT
Panel B
FIGURE 7·24 • (Conrfnued)
Laboratory Data
The ECG is a valuable tool in the diagnosis of these arrhythmias. Since anterograde conduction
occurs over 1 or more acc:essory pathways during tachycardia, it is important to compare the
12-lead ECG morphology of tachycardia with the ECG recorded during sinus rhythm. Electro-
physiologic evaluation will be necessary to identify the mechanism of pree:s:cited tachycardia
in most instances.
Electrophysiologic Evaluation
Preexcited tachycardias can be subdivided into those in which the AP is a requisite part of the
tachycardia circuit and those in which it is used only as a bystander for conduction of antero-
grade impulses to the ventricle (Figure 7-26). When the AP is a requisite part of the tachycardia
circuit, 2 basic types of reentrant wavefronts can occur. The most common form is antidromic
tachycardia (Figure 7-26, IA). demonstrated in Figure 7-27.45.46 Antidromic tachycardia uti-
lizes an AP for anterograde conduction and the normal AV node and His-Purkinje system for
retrograde conduction. In patients who have both AVRT and antidromic reciprocating tachy-
cardia. the rate of tachycardia is almost always faster with the antidromic type.46 Patients with
multiple APs, especially those with Ebstein's anomaly, can have a variety of preexclted tachycar-
dias that may utilize the normal conduction system as well as I or more APs in the tachycar-
dia circuit (Figure 7-26, IB). The tachycardia circuit depicted in this instance utilizes one AP
Atrium
''
.. '-:::::--. .
- --• Ventricfe
FIGURE 7·2J • Schematic of potential mechanism for loss of conduction over accessory pathway during cathe-
ter ablation. (See text for detalls).
for retrograde conduction and a second AP for anterograd.e conduction, with the normal AV
node-His-Pur.kinje system a nonfunctioning part of the tachycardia. a rare occurrence. How-
ever, several variations on this theme may occur,6 and these arrhythmic mechanisms can only
be identified at electrophysiologic study.
Preexcited tachycardia can also utilize the AP for anterograde conduction without requiring
AP conduction to maintain the tachyarrhythmia (Figure 7 -26, II). A potentially lethal variety
of these arrhythmias is atrial fibrillation or flutter with rapid preexcited ventricular rates
(Figures 7-3 and 7 -26, lIA). A relatively rare clinical occurrence but a diagnosis that must be
entertained is AV nodal reentrywith bystander AP participation (Figure 7-26, IIB). Points to
differentiate these arrhythmias are discussed in detail elsewhere. u
An unusual type of preexcited tachycardia may involve a nodoventricular pathway for

anterograde conduction.47 However. recent data suggest that most patients thought to have a
nodoventricular pathway actually have a right free-wall .AP that enters into the right bundle
(atriofascicular) and acts as the anterograde limb of the tachycardia circuit.SA Ifventriculoatrial
conduction is intermittent during persistence of tachycardia. the tachycardia circuit cannot
I. Aocesaory pathway requisite part of drcult
AVN
AP AP AP
HPS
PanelA PanelB
II. Accessory pathway used for bystander anterograde conduction
Atrial 'lhchyarThythmla AVN Reentry
AVN
AP AP
PalMIA PanelB
FIGURE 7·26 • Preexdted tachycardias with anterograde conduction over an accessory atriovenntcular connection. AP. acce55ory
pathway; AVN, atTioventria.llar node; HPS, His-Purkinje system. (See text for details.) (Reproduced with permission from Pry5towsky
EN, Packer OL Preexclted tachycardias. In: Zlpes OP, Jallfe J, eds. Qudfac E1ec:rrophyslology: From Cell to Bedside. Phlladelphla: Saunders;
1989:472-479. Copyrtght c Elsevler.)
involve an AV pathway-a helpful although. uncommonly identified finding. The usual situ-
ation is demonstrated in Figure 7-28. On the left-hand portion of the figure is a left bundle
branch block QRS morphology tachycardia with 1:1 retrograde conduction. Mapping during
tachycardia demonstrated earliest retrograde atrial activation to be in the His bundle area. Note
that the fifth QRS tachycardia complex is not foll.owed by retrograde atrial activation and tachy-
cardia terminates. The subsequent sinus complex demonstrates a normal QRS morphology
and a normal HV interval This beat is followed by a premature atrial complex that conducts
to the ventricle with a left bundle branch block QRS morphology, and the onset of the QRS
complex occurs just prior to His bundle activation. This patient has an atriofasdcular tract The
important clinical message is to consider atriofascicular reentry in the differential diagnosis of
a "typical.. left bundle branch block tachycardia, especially in a patient with a normal ventricle.
These pathways are amenable to catheter ablation.
Treatment
Consideration for chronic therapy in these individuals is similar to that in patients with AVRT.
However, it is more common for these patients to present with a rapid tachycardia with signifl-
cant symptoms; therefore chronic suppressive therapy is usually the rule. In patients without
heart disease who present with atrial fibrillation and conduction over an AP, it is highly likely
HBE
RV ---"1 11r---~.w 1,----...., ----..Jtr---....J ,----.-i
A'
PCS - - -
~ ~ J: ~ ~ ~
~A'
ocs - - - ~ ~ ~ ~ ~
I I
200ms
FIGURE 7·27 • Antldromlc reciprocating tachycardia. FO, foramen ovale. During tachycardia, earliest retrograde alTlal actlvcrtlon
occurs in the septum near the AV node, as identified on the HBE lead.The His bundle deflection occurs after the onset of the pre-
excited QRS complex. At electrcphyslologlc S1:Udy as well as at surgery to ablate this patient's left free-wall AP, only 1 AP was Identi-
fied and the diagnosis of antldromlc redprcc:.atlng tachycardia wu conflnned.
that atrial fibrillation is initiated by AVRT, as demonstrated at electrophysiologic study,1•48 or

possibly by involvement of the AP itself.49 In more than 95% of such patients, surgical ablation
of the AP will eliminate recurrent episodes of atrial fibrillation.4'.!0 Similar results occur after
catheter ablation of the accessory pathway. If there is adequate evidence that the atrial tach-
yarrhythmia is unrelated to AVRT-fur example, onset of the arrhythmia during long-term
event recordings-ablation of the AP will prevent the rapid preexcited ventricular response.
However, the patient may still require antiarrhythmic drug therapy or a separate ablation to
prevent the atrial arrhythmia. In this instance, the patient should know that nonpharmacologic
treatment may not eliminate the need to take drugs. Nonpharmacologic therapy still removes
the potential threat to life that can arise fur some ofthese patients.
Acute treatment fur a preexcited tachycardia is demonstrated in Figure 7-22. As with AVRT,
DC cardioversion is the treatment ofchoice ifthe arrhythmia is unstable. Intravenous procain-
amide or posaibly ihutilide is the preferred treatment in a stable hemodynamic situation; intra-
venous verapamil and especially digitalis should always be avoided. Beta blockers are usually
ineffective in these situations. Although these agents could theoretically terminate tachycardia
in a given individual by blocking retrograde conduction in the AV node, the exact mechanism
FIGURE 7·28 • Preexcited tachycardia utilizing an atriofascicular accessory pathway f'or anterograde conduction. (See text f'or
details.)
of the wide QRS tachycardia often cannot be determined from the ECG, and other forms of
preexcited tachycardia or ventricular tachycardia can be markedly worsened with these agents.
If intravenous procainamide does not terminate the arrhythmia or substantially slow the rate,
DC cardioversion is a reasonable option, although. an observation period may be acceptable in
some patients.
RISK STRATIFICATION OF PATIENTS WITH ASYMPTOMATIC VENTRICULAR PRE EXCITATION

A decision on whom to treat to prevent sudden cardiac death in an asymptomatic individual
is difficult even when the annual risk of death is a few percent, for example, in patients with
ischemic cardiomyopathy. but much harder when the annual estimated risk may be as low as
1/1000.'10 Yet, there are 2 certain axioms in risk stratification: you cannot make an asymptom-
atic person feel better, and you cannot develop a treatment plan for someone who has died.
Evaluation of a relatively large group of patients with WPW syndrome who had ventricular
fibrillation (VF) showed that at electrophysiologic study all had a preexcited RR interval of
250 ms or less, with the majority having 220 ms or less. 12 Consistent with this observation
was an anterograde AP effective refractory (AP-ERP) period of230 ms or less noted in almost
all patients who subsequently had VF.' Since 13/15 patients were 14 years of age or younger,
a group not expected to have primary AF, it is not surprising that 73% of them had AVRT
triggering AP at EP study:' It is well-appreciated that the mechanism of VF in patients with
WPW syndrome and normal hearts is AVRT-induced AF with subsequent rapid preexcited
responses degenerating to VF.
Catheter ablation to cure WPW has changed our approach to risk stratification ofthese patients.
However, our approach assumes the electrophysiologist performing the ablation has sufficient
experience in this area for a greater than 95% cure rate with no more than a I% significant corn -
plication rate. Further, there should be a detailed discussion of the risks of the study and the
fact that sudden death is a relatively rare initial presentation ofWPW, especially in adults. With
this in mind, we favor studying children with preexcitation for they appear to be at a higher risk
for VF,9 competitive athletes, and those with high-risk occupations such as airline pilots, and
any adult who opts for EP evaluation after considering all options. Ablation is recommended to
those with anterograde AP-ERP 240 ms or less, shortest preexcited RR interval in AF 250 ms or
less, and those with AVRT or ART induced.
REFERENCES
1. Prystowfilcy EN. Diagnosis and management of the precxcitation syndromes. Curr Prahl CardioL 1988;13:225.
2. Anderson RH, et al. Ventricular preexcitation: a proposed nomenclature for its substrates. Eur I Cardiol.
1975;3:27.
3. Critelli G, et al. The permanent form of junctional reciprocating tachycardia. In: Benditt DG, Benson DW, eds.
Cardiac Preexcitation Syndromes. Boston: Martinw Nijhoff, 1986:233-253.
4. Gallagher JJ, et al. Variants of preexcitation: Update 1989. In Zipes DP, Jalife J, eds. Cardiac Electrophysiology: From
Cell to Bedside. Philadelphia: WB Saunders; 1990:480-490.
5. Klein GJ, et al "Nodoventricular" accessory pathway: evidence for a distinct accessory atrioventriculer pathway
with atrioventricular node-like properties. I Am Coll CardioL 1988;11:1035.
6. Tchou P, et al Atriofasdcular connection or a nodo-ventricular Mahaim fiber? Electrophysiologic elucidation of
the pathway and associated reentrant circuit. Circulation. 1988;77:837.
7. Gallagher JJ, et al. The preexcitation syndromes. Prog Cardiovasc Dis. 1978;20:285.
8. Klein GJ, et al. Asymptomatic Wolff-Parkinson-White: should we intervene? Circulation. 1989;80:1902.
9. Pappone C, et al. Wolff-Parkinson-White syndrome in the era of catheter ablation. Insights from a registry study
of2169 patients. Circulation. 2014;130:811-819.
10. Klein GJ, et al. WPW pattern in the asymptomatic individual Has anything changed? CircArrhythmiaElectrophys-
ioL 2009;2:97-99.
11. Dreifus LS, et al. Ventricular fibrillation: a possible mechanism of sudden death in patients with Wolff-Parkinson-
White syndrome. Circulation. 1971;43:520.
12. Klein GJ, et al. Ventricular fibrillation in the Wolff-Parkinson-White syndrome. N Engl I Med. 1979;301:1080.
13. Prystowfilcy EN, Packer DL. Preexcited tachycardias. In: Zipes DP, Jalife J, eds. Cardiac Electrophysiology: From Cell
to Bedside. Philadelphia: Saunders; 1989:472-479.
14. Chang MS, et al. Supernormal conduction in accessory atrioventricular connections: an electrophysiologic study.
Am I CardioL 1987;59:852.
15. PrzbylsJci J, et al. Supernormal conduction in the accessory pathway of patients with overt or concealed ventricular
preexdtation. JAm CoU Cardiol. 1987;9:1269.
16. Fananapazier LK, et al Importance of preexcited QRS morphology during induced atrial :fibrillation to the diag-
nosis and localization of multiple accessory pathways. Circulation. 1990;81:578.
17. Wellens JHH, et al. Electrical stimulation of the heart in patients with Wolff-Parkinson-White syndrome, type A.
18. Baroid SS, Coumel P. Mechanisms of atrioventricular junctional tachycardia: role of reentry and concealed acces-
sory bypass tracts. Am I CardioL 1977;39:97.
19. Coumel P, Attuel P. Reciprocating tachycardia in overt and latent preexcitation: influence of bundle branch block
on the rate of the tachycardia. Bur J CardioL 1974;1:423.
20. Neuss H, et al. Analysis of reentry mechanisms in three patients with concealed Wolff-Parkinson-White syn-
drome. Circulation. 1975;51:75.
21. Pritchett ELC, et al. Supraventriculer tachycardia dependent upon accessory pathways in the absence of ventricu-
lar preexcitation. Am I Med. 1978;64:214.
22. Prystowfilcy EN, et al Postmyocardial infarction incessant supraventricular tachycardia due to concealed accessory
pathway. Am Heart]. l 982;103:426.
23. Akhtar M, et al. Role of retrograde His Purkinje block in the initiation of supraventricular tachycardia by ventric-
ular premature stimulation in the Wolff-Parkinson-White syndrome. I Clin Invest. 1981;64:1047.
24. Pritchett ELC, et al. Ventriculoatrial conduction time during reciprocating tachycardia with intermittent bundle
branch block in the Wolff-Parkinson-White syndrome. Br Heart J. 1976;38:1058.
25. Kerr CR, et al Changes in ventriculoatrial intervals with bundle branch block aberration during reciprocating
tachycardia in patients with accessory atrioventricular pathways. Circulation. l 982;66:196.
26. Motte G, et al. Disappearance of a bundle branch block with acceleration of reciprocal tachycardia in
Wolff-Parkinson-White syndrome. Ann Cardio/ AngeioL 1973;22:343.
27. Green M, et al Value of QRS alternation in determining the site of origin of narrow QRS supraventricular tachy-
cardia. Circulation. 1983;68:368.
28. Kay GN, et al. Value of the 12-lead electrocardiogram in discriminating atrioventricular nodal reciprocating
tachycardia from circus movement atrioventricular tachycardia utilizing a retrograde accessory pathway. Am J
Cardiol. 1987;59:296.
29. Morady F, et al. Determinants of QRS altemans during narrow QRS tachycardia. JAm Coll CardioL 1987;9:489.
30. Pritchett BLC, et al. "Dual atrioventricular nodal pathways~ in patients with Wolff-Parkinson-White syndrome.
Br Heart J. 1980;43:7.
31. Pressley JC, et al The effect ofEbstein's anomaly on the short and long-term outcome of surgically treated patients
with Wolff-Parkinson-White syndrome. Circulation. 1992;86:1147.
32. Prystowsky EN. Indications for intracardiac electrophysiologic studies in patients with supraventricular tachycar-
dia. Circulation. 1987;75:111.
33. Milstein S, et al. An algorithm for the electrocardiographic localization of accessory pathways in the Wolff.
Parkinson-White syndrome. PACE. 1987;10:555.
34. Miles WM, et al. The preexcitation index: an aid in determining the mechanism of supraventricular tachycardia
and localizing accessory pathwap. Circulation. 1986;74:493.
35. Packer DL, et al. Effect of left free wall accessory pathway location and left bundle branch aberrancy on the
response to ventricular premature complexes during reciprocating tachycardia. PACE. 1987;10:408.
36. Wm.die JR, et al. Determination of the earliest site of ventricular activation in Wolff-Parkinson-White syndrome:
application of digital continuous loop two dimensional echocardiography. J Am Coll Cardiol. 1986;7:1286.
37. Nakajima K, et al Phase analysis in the Wolff-Parkinson-White syndrome with surgically proven accessory con-
duction pathways: concise communication. J Nucl Med. 1984;25:7.
38. Prystowslcy EN, et al The quality of life and arrhythmia status after surgery for Wolff-Parkinson-White syndrome:
an 18 year perspective.! Am Coll Cardiol. 1987;9:100A.
39. Warin JF, et al. Catheter ablation of accessory pathwap with a direct approach. Circulation. 1988;78:800.
40. Jackman WM, et al Catheter ablation of accessory atrioventricular pathways (Wolff-Parkinson-White syndrome)
by radiofrequency current. N Engl JMed. 1991;324:1605.
41. Cal.kins H, et al. Diagnosis and cure of the Wolff-Parkinson-White syndrome or paroxysmal supraventricular
tachycardias during a single electrophysiologic test. N Engl JMed. 1991 ;324:1612.
42. Kuck KH, et al Radiofrequency current catheter ablation of accessory atrioventricular pathways. Lancet.
1991;337:1557.
43. Leather RA, et al Radiofrequency catheter ablation of accessory pathways: a learning experience. Am J CardioL
1991;68:1651.
44. Sellers RD, et al. Digitalis in the preexcitation syndrome: analysis during atrial fibrillation. Circulation. 1977;56:260.
45. Bardy GH, et al Preexcited reciprocating tachycardia in patients with Wolff-Parkinson-White syndrome: incidence
and mechanisms. Circulation.1984;70:377.
46. Packer DL, et al. Physiologic substrate for antidromic reciprocating tachycardia: prerequisite characteristics of the
accessory pathway and AV conduction system. Circulation. 1992;85:574.
47. Gallagher JJ, et al Role of Mahaim fibers in cardiac arrhythmias in man. Circulation. 1981;64: 176.
48. Campbell RWF, et al Atrial fibrillation in the preexcitation syndrome. Am J Cardiol. 1977;40:514.
49. Chen PS, et al. New observations on atrial fibrillation before and after surgery in patients with Wolff-Parkinson-
White syndrome.! Am CoU Cardiol. 1992;19:974.
50. Sharma AD, et al Atrial fibrillation in patients with Wolff-Parkinson-White syndrome: incidence after surgical
ablation of the accessory pathway. Circulation. 1985;72:161.
Ventricular Tachycardia
Ventricular tachycardia (VT) is protean in form, duration, clinical setting, and prognosis. There
is no uniformly accepted classification of VT, and this arrhythmia may be subdivided using
many factors, as noted in Table 8-1. Unfortunately, no single subcategory provides enough
information for correct classification ofall patients with VT, and in many instances there is sub-
stantial crossover. For example, in many patients the mechanism of tachycardia is not certain.
Whereas reentry is the presumptive mechanism for sustained VT in patients who have coro-
nary artery disease with a previous myocardial infarction and ventricular scar, the mechanism
of exercise-induced VT may include enhanced automaticity. triggered activity, and probably
reentry. Thus, our present state of knowledge regarding mechanism of VT precludes use of this
sole criterion for classification. The other potential classification variables listed in Table 8-1
also have deficiencies. It is often more useful to define a set of variables for a particular type of
tachycardia so as to provide the clinician with a meaningful approach to the patient who has
that arrhythmia. For example, patients with no definable structural heart disease who have
right bundle branch block, left axis morphology sustained VT are a select subgroup for whom
the location of this tachycardia is known and response to therapy-for example, endocardial
radiofrequency catheter ablation or oral verapamil-has been well-documented.1•3 We will
approach the classification of VT by clinical presentation in order to aid the clinician taking
care of these patients.
ACCELERATED IDIOVENTRICULAR RHYTHM

Accelerated idioventricular rhytlun (AlVR) is a form of VT that is probably due to automaticity.
The rate of tachycardia is usually between SO and 110/min, and it becomes manifest in most
instances as sinus slowing occurs. Thus, the sinus node competes with the idioventricular focus
for capture of the ventricles. Although this arrhythmia usually occurs in the presence of heart
disease, we have noted it in patients with no definable structural heart disease. The arrhythmia
is self-terminating and rarely requires any therapeutic intervention. In some prolonged epi-
sodes of AIVR with sinus nodal dysfunction, there may be a decrease in blood pressure because
of the ventricular origin of the arrhythmia and lack ofatrioventricular synchrony, and enhance-
ment of the sinus rate or suppression of the ventricular focus may be necessary. The former
can be accomplished with drugs such as atropine or isoproterenol if not contraindicated, or
by atrial pacing. Examples of AlVR are noted in Flgures 8-1 and 8-2. Note that in Figure 8-1
the fourth QRS complex is slightly premature, 120 ms in duration, and ventricular in origin.
TABLE8-1 Classlflcatlon of ventricular tachycardia.

Mechanism
Location
Morphology
Duration
Cardiac pathology
Exerclse-Jelated
Drug responsiveness
lsoproterenol lndudblllty
EJectrophyslologlc: lnduc:lblllty
The PR interval is suddenly shortened, consistent with the ventricular origin of the QRS com-
plex. The last 4 QRS complexes represent AIVR, with a rate of approximately 65/min, a rate
only slightly faster than that of the underlying sinus rhythm. There also appears to be some
slight variability in the QRS morphology during AlVR (Figure 8-1). The QRS complexes with
the longer PR intervals during AIVR most likely have slight degrees of fusion due to partial
depolarization of the ventricles from the supraventricular impulse. Figure 8-2 demonstrates
AIVR at a faster rate of approximately 107/min and, as expected, the underlying sinus rate is
also faster than that noted in Figure 8-1.
NONSUSTAINED VENTRICULAR TACHYCARDIA

The definition of nonsustained VT (VT-NS) differs among investigators in the field of clini-
cal electrophysiology. We cunently define VT-NS as a tachycardia lasting from 3 consecutive
ventricular complexes to <30 s in duration with a rate ~110/min. In most instances VT-NS is
relatively briefin duration, usually less than 10 complexes. As noted below, VT-NS can be mon-
omorphic or polymorphic, and patients can have both forms of tachycardia at different times.
The prognostic importance of VT-NS depends on whether it is monomorphic or polymorphic,
the clinical setting in which it occurs, and the frequency of it along with premature ventricular
complexes that often accompany it Very frequent ventricular ectopy can lead to a cardi.omyo-
pathy as noted below.
I I' !ll 1111 lin. I flll !I!! 1!1!!1 II Ill

I. I Ii!! !i!i Hli 'I! !IH ilii ! I! !Iii .
'I I! I
! . •l: illi ! l I . I ! !; ! ;
. l '' 11 I' ' l 't !
! •
11
FIGURE •1 • Accelerated idioventric:ular ritythm. {See text f'or details.)

CHAPTER 8 • Ventricular Tachycardia 173
FIGURE l·:Z • Electrocardlographlc tracing of accelerated ldloventTlcular rhythm for the fourth through sixth complexes. The P-P
intervals are relatively consl'Clnt throughout
Repetitive Monomorphic Ventricular Tachycardia

Repetitive monomorphic VT (RMVT) is an arrhythmia characterized by runs of mo.nomorphic
vr or single or paired ventricular QRS complexes. all with the same QRS morphology, which
occur in a patient with no definable structural. heart disease. The intervening supraventricular
QRS complexes are normal. An example of this arrhythmia is noted in Figure 8-3 in a patient
lsoproterenol 3 MCGMlmln 70° tllt
ffillltliii!B·
11t11tiim1•-·
•111--
FIGURE •3 • Repettttw monomorphlcVTln a pa'dentwho has noorallymedlated syncope. The arrhythmia noted In the top and
mlddle ECG strtps ls repetltllle monomorphlc VT that U'le patient had throughout U'le day and was never associated with any symptoms.
The patient had repeated episodes of presynaipe and undefwent hekl-up tllt evaluation. In the absence of lsoproterenoi no symptoms
ocaured. During heed-up tllt at 7'1' with lsoprot!fenol at 3 IJ.9/mln Infusion, U'le patient's dlnlcal sympmms at presyncope were repro-
duced and the blood pressure was not palpable.The repetitive monomorphlcVT was unchanged U'lroughout the pretllt evaluation and
during tilt testing. Thus, U'le patient's syrnpmms were unrelated t:o VT. Of note, this patient had normal cardiac function.
who had recurrent presyncope that was replicated during a tilt-table evaluation. The syndrome
of RM.VT has been well-documented in the medical literature for many years.4-9 Froment et al.6
recognized the benign course of patients with RM.VT and labeled it "curable and mild mo.nomor-
phic ventricular extrasystoles with paroxysms of tachycardia.'" Rahilly and colleagues7 reported
on 18 patients with RM.VT. Of these, 10 were men and 8 women; the mean age was 37 years.
Only 2 patients had syncope, and there were 8 without any symptoms. The QRS morphology
during ventricular tachycardia was left bundle branch block in 10 patients. 9 with a normal axis.
Tachycardia rates were quite variable but in 16 patients ranged from 100 to 150/min. Exercise
testing increased episodes of tachycardia in 5 patients, decreased episodes in 5 patients. and there
was no change in 3. Of note, during Holter monitoring. there we.re frequently large variations in
number ofepisodes oftachycardia throughout the day. and clustering ofepisodes was not uncom-
mon. Programmed electrical stimulation initiated VT in 2 of 9 patients. During a 2-year mean
follow-up evaluation there were no deaths, although many patients were treated because ofinitial
symptoms. In 5 of6 patients who were not treated. no VT was identified during Holter evaluation
several years later. Thus. this arrhythmia can resolve spontaneously in some patients.
In another series of patients with RMVT, all 22 had left bundle branch block, inferior axis
morphology.8 This suggests a right ventricular outflow tract site, which has been success-
fully approached using endocardial catheter ablation techniques (see Chapter 18).1°"11 Of the
22 patients reported by Buxton et al.,8 7 were induced during electrophysiologi.c testing. 9 with
isoproterenol infusion. and 11 of 18 during exercise testing. This series of patients clearly dif-
fers from those reported by Rahilly et al.,1 and it is quite possible that RMVT can be caused by
various mechanisms. high1ighting the difficulty of attempting to subclassify even a relatively
narrow clinical syndrome. Coumel et al.9 discussed 70 patients with RM.VT who had a mean
age of 40 years. Left bundle branch block with normal or right uis morphology occurred in
51%. These authors suggested that the arrhythmia was related to sympathetic tone and there
were sinus rates below which repetitive beating did not occur.
Episodes of VT that are repetitive and monomorphic can occur in patients who have underly-
ing structural heart disease, and the arrhythmia may not presage as good a clinical outcome in
these patients as it does in patients with no structural heart disease. Two examples are demon-
strated in Figures 8-4 and 8-5. The arrhythmia noted in Figure 8-4 demonstrates single prema-
ture ventricular complexes with a fixed coupling interval to the preceding sinus QRS complex
and 1 run (3 complexes) ofVT-NS. In this single-lead tracing, all QRS ventricular complexes
appear similar. This patient had underlying structural heart disease, and this arrhythmia should
not be characterized as RMVT. In Figure 8-5, the patient has runs of rapid monomorphic VT
. . . .. ·.: l· ·> . : ... : · :' · :.:" n.. ::-, ·::I.;·:::::;;:: !::. .. : :.·.
FIGURE H • Nonsustained monomorphic VT. (See text for details.)

FIGURE •s • Run5 of rapid monomorphic nonsustained VT.
with only infrequent sinus complexes. This patient with heart disease was highly symptomatic
and required urgent therapy to suppress the VT. Thus, runs of nonsustained monomorphic VT
can occur in patients with and without structural heart disease, but the syndrome of repetitive
monomorphic VT requires the absence of underlying structural heart disease.
It is always important to consider the diagnosis of supraventricular tachycardia (SVT) with fixed
o.r functional bundle branch block aberrancy o.r a preexcited QRS morphology in patients with a
wide QRS complex tachycardia. Figure 8-6 shows a patient with no structural heart disease who
was referred with a diagnosis ofRMVT. The recurrent episodes ofwide QRS complex tachycardia
are due to a supraventricular tachycardia with conduction over a left lateral accessory pathway in
this patient, who had no previous electrocardiogram (ECG) for comparison. This diagnosis was
confirmed at electrophysiologic study. Thus, although one should always consider VT as the ini-
tial diagnosis in such a patient, one must also realize that alternative mechanisms can be present
Treatment of patients with RMVT should be directed primarily at relief of symptoms, since the
occurrence of sudden cardiac death in an otherwise asymptomatic patient with RMVT is rare.
Drug therapy or endocardial radiofrequency catheter ablation in symptomatic individuals are
acceptable therapies. Beta blockers are good first-line agents, and verapamil can be useful in
some cases, e.g., outtlow tract origins of ectopy. If these drugs are not effective, and the patient
prefers to avoid an ablation procedure, use of antiarrhythmic drugs with a direct effect on the
sodium or potassium channels c.an be given, including mexiletine, sotal.ol, propafenone, and
flecainide. While amiodarone can be very useful to suppress ventricular ectopy and VT-NS, it
has potentially significant noncardiac side effects, e.g., puhnonary, thyroid, and liver toxicity,
and should be avoided if possible in these patients with normal ventricular function. We rou-
tinely begin drug therapy with a beta blocker or verapamil on an outpatient basis, but we prefer
to start the other agents, exc:Iuding amiodarone, in the hospital to maximize safety regard-
ing proarrhythmia. The necessity for long-term drug therapy should be reevaluated after 1 to
2 years of treatment, because the arrhythmia can resolve over time.
Tachycardia-Related Cardlomyopathy
Patients with high daily burdens of VT-NS, but much more commonly PVCs, can develop
a tachycardia-related cardiomyopathy (T-CM).1i-14 This can also occur with other arrhyth-
mias, most commonly atrial fibrillation. The mechanism for T-CM may differ depending on
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. ·. ~- - . ~ !'!: . -- ~~--t--t-·+-t-1---t-......,,. .,..
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. ', t , , ,, , ... . , , i: ;j I;,, ..... , ..:... - , :: :' : !:° , , - ....._ _,__.__~- - i.-- - _ . _ _ . _ _ " ' - ' - - ' - - ' - " '' "
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- -"·+ ··~t-
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:;;+ ··-t:.....
:::... :: +. •.....'·...·'~'·,...
=::+. '.Lii-,~;-t
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·::+· ·_· ·-1-
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: :_·:.+--ir- 2$
--+--+--i--+-~f.-1 ·--+--+--+-·t---<i-+--+--+--+ +--......t--+-1---t-· - 1--- - ~- - -· ~- - .:..,_ ,._~
FIGURE W • Repetitive episodes of a wide QRS complex tachycardia diagnosed as a preexclted tachycardia at electrophys!ologlc
study. (See text for details.)
the arrhythmia, but is possibly related to calcium overload and mishandling in PVCNT-NS
arrhythmia.n.14 Patients at risk to develop T-CM require a requisite number of PVCs per day,
but this threshold ofPVC burden has wide variation in the literature. Daily thresholds of PVCs
as low as 16% to as high as 31% have been reported, as well as >17,000 ectopic beats daily.12
Patients who have >10,000 PVCs per day over prolonged periods of time seem to be at risk to
develop T-CM, but recent data suggest improvement in LV function with suppression ofPVCs
in daily burdens of only 696-8%.13 Further, even when the PVC burden is high, it does not mean
that a T-CM will develop, ocaming in only 7% of patients in one study.12 Other factors con-
tributing to T-CM are male gender, PVC durations> 150 ms, lack of diurnal variation in PVCs,
duration >30 months, and asymptomatic ectopy. Because there is no clear indicator(s) of which
asymptomatic patient with a high PVC burden and normal ventricular function will develop
T-CM, our approach. is to do yearly echocardiograms and long-term monitoring and treat those
who develop symptoms or reduction in left ventricular ejection fraction (LVEF).
Treatment of patients with T-CM involves good medical therapy for their myocardial dysfunc-
tion and heart failure, and appropriate tests to determine whether there is any other reason
for the myopathy. In essence, T-CM is a diagnosis of exclusion. Cardiac magnetic resonance
imaging (CMR) is particularly helpful and the lack of scar portends a better improvement in
LV.EF with PVC suppression than if scar is present. Ablation of the PVCs and VT-NS is first-
line treatment in our opinion, but drug therapy can be used, most often amiodarone or sotalol.
In some patients in which the cause of the LV dysfunction is not clear, a trial of amiodarone to
suppress the ectopy and reevaluation ofLVEF can be useful-if there is substantial improve-
ment, we tend to discontinue the amiodarone and treat with ablation when the ectopy returns.
Paroxysmal Nonsustained Ventricular Tachycardia

Isolated episodes of nonsustained VT are common in patients with structural heart disease but
infrequently occur in patients who have normal ventricular function. Ventricular tachycardia
can be monomorphic, polymorphic, or monomorphic with each episode but with more than 1
morphology being noted in a given patient. Typically patients have only a few episodes a day,
often merely I, and the duration is less than 10 complexes with a rate <160/min. However,
VT-NS is highly variable and may be much more rapid and longer in duration. Patients are
often asymptomatic and the arrhythmia is discovered incidentally, e.g., on a routine pacemaker
check. When symptoms occur, they are most commonly palpitations, but presyncope and diz-
ziness are occasionally noted. The significance ofVT-NS in asymptomatic individuals depends
on the presence and severity of underlying heart disease.
Patients with structural heart disease, especially those with substantial deaease in left ventric-
ular function, frequently have episodes of asymptomatic VT-NS recorded during 24-h ambu-
latory ECG monitoring. 1>-ll Some investigators have documented an independent association
of VT-NS with subsequent sudden cardiac death in patients with dilated cardiomyopathy. 11-19
Figure 8-7 is a common example of nonsustained VT. The rate of tachycardia is somewhat
variable, ±150/min, and the duration is short, 8 complexes. Figure 8-8 represents a run of rapid
polymorphic VT that occurs less commonly but is not rare. The rapidity of the VT and its onset
on the T wave are worrisome characteristics that suggest a risk for sudden cardiac death.
A poor correlation has been noted between characteristics of VT-NS and mortality or sudden
cardiac death. For example, Meinertz et al.18 reported that ~20 episodes of ventricular pairs or
~I --------+----t----~ l---+-1--1-+ -1-1-+-
;· . \ .
. .~ .... -
;' --+--1-t-jl--+-+-t- _,__ - -- - .. . .. ·- - - . 1- ••• ~. -.+--J:.Li-:-4-+-l--+-+--ll- + -
~-+-1--1--t- - ·- - I " - .... -..-•• t - - · - • •• •••• • · - ••• •• ... ••• · - -~ - ··I- ·- _l ·- -· ·----··I--··· - - 1 - - - 1 - - + - - 1 - -
r:
:: ·- -· • -- - ...- ... _ . ...... i...- •• - ~-- · ,__ - --- ·--- -- -
~ ... ~ --- - i - - - - - f - - -
. -+-l--f--t-j·-i--1·-·
i--,-+ - -- -t-.. - · -· ~ ·-·r---- ,_, .. -- - ~to--•_.. ,.._.f-.. ... -- -
FIGURE 1-7 • Example of nonsustalned VT thBt starts with the fourth QRS complex and Is 8 complexes In duration. Ventrlculoa-
trlal dissociation ls present and the first complex of tachycardia merges with the end of the sinus P wave. Emergence ofVT lam In
diastole (R-on-P wave) is not unusual.
I 1
1 ·~
FIGURE•• • Rapid polymorphlc nonsustalned VT.
VT-NS in a 24-h ECG recording correlated with sudden cardiac death in patients with idio-
pathic dilated cardiomyopathy. However, the authors did not suggest that any characteristics
of VT-such as rate, duration, or morphology-were prognostically useful. In a retrospective
analysis of the outcome of patients who had VT-NS during 24-h ambulatory monitoring,15
10of37 patients died suddenly. All 10 had structural heart disease and 9of10 had congestive
heart failure, compared with only 10 of27 patients with VT-NS who did not experience sud-
den death. Patients who died suddenly had 2.4 episodes of VT per day and 3.8 complexes per
episode; the rate was 160 ± 36/min. Importantly, these characteristics were similar to those
noted in patients who did not die suddenly. Nonsu.stained VT is also an independent risk factor
for arrhythmic mortality in patients in whom it was identified a mean of 11 days after acute
myocardial infarction, but individual parameters of the nonsustained VT episodes were not
predictive of sudden death.21 Nonsu.stained VT also occurs commonly in patients with hyper-
trophic cardiomyopathy, but some data suggest its significance is minimal in asymptomatic
individuals.23
There are several potential explanations for the poor predictive capability of individual param-
eters ofVT-NS-such as rate, duration, and morphology-in patients who are asymptomatic
from this arrhythmia. The assumption that patients have only 1 type ofVT-NS is incorrect.24
Quite frequently patients have multiple types of VT with variable duration and rate, and the
more episodes per day of tachycardia the greater is the variability in rate.24 Flgure 8-9 is taken
from a patient with atrial fibrillation and multiple runs of VT recorded during continuous
in-hospital ECG telemetry. All 3 episodes of VT differ from each other in morphology. dura-
tion, and rate. It would be impossible to predict which one of these arrhythmias, if any, would
correlate with a future episode of sustained VT. Further, if this patient were included in an
epidemiologic study, it would be very difficult to characterize the various tachycardias and risks
for future occurrence of sudden cardiac death.
The assumption that the nonsustained VT will resemble sustained VT is also incorrect,24 as
noted in Figure• 8-10 and 8-11. In Figure 8-10, Panel A, 2 runs of VT-NS that are poly-
morphic but with similar appearance are followed at the end of the tracing with the initiation
. !i!i 1H; ll !l ji !I
: !! !ill !l!l 11i :I II
111.i P'l jl~ ii!
il!ill .!:: L. :ii
:: ·: :1
I: !I! : : I :i: ! ii: . . . ' :::: ' : I~: II!: :::::::: ::: ~nl i:f!'ITTI . f:~
Ii.I!: · i! .!i !'!
tl; 1111 !:' ! I • I I!· !P Ii!
Panel A
: i iii! ·iii 'j:
I p: Iii! 11
!.!ii i!!1i.
" 1. i! ::· ::! ! 1! :; :: m! 'l :m g ~i: 1 :::: :,,, :·: :!r: ,,,, :::: ~= =~
•!Ji I
'Ii Ii
I· .i: II! illl
PanelB
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l!I!
iili
1111111; .!!! l i i!i
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PanelC
FIGURE H • Multiple episodes of VT in a patient with underlying atrial fibrillation. The 3 episodes noted in
Panels A. B, and Cdiffer in rate, duration, and morphology.
of sustained monomorphic VT, which is also demonstrated in Panel B. The rate of sustained
VT is approximately 167/min, whereas some portions of the nonsustained VT are as rapid as
250/min. In Figure 8-11. 3 panels of simultaneously recorded 12-lead ECGs are demonstrated.
In Panel A. single and paired ventricular premature complexes have a similar morphology. In
Panel B, a nonsustained VT run begins with a QRS complex that has a similar morphology
to the premature QRS complexes noted in Panel A. but the subsequent 2 QRS complexes
of tachycardia are clearly different. Sustained VT in this patient (Panel C) resembles the
12-lead ECG morphology noted in Panel A. Thus, one premature ventricular complex mor-
phology presaged the morphology noted during VT, whereas the other was markedly different.
PlnelA
PlnelB
FIGURE 8·1 O • Nonsustained {Panel A) and sustained (Panel B} VT. (See text for details.)
In summary, except for the observations noted by Meinertz et al18 regarding frequency of runs
ofVT-NS, our own experience and that documented by other investigators suggests that the
presence ofVT-NS in patients with heart disease, especially those with significant left ventric-
ular dysfunction, is a risk factor for the future occurrence of sudden cardiac death. Individual
characteristics of VT, except for possibly those shown in Figure 8-8, are of no prognostic signif-
icance in patients with asymptomatic nonsustained VT.
Sinus Sustained VT
1~
. I ..I
·1
I I I •.
II 1l1r'.\f.1rW
Ill ~
aVR J\.Mm
aVL ~
V1
V2
Va
V4
vs _.......__...._,_,....,
vfJ _,.,__.__,'--"!
I.
I'
PllnelA PllnelB PllnelC
FIGURE 8-11 • Single and repetitive ventrlcular complexes of different morphology (Panels A and BJ and sus-
tained VT that resembles one of the ectopic morphologies {Panel C).
Apparently healthy individuals with asymptomatic VT-NS are at minimal risk for sudden car-
diac death.25 Kennedy and colleagues25 evaluated 73 such patients with a mean age of 46 ± 13
years, and the mean follow-up was 6.5 years. One patient had a cardiac arrest, survived, and
was documented to have disease of the right coronary artery. Another patient died suddenly
approximately 7 years after entry into the study and was known to have normal coronary angi-
ography when initially evaluated. The incidence of sudden death during follow-up was there-
fore very low. Because the risk of sudden cardiac death is minimal in patients with no structural
heart disease, therapy should be given only to those individuals who have substantial symptoms
associated with VT-NS. In general, we recommend reassurance for those patients who have
palpitations, but symptoms such as presyncope or syncope need to be evaluated in more detail.
Noninvasive and invasive electrophysiologic testing may be needed to define the problem, and
therapy is warranted to suppress ventricular arrhythmias if they are documented to be the
cause of the symptoms. Therapy should be individualized to the patient; some may require
only beta blockers, whereas others may need more potent antiarrhythmic agents, for example,
sotalol, or catheter ablation.
Treatment to suppress symptoms may also be warranted in patients who have structural heart
disease. Such therapy should be individualized to the nature and extent of heart disease. Beta
blockers may be useful in some patients, whereas antiarrhythmic agents such as mexiletine,
sotalol, and amiodarone are better choices, and for others catheter ablation is preferred.
EXERCISE-INDUCED VENTRICULAR TACHYCARDIA

Exercise is associated with many physiologic changes, including an increase in systolic blood
pressure, heart rate, contractility, sympathetic tone, secretion of catecholamines, and decreased
parasympathetic tone. The role of decreased parasympathetic tone in arrhythmogenesis has
been evaluated in many models. For example, atropine can facilitate initiation ofAV nodal reen-
trant tachycardia at electrophysiologic study in some patients in whom heightened vagal tone
has prolonged AV nodal refractoriness and depressed conduction.26 In canine models as well as
humans, data are available to suggest that a decrease in parasympathetic tone after myocardial
infarction increases the risk of mortality.27.2• The relative contribution of parasympathetic with-
drawal or heightened sympathetic tone to initiation of ventricular arrhythmias during exercise
is unclear. The changes in autonomic tone can facilitate initiation of VT by a variety of mech-
anisms including reentry, automaticity, and triggered automaticity.29 Further, patients with or
without structural heart disease can have exercise-induced ventricular arrhythmias by one of
several mechanisms. Thus, the appearance of VT, whether sustained or nonsustained, during
exercise requires further investigation to determine, if possible, the electrophysiologic mech-
anism and to define whether cardiac structural abnormalities are presenL There may be an
increased risk of sudden death in patients with exercise-induced PVCs and VT who have struc-
tural heart disease,30•31 but not so in well-trained athletes with normal hearts.32 Of 5011 athletes
<35 years old undergoing exercise testing prior to participating in competitive sports, 6.6%
had at least 1 PVC, and 0.7% had >10 PVCs, and some had VT-NS32; all had a benign clinical
course. Exercise can also induce ischemia, and it is critically important to identify patients with
ischemia-initiated VT. In our experience such VT is typically polymorphic, not infrequently
degenerating to ventricular fibrillation. The approach to patients with ischemia-provoked
malignant arrhythmias is quite different, as noted below. Table 8-2 lists several studies ofpatients
with exercise-induced VT and demonstrates the diversity of findings in these patients.33-41
Woelfel34 14 NHD~ RBBB-6 VT-S-5 10/11 (IV)

CAD-6 LBBB-5 VT-NS-9
NCAD-2 Pleo-3
WoelfeP 5 16 NHD-5 RBBB-5 VT-S-6 12/16 (IV)
CAD-7 LBBB-7 VT-NS-10 8/12 (0)
NCAD--4 Pleo--4
Sung'" 12 NHD-3 RBBB-7 VT-S-12 3/6 (1V)
CAD-6 LBBB-5
NCAD-3
Wul1 3 NHD-3 LBBB-3 VT-S-3 3/3 (0) 3/3 (IV)
38
Pallleo 6 NHD-2 LBBB~ 6/6>10sbut 6/6 (0)
RVCM-3 self-terminating
MVP-1
O'Hara,. 17 CAD-17 RBBB-16 VT-S-17
Other-1
Mont'O 37 NHD-37 RBBB-22 VT-S-19 2/8
LBBB-9 VT-NS-18
Sokoloff" 10 NHD-3 LBBB-10 VT-N5-10 9/10 (IV)
CAD-4
NCAD-3
33
Lennan 4 NHD--4 LBBB-3 VT-S--4 3/3 (IV) 3/3 (IV)
LBBB/RBBB-1
Abbreviations: CAD, coronary artery disease; NCAD. no CAD; NHD. no obvious heart disease; RVCM. right ventricular cardlomyopathy; MVP, mltral valve
prolapse; VT-5, sustained VT; VT-NS, nonsustalned VT; pleo, pleomorphlc; RBBB. right bundle branch block; LBBB, left bundle bronch block.
Therapy
In most cases, patients with sustained VT, regardless of mechanism, should be treated, and
the method of treatment will depend upon the mechanism of the arrhythmia and the type of
heart disease present For example, patients with ischemia-initiated polymorphic VT or ven-
tricular fibrillation 42 require anti-ischernic therapy, pharmacologic or nonpharmacologic, as
primary treatment and reevaluation afterward for the need for specific antiarrhythmic drugs
or an implantable cardioverter-defibrillator (ICD). The arrhythmia of patients with no obvious
structural heart disease may be suppressed with beta blockers, verapamil, or one of several
membrane-active antiarrhythmic drugs. The use of verapamil to treat patients with VT is not
advisable except in very specific circumstances such as tachycardia originating from the right
or left ventricular outflow tract or idiopathic left ventricular VT (see Figure 5-12). Of note,
Lerman et al.33 reported that some patients with verapamil-sensitive VT are also responsive to
intravenous adenosine, propranolol, and heightened vagal tone. These authors suggested that
VT was due to cyclic AMP-mediated triggered activity.
Therapy will have to be individualized to the patient. In some of these patients, radiofrequency
endocardial catheter ablation can be used to cure VT; this will be discussed in more detail
in Chapter 18. Patients with structural heart disease and exercise-induced sustained VT will
Yang"" 55/3351 NHD-5 During ex-28 VT-S-50 None

(1.6%) CAD--45 Recovery-27 VT-NS-5
NCAD-5
Mllanes47 48/2600 NHD-5 During ex-76% VT-S-1
(1.9%) CAD-36 Recovery-53% VT-NS--47
NCAD-7
Codini.,. 47/5730 NHD-7 During ex-17 VT-S-5
(0.8%) CAD-30 Recovery-23 VT-NS--42
NCAD-10 Both-7
BusbySO 18/1160 NHD-18 VT-S-1 None
(1.6%) VT-NS-17
Mokotoft"' 26 NHD-8 During ex-13 None
CAD-16 Recovery-13
NCAD-2
Abbreviations: NHD. no obvious heart disease; CAD. coronary artery disease; NCAD. no CAD; El(. exercise; VT-S, sustained ventricular tachycardia; VT-NS,
nonsustained VT; SCD. sudden cardiac death.
almost always require therapy with specific antiarrhythmic drugs and/or an ICD, although beta
blockers may be useful adjunctive therapy.
The need for therapy of patients who have asymptomatic nonsustained VT detected during
treadmill evaluation is uncertain and controversial. The incidence of sudden cardiac death dur-
ing exercise is rare-for example, 1 death in 396,000 person hours of activity during jogging-
but it appears to be more prevalent in patients who have underlying structural heart disease.43
Cardiac arrest due to ventricular fibrillation during exercise in a patient with no obvious struc-
tural heart disease appears to occur rarely.«
The incidence and predictability for survival of patients with exercise-induced VT during
routine treadmill testing has been extensively investigated (Table 8-3).45- 53 In essence, these
studies demonstrate that asymptomatic nonsustained VT occurring during exercise is much
more common in patients with underlying structural heart disease, especially coronary artery
disease; has an incidence of approximately 1% to 2%; is usually of short duration; frequently
presents in the early recovery period; and is not predictive of subsequent sudden cardiac death.
However, some other studies suggest an increased risk of sudden death in such patients.30.3 1 It
seems reasonable to treat these patients with a beta blocker, and to consider an ICD if they meet
guideline criteria for it (see Chapter 15).
MALIGNANT MITRAL VALVE PROLAPSE SYNDROME

Patients with mitral valve prolapse (MVP) typically have a benign course regarding arrhyth-
mias. They may have ventricular ectopy that often responds to beta blocker therapy. It has been
known for decades that a very small subset of patients with MVP can develop life-threatening
ventricular arrhythmias and sudden cardiac death. The earlier literature stressed the impor-
tance of marked redundancy of the mitral leaflets and ECG evidence of T-wave inversions in
leads 2, 3, and aVF in patients who died suddenly. Sriram et al.54 reported on 10 patients with
MVP who had a VF arrest out of hospital and were successfully resuscitated. All had bileaflet
involvement, 9 were women, 5 had moderate to severe mitral regurgitation, most had T-wave
abnormalities in the inferior leads, and polymorphic VT was present on Holter monitoring in
nearly half of the patients. Of note, 8 had cardiac arrest during wakeful rest, and only 2 with
emotional or physical stress. In our experience, patients with T-wave inversions are more likely
to have positive delayed enhancement on CMR, and typically located in the region of the left
papillary muscles. Treatment for those who survive a VF arrest is an !CD, but suppressive anti-
arrhythmic drug therapy or catheter ablation may also be needed.55
What is the "best" approach to patients who have many of the characteristics of the malignant
MVP syndrome but who have minimal or no symptoms? Such patients are at risk for SCD, but
there are no good data on stratifying their risk and deciding who should receive an ICD or suppres-
sive arrhythmia therapy. Our initial approach is to determine whether they require MV surgery,
but most do not Next, we obtain CMR to evaluate LV function and the presence of scar. While the
ejection fraction is typically normal, in patients with very frequent PVCs and VT-NS, LV dilatation
may be present. In this situation, we recommend therapy to reduce the VT and PVC burden, typi-
cally catheter ablation. In patients with nonvagal/unexplained syncope, an ICD is considered after
a thorough discussion with the patient. Hopefully future studies will add clarity to the approach to
this MVP subset of patients. The role of mitral annulus disjunction in SCD requires more study.
SUSTAINED VENTRICULAR TACHYCARDIA

We define sustained VT as tachycardia that lasts at least 30 s or has to be terminated prior to 30 s
because of hemodynamic compromise.56 Although this definition was proposed to classify VT
induced at electrophysiologic testing, it can also be used to define spontaneous sustained VT,
because there is no alternative, universally accepted definition. However, some suggest that the
term sustained be applied only to VT that requires therapy to terminate it, but then would an
episode that occurs for hours be considered "nonsustained"? Such is the problem with artifi-
cial definitions. Sustained VT can be monomorphic, polymorphic, or combinations of the 2. An
episode of sustained monomorphic VT is noted in Figure 8-12 and is characterized by a similar
QRS morphology throughout the episode of tachycardia and usually minimal variability in cycle
length between QRS complexes. Sustained polymorphic VT displays changes in QRS morphol-
ogy throughout the episode of tachycardia, sometimes as frequently as every few QRS complexes,
and frequently degenerates into ventricular fibrillation; alterations in cycle length throughout
the episode of tachycardia are also frequent {Figure 8-13). In 1 sense, ventricular fibrillation is
the ultimate polymorphic VT. In some patients, polymorphic nonsustained VT can organize
into monomorphic sustained VT (Figure 8-14). In this patient with a history of monomorphic
sustained VT, nonsustained polymorphic VT was initiated at electrophysiologic testing with 2
extrastimuli (S2S3) introduced during right ventricular pacing {S). There was ventriculoatrial
dissociation, as noted in the His bundle electrogram. This same phenomenon can occur during
spontaneous initiation of monomorphic VT. Some patients will demonstrate long runs of mono-
morphic VT that spontaneously change into a different monomorphic QRS morphology lasting
for some time. In these individuals, it is difficult to characterize this arrhythmia as either mono-
morphic sustained VT or polymorphic sustained VT. In our opinion, these arrhythmias are often
stable and more closely fit the clinical characteristics of a monomorphic sustained VT. Sustained
monomorphic VT is covered in more detail later in this chapter and also in Chapter 15.
FIGURE 8"12 • Sustillned monomorphlcVTwlth a right bundle branch block morphology.
ITTTTTTTTTTTTTTTTTmmnTTTTllll ll llil ll llll lll lll llllll llll ll lllllllllllllllllllllllllllllll iiii ii illlili i
FIGUREl-U • Polymorphic VT Initiated with 2 premature stlmull (525,J Introduced during sinus rhythm. Simultaneous ECG
leads I, u. IU, and V1 are recorded with lntracardlac leads from the high rig ht atrium (HRA) and rlgtrt ventrlde (RV). Note the
frequent afteratlons In Q.RS morphology and cycle length between QRS complexes. (Reprinted with permission from Prystowsky
EN. Electrophysio logic-electrophannacologic testing in patients with ventricu lar arrhythmiu. Pl\CF. 1988;11:225.)
I'
2000 3000 -4000
PVT-NS MVT..S
II
Ill
AVF
V1
V8
A A
HIS
FIGURE •14 • Polymorphic nonsustained VT (P\IT-NS} that organizes into sustained monomorphicVT {MVT-S}. {See text f'or details.)
VENTRICULAR FLUTTERNENTRICULAR FIBRILLATION

Ventricular flutter and ventricular fibrillation are 2 forms of tachycardia that are very rapid
and result in cardiac arrest if not promptly terminated. Cardiac arrest is discussed in detail in
Chapter 15. Ventricular flutter is often very difficult to distinguish from a very rapid monomor-
phic sustained VT. The QRS complexes have a sine wave appearance, as noted in Figure 8-15.
In this 71-year-old man with a history of syncope and an inferior wall myocardial infarction,
2 ventricular premature ext:rastimuli introduced during pacing cycle length SOO ms, initiated ven-
tricular flutter that caused rapid loss of consciousness. One could argue that this is a very rapid
sustained monomorphic VT, but the distinction is of no real clinical significance because the con-
sequences are the same and it is often very difficult to differentiate these 2 arrhythmias. Ventticular
fibrillatio.n (Figure 8-16) is a rapid VT with grossly disorganized QRS complexts that will lead to
cardiac arrest and sudden death ifnot promptly terminated. Patients with ventricular flutter or ven-
tricular fibrillatio.n will usually present with cardiac arrest or, ifthe arrhythmia tenninates sponta-
neously. syncope; these indMduals require aggressive workup and therapy, as noted in Chapter 1s.
TORSADE DE POINTES
Torsade de pointes (TdP) VT is a serious type of VT initially described by Dessertenne.!;/It is
characteriud by a prolonged QT interval during baseline rhythm and a rapid VT with aphasic
continuous alteration of QRS morphology (Figure 8-17). It is also important to realize that
Control EP
II
Ill
AVF
V1
V6
S1 S1
500'2~190 VTCL=220
71 Y/O WM WITH REMOTE INFERIOR Ml AND SYNCOPE
FIGURE 1-15 • lnltlatton ofventrfc:ularflutterwtth a wmrtc:ular pacing cycle length of SOO ms (S,) and 2 extrastimuli CS:iSJ·
artifacts of recording techniques can give the appearance of TdP (Figure 8-18). We feel that
it is very important to include a prolonged QT interval at baseline rhythm as part of this syn-
drome for diagnostic as well as therapeutic reasons. For example. patients with a normal QT
interval at baseline rhythm can have polymorphic VT with a morphology that resembles TdP.
These individuals may be treated successfully with antiarrhythmic agents that prolong the QT
interval; one would not administer such a drug. with the possible exception ofamiodarone. to a
patient with TdP VT. The etiology for TdP is linked to the QT prolongation. IfTdP is suspected,
conditions or agents that prolong the QT interval should be sought Patients can also have con-
genital long QT syndrome (LQTS). which is discussed in Chapter 15. However, although drugs
or other conditions that prolong ventricular repolarization may be the cause ofacquired LQTS,
they could also greatly exacerbate arrhythmias in a patient with congenital LQTS.
Acquired LQTS
The most common cause of acquired LQTS in our experience is associated with the use ofanti-
arrhythmic agents that can block outward potassiwn ions from cardiac cells and prolong the
QT interval.. These patients often undergo concomitant diuretic therapy and have hypokalemia
that can worsen the situation. Hypokalemia, hypomagnesemia, phenothiazines, tri and tetra-
cyclic antidepressants, and many other drugs including some antibiotics can also prolong the
QT interval and cause TdP VT (see crediblemeds.org for a detailed list ofdrugs prolonging the
QT interval.). It is possible that patients with a baseline normal QT interval who develop TdP
II
Ill
AVF
V1
FIGURE 8-16 • Induction of ventricular flbrlllatlon with 1 extrastimulus (S:) Introduced during ventTlcular padng (S1). The patient
had a low left ventricular ejection fraction and spontaneous nonsustalned VT (VT-NS) 7 days after coronary artery bypass graft
(CABG} surgery.
taking drugs that typically cause only minimal QT lengthening have a genetic abnormality in
their genes that control ventricular repolarization. Female gender appears to be a separate risk
factor for TdP in acquired AV block.58
The mechanism of TdP in acquired LQTS is postulated to be triggered activity with EADs,
but reentry is not discounted. The tachycardia commonly occurs with a short-long-short QRS
complex sequence (F~ 8-19). This ECG rhythm strip is taken from a patient receiving qui-
nidine therapy. The patient has premature atrial complexes followed by pauses and a marked
abnormality in repolarization, with a pronounced inverted T wave in the QRS complexes
: II
FIGURE •17 • Torsade de pointes VT. {See text i'or details.}

m11111111~11111111111111m~:::~m:1111111~11111111111111111~11111111mm111~11111m11111111111~m~111111~~~m1111111m~m11mm~1111~
FIGURE 1-11 • Simultaneous ECG recordings of a patient In sinus rhythm at elec:trophy:slologlc study In whom me recording wire
connected n:> the patient was jlggled at regular Intervals to give the artlfactual appearance of torsade de polntes.
closing a pause. After the second premature atrial comple.i: (fourth QRS complex). there is a
relatively long pause, and the QRS complex ending the pause has a more marked inversion of
the T wave and is followed by TdP. This short-long-short QRS comple.i: sequence is very typical
for the initiation of pause-dependent TdP in acquired LQTS.
Therapy
Probably the most important aspea of treatment for patients with acquired LQTS is a correct
diagnosis. It is critically important to obtain an ECG during baseline rhythm between epi-
sodes of TdP to evaluate the QTc interval It is also necessary to review the electrolyte status
and drugs the patient is receiving. Therapy consists of discontinuing the implicated drug and
correcting any electrolyte abnormality. It is important to suppress subsequent episodes of TdP
while the offending drug is being eliminated from the patient. and several methods are avail-
able to accomplish this.59 Temporary overdrive ventricular or atrial pacing is a proven, excellent
method to prevent the recurrence of arrhythmia. It may not be possible to initiate pacing in a
timely fashion. however. and other treatment options are available.
FIGURE 1-19 • Typical Initiation of torsede de polntes VT. The f'ourth QRS complex Is premature and ls followed by a relatively
long pause. The QRS complex dosing the pause Is a550clated with a marked Increase In the amplitude and duration of the Inverted
T and possibly U wave, and torsade de pointes tachycardia follows.
Tzivoni and colleagues60 clearly demonstrated the success of intravenous magnesium sulfate to
treat TdP. Using a 25% or 50% solution of magnesium sulfate, they suggested that a 2 g intrave-
nous bolus be given over 1to 2 min, which can be followed by a second 2 g bolus 5 to 15 min later
if needed. A continuous infusion of 3 to 20 mg/min of magnesium sulfate can also be used. In
12 patients with acquired LQTS and TdP with a mean QTc of 0.64 s, they noted that 9 had no
more TdP after the first dose of magnesium sulfate and the other 3 had a partial response.60
Importantly, in 5 patients with coronary artery disease and polymorphic ventricular tachycar-
dia with a normal QT interval, intravenous magnesium sulfate was ineffective and 3 patients
responded to intravenous lidocaine and 2 to intravenous procainamide. This observation sup-
ports the concept that TdP should be diagnosed only in the presence of a prolonged QTc interval,
measured either immediately before the onset of ventricular tachycardia or at baseline, because
therapy that can acutely exacerbate 1 type of arrhythmia-for example, procainamide in TdP-
can be lifesaving in another patient. Temporary overdrive ventricular or atrial pacing or intra-
venous isoproterenol to increase the heart rate can effectively suppress TdP in acquired LQTS.
The highest priority should be given to prevention ofTd.P. Drugs that are known to prolong the
QT interval should be given cautiously to patients who have a propensity for conditions such
as hypokalemia and avoided whenever possible in patients who have a baseline prolonged QTc
interval. One should be careful when administering 2 or more agents that can prolong the QT
interval in a given patient and preferably do this in-hospital during continuous ECG monitoring.
BIDIRECTIONAL TACHYCARDIA
Bidirectional VT is usually a manifestation of digitalis toxicity. It is characterized by right bun-
dle branch block morphology with alternating frontal-plane polarity.61 It is important to rec-
ognize that this can be a digitalis toxic arrhythmia and to determine whether the patient is
receiving digitalis. If digitalis toxicity is noted, methods to treat this-such as administration of
potassium, lidocaine, or phenytoin-can be considered, but we recommend as initial therapy
in this potentially life-threatening situation the administration of cardiac glycoside-specific Fab
fragments. Other rare causes of bidirectional VT are Anderson-Tawil syndrome and catechola-
minergic polymorphic VT (CPVT).
GENETIC SYNDROMES AND ARRHYTHMOGENIC CARDIOMYOPATHIES

Life-threatening sustained ventricular tachycardia, typically polymorphic, can occur in patients
with normal ventricular function who have certain genetic syndromes-LQTS, Brugada (may
also have some myocardial abnormalities), CPVT, short QT, and idiopathic ventricular fibril-
lation with or without early repolarization. 12 Patients with hypertrophic cardiomyopathy and
a variety of arrhythmogenic cardiomyopathies, for example, sarcoidosis and arrhythmogenic
right/left ventricular cardiomyopathy, can also develop sustained VT.62 These syndromes and
cardiomyopathies are discussed in Chapter 15.
SUSTAINED MONOMORPHICVENTRICULARTACHYCARDIA
Sustained monomorphic ventricular tachycardia (VT) has a uniform QRS configuration
throughout the duration of tachycardia. Categorizing VT by mechanism or other specific char-
acteristics is often difficult. The overwhelming majority of patients who have sustained mono-
morphic VT have some form of heart disease, usually coronary artery disease.63.64
History and Physical Examination

Patients who have sustained monomorphic VT may have a variety of symptoms that depend
primarily on the hemodynamic effect of VT in a particular patient. The major determinants of
hemodynamic response to VT are the rate of tachycardia, degree of myocardial dysfunction,
and peripheral vascular adaptation. Common presenting symptoms range from palpitations
and presyncope to syncope and cardiac arrest In some patients symptoms may reflect concom-
itant organ disease-for example, angina in a patient with significant coronary artery obstruc-
tion. The level of myocardial dysfunction is not merely based on the left ventricular ejection
fraction. Figure 8-20 shows examples of sustained monomorphic VT in 2 patients with a his-
tory of heart disease. Although the rates of tachycardia are similar, one patient (Panel A) pre-
sented with palpitations whereas the other {Panel B) had syncope. Note that the left ventricular
NYHAll-111 CHF
No History of CHF LVEF 19%
LVEF 10% BPwithVT-S
BP with VT-S 112189 mmHg 40 mmHg Sys., Syncope
:r.I I
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Panel A PanalB
FIGURE 8-20 • Examples of sustained monomorphlc VT In 2 patients with myocardial dysfunction. (See text for details.) CHF, con-
gestive heart failure; LVEF, left ventricular ejection fraction; BP; blood pressure; VT-S, sustained ventricular tachycardia; VTct' ventric-
ular tachycardia cycle length; Sys, systolic; NYHA, New York Heart Association classification.
ejection fraction was only 10% in the patient presenting with palpitations, but there was no
history of congestive heart failure. In contrast, the patient who had syncope had an ejection
fraction of 19% but was also ranked in New York Heart Association (NYHA) class II-III for
congestive heart failure. In our experience, syncope is more likely to occur in patients with a
history of heart failure during sinus rhythm, which signifies a heart that will have limited com-
pensatory ability during VT.
The most important historical information is determination of the presence of heart disease.
Akhtar and colleagues64 noted that structural heart disease occurred in 112 of 122 (92%)
patients with VT compared with only 6 of 28 (21 %) patients with supraventricular tachycardia
(SVT). These authors also noted that VT was frequently misdiagnosed as SVT.64 In our expe-
rience, this usually occurs when a patient presents with a wide QRS complex tachycardia and
a relatively stable blood pressure (Figure 8-20A). It is critical to remember that hemodynamic
stability during a wide QRS complex tachycardia does not exclude VT and hemodynamic insta-
bility during tachycardia does not exclude SVT.
Physical examination of the patient during tachycardia may disclose signs of ventriculoatrial
dissociation, which rarely occur with SVT. During ventriculoatrial dissociation, the normal
synchronized atrial to ventricular activation sequence is lost and the 2 chambers contract
independently of each other. Thus, the relative position of the tricuspid and mitral valves
in the ventricle at the time of ventricular contraction may vary from beat to beat and lead
to cannon A waves in the neck veins, variable intensity of S1, and variable systolic blood
pressure. After restoration of sinus rhythm, the physical examination should be directed
to uncovering signs of heart disease such as neck vein distension, pulmonary congestion,
pathologic murmurs or gallops, and peripheral edema. The presence of decreased arterial
pulsations or bruits over carotid or other arteries may suggest the presence of atherosclerotic
disease.
Electrocardiographic Evaluation
It is very important to obtain ECG documentation of the wide complex QRS tachycardia, pref-
erably a 12-lead ECG. An in-depth discussion of the differential diagnosis for wide complex
QRS tachycardia is presented in Chapter 13, and only key points will be reviewed here. ECG
signs of ventriculoatrial dissociation are independent P waves and QRS complexes and fusion
and capture QRS complexes. Figure 8-21 demonstrates the normal QRS complex for this
patient in Panel A and the presence of capture <.first arrow) and fusion (second and third arrow)
QRS complexes in Panel B. Note that the morphology of the fusion complexes is intermediate
between the normal and VT QRS complexes. Fusion and capture QRS complexes occur when a
supraventricular impulse activates all (capture) or part (fusion) of the ventricles during tachy-
cardia. This may occur in patients who have slower VTs but, in our experience, is rarely seen
in patients in whom the rate of tachycardia is 180 or greater. Figure 8-22 shows the electro-
physiologic mechanism of fusion and capture QRS complexes. In Figure 8-22A, the third QRS
complex is narrow and generated from the sinus atrial impulse that captures the ventricles and
yields a normal HV interval of 50 ms for this patient. In Figure 8-22B, 2 fusion QRS complexes
are noted with an HV interval of 40 ms, which is 10 ms shorter than that noted during sinus
rhythm in this patient, and the QRS morphologies are intermediate between the sinus-gen-
erated complexes and those that occur during tachycardia. In some patients, ventriculoatrial
....
Panel A
:: .. .. ·+
:: : .. .. : .. .. tt
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1 .\ :: I ·- i J
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IT
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lt1 lt1 1 '" TI:
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PanelB
FIGURE 8·21 • Fusion and capture QRS complexes during VT. (See text for details.)
block but not total dissociation is present and may be identified on the ECG. In Figure 8-23,
2:1 ventriculoatrial conduction is noted during VT. Note that a His bundle depolarization is
present with each QRS complex regardless of the presence of an atrial depolarization. However,
the His activation occurs within the QRS complex and represents retrograde activation of the
His bundle during VT in this patient. The arrows in ECG lead III point to atrial activation on
the ECG after every other QRS complex. Although the P waves are clearly seen in ECG lead III,
they are not easily identified in several other leads, which reinforces the importance of obtain-
ing a 12-lead ECG whenever possible during tachycardia.
Ventricular tachycardia can be left bundle branch block (Figure 8-24) or right bundle branch
block (Figure 8-25) morphology, and the QRS duration is typically 120 ms or greater. Very
uncommonly a rdativdy narrow QRS complex can occur during VT (Figure 8-26). Hayes et al.65
reviewed 12-lead ECGs of 106 patients with induced VT at dectrophysiologic study. Of these
patients, 5 (4.7%) had a QRS duration of 110 ms or less. Of the 5 patients, 4 had coronary artery
disease and only 1 patient had no obvious structural heart disease. In patients with a rdativdy
narrow QRS complex during VT, it is possible that the origin of tachycardia is in the proximal
His-Purkinje system, which would allow activation of most of the ventricles over the normal
conduction system. Although this is theoretically possible, it is difficult to confirm even at
dectrophysiologic study. The fact that VT can occur with a QRS duration <120 ms emphasizes
the importance of considering any rdativdy wide QRS complex tachycardia in a patient with
structural heart disease as VT until proven otherwise.
V1
~
I I
HRA-1 1J
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550
Panel A
111111111111 11ll+llH H~liHI HHlll 111111111111111HHHH#l+l+l111111 11111111111 111
II
Ill
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Panel B
t-+-
FIGURE •22 • Elec.trophyslologlc mechanism offusion and apture QRS complexes during VT. Panel A. Th~ third QRS complex Is
narrow, with an HV Interval ofSO ms, Identical to that seen during sinus rhythm, and this represents a capture (Q QRS complex. Panel B.
The third and seventh QRS complexes are fusion (F) complexes with an Intermediate QRS mOJphology between that ofsinus rhythm
and VT. The HV Interval Is 40 ms. less than that noted during sinus rhythm. For the time llnes, each major dlvlslon equals SO ms.
II
Ill
V1
Ve
HBE
~ ~ ~~ ~ ~ t ~ t
RV
FIGURE 8-23 • Venb'ia.ilar tachycardia with 2:1 venb'iculoatrial conduction. (See text for details.)
FIGURE 1-24 • Left bundle branch block VT terminates spontaneously and sinus rhythm resumes for the last 3 ORS complexes in
this tracing.
I, II, Ill aVR, aVL, aVF v,,V2,V3

I I 1 ! t I • I f : •
~+-1-+-+-t'-'T-~-+-"-'--~-'-.........- - - -- - - - - - - - - - -- - - -
··· ···.
.. ------. - - -· - - - - - - -
FIGURE •Z5 • Right bundle branch block sustained rnonomorphlc VT.
FIGURE •26 • Relatively narrow ORS complex VT.

Electrophysiologic Testing
An in-depth review of methods of electrophysiologic testing is noted elsewhere.63M Pro-
grammed electrical stimulation of the heart, in particular ventricular stimulation, is used to
initiate sustained VT. Induction of VT using programmed stimulation techniques can occur in
patients in whom the mechanism of tachycardia is due to reentry or triggered activity related to
delayed afterdepolarizations but not when it is due to abnormal automaticity. Further, success-
ful initiation of tachycardia at electrophysiologic testing depends on the type of arrhythmia and
heart disease being studied as well as the stimulation techniques employed.63M For example, in
patients with a history of sustained monomorphic VT, the frequency of initiation of sustained
monomorphic VT is approximately 95% in patients who have coronary artery disease but only
approximately 80% to 85% in patients with idiopathic dilated cardiomyopathy.
Successful induction of sustained monomorphic VT depends on the pacing technique

employed, with the use of 3 extrastimuli having a higher inducibility rate than that of 1 extra-
stimulus. However, there is a trade-off of specificity for sensitivity as more aggressive pacing
techniques are employed. Thus, a very rapid-for example, with a cycle length <220 ms-
monomorphic sustained VT initiated with triple extrastimuli may be a nonspecific arrhyth-
mia in a patient who has documented hemodynamically stable slower VT. Unfortunately,
some patients may have more than 1 clinical tachycardia, but only a slower VT has been
documented. In these instances, the more rapid VT initiated with triple extrastimuli might
have important clinical consequences, and these decisions have to be made on an individual
basis. We do consider sustained polymorphic VT or ventricular fibrillation initiated with tri-
ple extrastimuli in patients with a history of only sustained monomorphic VT as nonclinical
arrhythmias because of the lack of specificity of these tachycardias initiated with very aggres-
sive pacing techniques.
Initiation of sustained monomorphic VT using atrial and ventricular pacing techniques is

demonstrated in Figures 8-27 and 8-28.
To increase yield of induction of VT, multiple pacing cycle lengths are employed as well as
stimulation at 2 or more right ventricular sites using 1 to 3 ventricular extrastimuli. In some
individuals, infusion of isoproterenol is necessary as an adjunct for the induction of VT dur-
ing programmed electrical stimulation. In other patients, infusion of isoproterenol alone may
initiate tachycardia.
SUSTAINED MONOMORPHICVENTRICULARTACHYCARDIA IN PATIENTS WITH

STRUCTURAL HEART DISEASE
Coronary Artery Disease
The most common cause of sustained monomorphic VT is coronary artery disease.63.64 When
sustained VT occurs in a patient with chronic coronary artery disease, typically originating
from an area of the ventricle associated with a healed myocardial infarction, the overwhelming
evidence in experimental models as well as in humans suggests reentry as the mechanism for
tachycardia.67- 70 Although most electrophysiologists accept reentry as the cause of VT in the
majority of patients in whom sustained VT can be initiated by programmed electrical stimula-
tion, triggered activity often cannot be excluded.71
1uu11111r11' l''''l'ml11"rmr"'l"ul""l11"l""l'"l'111l'"'l""l"11l'11'l"11l11"l''''r111i•11T"'lnu1... ,1,11111111111111111•i""l""' 11'l'"'l111'l''"l'"'l''''l""l''"l'"'l'"'l"''l"'i'"'l'"T"'l"''l"'T"'l"'T'"r" 1
V1 - ---"" - - - - - -.... ,.- - - -......
FIGURE 8-27 • Initiation of sustained rnonomorphicVT during atrial pacing. The atrial pacing cycle length is fixed at 550 ms. Note
that the first 2 QRS complexes are conducted from the high right atrial pacing site to the ventricle over the normal AV conduction
system, with a His bundle elect!Ogram prececilng each QRS complex with the same HV Interval ldentlfted during sinus rhythm. Ven-
tricular tac:hycan:ila begins with the third QRS complex and was sustained In this lndlvldual. Ventrlcular tachycardia was Initiated
during Incremental atria I pacing and only the last 2 normal QRS complexes are Illustrated prior to the Initiation of tachycardia. Note
that the third atrial pacing stimulus to QRS Interval ls too short forthls QRS complex to have been genet'ated from the alTlum.
1000
II
Ill
AVF
V1
600 330
FIGURE 8-28 • Induction of sustained monomorphlcVT with 1 ventrlcular stlmulus Introduced during ventrlcular pacing. Padng
at the right ventrlcular apex at cycle length 600 ms and Introduction of a premature ventricular complex with an S1S2 interval of
330 ms initiates sustained monomorphic VT of a right bundle branch block superior or northwest axis morphology.
The QRS morphology during VT can either be right bundle branch block, left bundle branch
block, or both in a patient in whom the interventricular septum is part ofthe tachycardia circuit.
The morphology of VT will reflect the site of origin for the arrhythmia. For example, tachycar-
dia originating in the posterior wall of the left ventricle near the interventricular septum that
occurs after an inferior wall myocardial infarction commonly has a right bundle branch block,
superior axis morphology.
The most frequent form of sustained monomorphic VT occurs months or years after acute
myocardial infarction.63•61.li• The reason for the occurrence of VT is usually enigmatic. In most
instances there are no acute pathophysiologic derangements such as heart failure, electrolyte
imbalance, or ischemia, and patients appear to present in an otherwise stable state with sus-
tained monomorphic VT. Regardless, any reversible cause for the tachyarrhythmia should be
investigated and corrected if found. With rare exception, patients with sustained monomor-
phic VT should undergo antiarrhythmic therapy. Multiple therapeutic options are available and
include antiarrhythmic drugs, most commonly sotalol or amiodarone; ICD; catheter ablation;
or infrequently directed surgery to isolate, destroy, or remove the area involved in tachycardia
(see Chapters 15 and 18).63·12.13
ICDs are the usual therapy in these patients. Figure 8-29 is an example of an ICD with anti-
tachycardia pacing functions. In Panel A, a monomorphic sustained VT of cycle length 325 ms
is terminated by a pacing train of stimuli at cycle length 280 ms.
In Panel B, a second episode of VT occurred in this patient that was faster with a cycle length
of 295 ms. A burst of ventricular stimuli with cycle length of 250 ms not only fails to terminate
tachycardia but accelerates it to a cycle length of 270 ms, which is recognized by the device as
an arrhythmia that will require more aggressive treatment and, as noted in the bottom panel,
a 20-J shock is given that restores sinus rhythm. The use of these devices is covered in more
detail in Chapter 19.
Cardiomyopathy
Various forms of cardiomyopathy can be associated with sustained monomorphic VT (see
Chapter 15). Bundle branch QRS morphology during tachycardia depends on the origin of
the arrhythmia. Many diseases may cause a cardiomyopathy, but in our experience idiopathic
dilated cardiomyopathy is most frequently associated with sustained VT. Most patients with
dilated cardiomyopathy can have their ventricular tachycardia initiated at dectrophysiologic
testing, although less frequently than with coronary artery disease.66 Bundle branch reentrant
VT (BBR-VT) commonly, but not exclusively, occurs with markedly dilated cardiomyopathy
and typically can be induced at electrophysiology study.7•
Patients with sustained VT and dilated cardiomyopathy require therapy to prevent recurrences
of the arrhythmia. We currently consider an ICD as early therapy in these patients. Pharma-
cologic treatment may be an important adjunct to decrease the frequency of tachycardia epi-
sodes and to slow the rate of tachycardia if it occurs. Catheter ablation is often useful to treat
these patients, especially those with BBR-VT.73 Surgery is less likely to be successful because of
the diffuse nature of this process, and it is usually not considered as prime therapy for these
individuals.
Ill
V1
ZONEll
PanelA
Continuous
- 20J
ZONElll
Panel B
FIGURE •2t • Treatment of sustained VT by an implanted cardiovertet' defibrillator with antitachycardia pacing functions. (See
text for detalls.} a.
cycle length ofVT; PCL, pacing cycle length. Zone II and zone Ill are programmed rate zones, each of which
has specific therape4.1tlc modalltles programmed to tennlnate the VT. In this devtce, zone Ill aul'Cmatlcalty requires hlgh-enefgy
deflbrlllatlon.
Bundle Branch Reentrant VentTicular Tachycardia

A specific type of VT exists that incorporates the right and left bundle branches in the tachy-
cardia circuit and is termed bundle branch reentry.7"'7S Patients with bundle branch reentrant
VT typically have substantial cardiac enlargement, a history of congestive heart failure, and
either idiopathic dilated cardiomyopathy o.r coronary artery disease.74 Occasionally. patients
with normal ventricular function but with marked delay in His-Purkinje conduction can
have BBR-VT. His-Purkinje dysfunction is usually present and manifested by a prolonged HV
ITITl1 Il'I M1Tlii1rrn!TIInn111111111111 111111 11111 11 11111111 ITl'rl 111'11111111 ml'lIID1TI llfl11'M1'fl
JV\..r-
II ~
Ill f\f\r-
r\/V'-
HVSOmeec
Panel A PanalB PanalC
FIGURE •30 • Initiation of sustained bundle branch reentrantVT. Arrows In Panel C point to His bundle depolarizatlons. {See text
fordetallsJ (Reproduced with psmlsslon from Lloyd EA. etal. SustBined ventrlculartllchycardla due to bundle branch reentTy.Am
HeartJ. 1982;104:1095. Copyright C> Elsevier.)
interval during supraventricular rhythm and nonspecific interventricular conduction delay,

often with a pattern of the left bundle branch block type. Left bundle branch block morphology
during tachycardia is most commonly observed, although macroreentrant VT can also have
right bundle branch block morphology.
Initiation of bundle branch reentrant VT in the clinical electrophysiology laboratory is demon-

strated in Figure 8-30 with a schematic representation in Figure 8-31. In this patient 2 ven-
tricular extrastimuli were necessary to initiate tachycardia. In Figure 8-30, Panel A, note that
the S1S1 interval is 250 ms, which is kept constant in Panels Band C. After the first premature
complex (S1). a retrograde H2 is present with an S2Ha interval of 230 ms. Retrograde activation
of the His bundle is presumably due to retrograde block in the right bundle branch with trans-
septal conduction and activation of the His bundle over the left bundle branch (Figure 8-31,
Panel A). The SA interval is 340 ms and yields an S,H, interval of 180 ms without initiation
of tachycardia. In Figure 8-30, Panel B, the S2S3 interval is shortened to 320 ms, and this results
in an increased conduction delay from S3 to H3 , which is now 200 ms. This is most likely due to
slowing of conduction in the left bundle branch, ventricular myocardium, or both (Figure 8-31,
Panel B). Bundle branch reentrant VT is finally initiated in Figure 8-30, Panel C when the SA
interval is shortened to 300 ms with a corresponding increase in S3 H3 interval to 220 ms and
completion of the reentrant circuit Figure 8-31, Panel C depicts even more conduction delay
than is noted in Panel B, which allows enough time for the distal right bundle branch to recover
from refractoriness and allow reexcitation of this area with completion of the reentrant circuit.
The bundle branch macroreentrant circuit in this patient includes anterograde conduction over
PanelA PanelB PanalC
FIGURE 8-31 • Schematic representation of Initiation of bundle branch reentrant VT. (See text for detallsJ The zigzag portion of
dte conduction llne represents slowed conduction.
the right bundle branch, transseptal conduction, and retrograde conduction over the left bun-
dle branch. Thus, the QRS morphology is left bundle branch block and will resemble a typical
left bundle branch block morphology (Chapter 3). In this type of tachycardia the His bundle
actively participates in the reentrant circuit. In contrast, other forms of VT may demonstrate
retrograde His bundle depolarization, but His bundle conduction is not needed for mainte-
nance of tachycardia (Figure 8-23).
One should remember that there are many types of tachycardia other than bundle branch reen-
try that c:an have a left bundle branch block morphology ('Iable 8-4). Etiologies can include
various forms ofVt SVT with bundle branch block or aberrancy. or preexc:ited tachycardia with
anterograde conduction over an accessory pathway. Differentiation of these forms of tachycardia
is critically important to the appropriate management of the patient, and in many if not most
instances will require electrophysiologic study. In general, if the 12-lead ECG is identical during
tachycardia and sinus rhythm, the mechanism is usually supraventricular. When the QRS com-
plex resembles "typical'" left bundle branch block morphology (Chapter 3), conduction usually
proceeds over the right bundle branch to activate the ventricles; differential diagnosis includes
bundle branch reentrant VT, SVT with left bundle branch block or aberrancy. and atriofascicular
and nodofascicular reentry utilizing aa:essory pathways (F:lgure 8-32). The more "atypical" the
left bundle branch block morphology. the more likdy it is that VT is the mechanism, excluding
Coionary artery disease SVT wldt aberranc:y

SVT'widt888
Arrhythmogenlc RV dy.splasla Preexclted tachycardia
Antfdromlc RT
RV cardlornyopathy Atrlofasclcular RT
Bundle branch reentry Nocloventrtcular RT
RV outflow tract Noclofasclcular RT
After TOF repair Bystander participation
Abbmitatlom: WF, tnm/ogy of Fa/lot; SVT, ruprawntrlctllar tachymrdla; .!IV, right wntTlcff!; R1; rttntrant tl1chyaudll1; BBa. bundfe
branch block.
SVT/LBBB A1riofascicular RT
Atrium
Panel A Panel B
Nodofascicular RT BB Reentry
AVN
Atrium
PanelC Panel D
FIGURE 1-32 • "'fyplal' left bundle branch block tachycardia mechanisms. As noted In the~ activation of
the ventrldes over the rtght bundle branch tends to give an ECG pattern of a typical left bundle branch block
morphology. Panel A. Any supravenulcular tachycardia (SVT) with left bundle branch block aberrancy Is 1 mech-
anism. Pan1I B. Atrlofasclculer redprocating tachycardia utlllzes an accessory atrloventrlculer tract that connects
the right atrium with the right bundle and subsequent conduction to the ventricle over the right bundle with
retrograde conduction to the His bundle and AV node and then back to the right atrium. Panel C. Nodofascicular
reclpnxattng tachycardia In wttlch the reentrant drcult uttllzes a nodofasc:lcular tract originating from the AV
node and entering Into the right bundle for anten>grade c:onducUon and ~regrade conduction over the His
bundle and through the AV node. This Is cllnlailly rare compared with atrlofasdcular reciprocating tachycardia.
Pa Ml D. Bundle branch reentry with anterograde conduction over the right bundle branch and retrograde con-
duction over the left bundle branch can give a typical left bundle branch block morphology even though this
Is a form ofVT. Abbreviations: AVN, auloventrlcular node; Ar-. aulofasclcular; NF, nodofasdcular; 1.8, left bundle
branch; RB, right bundle branch; RT, reentrant tachycardia.
various forms of prcexcited tachycardias (Egure 8-33). The electrophysiologic differentiatio.n of

the various forms of tachycardia noted in Table 8-4 is complex and beyond the scope of this
discussion. However, several examples of left bundle branch block morphology tachycardia are
illustrated in Figures 8-34 through 8-36.
SUSTAIN ED MONOMORPH IC VENTRICULAR TACHYCARDIA IN PATIENTS WITHOUT

STRUCTURAL HEART DISEASE
Sustained monomorphic VT can occur in patients with normal ventricular function from
various locations and be caused by reentry or automaticity.12 Two of the more common vari-
eties are idiopathic left VT (ILVT) and those arising from the outflow tract region (OT-VT).
Ventricular Tachycardia Pmexctted Tachycardia
Atrium Atrium
AP
Panel A PanelB
Nodoventrlcular Tachycardia
PanelC
FIGURE 1-33 • '"Atyplcal"left bundle branch block mechanisms. P~nel A.AnyVT orlglnattng In the right ventric-
ular free wall or In some cases from the right ventrlcular septum can give a left bundle branch block morphology
pattem, but It Is usually atyplcal In form. Panel B. Many forms of preexcited tachycardia I.fort ut111ze a right free
wall accessory pathway connecting to the right ventricle can yleld an atyplcal left bundle branch block mor-
phology. These Include any atrial tachycardia with conduction over the accessory pathway as well as antidromlc
reciprocating tachycardia in which the accessory pathway is used f'or antefograde conduction and the nonnal
ventrtculoattlal conduction system for retrograde conduction, AV nodal reentty with anterograde conduc:tton
as a bystander over a rtght free wall pathway, and nodoventrlcular reciprocating tachyardla with an acce$SOry
pathway originating In the AV node and entering Into the right ventricle {Panel C).
ILVT can involve the left posterior, anterior, or high septal fascicles.11 OT-VT may be on the
right or left side, from the aortic sinus ofValsalva, or in the peri-His region.12 Two specific types
are discussed below.
Right Bundle Branch Block/Left Axis Morphology

An example of sustained monomorphic VT with right bundle branch block. left axis devia-
tion morphology is shown in Flgure 8-37.76-aO Very infrequently patients can have right bundle
branch block. right axis deviation morphology during VT,u.n.79 with electrophysiologic char-
acteristics and responsiveness to verapamil therapy indistinguishable from individuals with
right bundle branch block. left axis deviation vr. Some investigators have observed inferior
and/or inferolateral T-wave inversions after the termination of tachycardia7m and others have
reported T-wave inversions in ECG leads :a:. m, and aVF as well as in the lateral precordial leads
during sinus rhythm.ao.a1 However, these ECG findings in sinus rhythm have not been present
in the majority of patients with this form of vr (Flgure 8-38). Patients are typically young and
most are men. and symptoms during tachycardia are usually palpitations although occasionally
syncope has been reported. Sudden death is rare in these patients.
~~N'f[ffl
l.h
.
ft h .A A A
:vs/\rJ""J\,J~\,/\tJ':
h~
I
I
1 •
FIGURE •S4 • Left bundle branch block Sllltalned VT In a patient with coronary artery disease and previous myocardial Infarc-
tion. Note the prolonged time from onset of the QRS complex to Its nadir In ECG leads V1 and V1! and the fractionation In some of
the ORS complexes. This is consistent with VT.
FIGURE •ss • AV nodal (AVN) reentrant tachycardia with left bundle branch block aberrancy Initiated at electrophyslologlc
study. Nate the rapid downstroke of the 5 wave In V1 and v,,, with minimal duration of the r wave. This patient has 'typical' left
bundle branch block morphology during tachycardia, consistent with a supraventricular origin but not exclusive of some types
of VT.
FIGURE 8-36 • Left bundle branch block morphology during VT that occurred In the right ventricular outflow tract In a patient
with nonnal ventTfcular function. The QRS complexes are Rlatlvely narrow and not too dlsslmllar from •typtcal• left bundle branch
block morphology. Patients with structurally normal ventricles who have right ventricular outflow tract tachycardia an have a left
bundle branch block morphology that may mimic the typical form of left bundle branch block even though conduction to the
ventricles does not proceed exclusively over the right bundle branch. (Reproduced with permission from Prystowsky- EN, Noble RJ.
Electrophyslologlc studies: who to refer. Heart Dis Stroke. 1992;1 :188J
FIGURE 8-37 • Sustained right bundle branch block, left axis deviation VT that occurred In a patient with no obvious structural
heart dlsease. lsoproterenol Infusion was necessary to help fadlltBte Initiation of tachycardia with programmed ventricular stlmula-
tion at efectrophysiologic study in this patient.
~ij "ii1 :ii!;;; :[:: ·i:::·····. ' ·'--aVF-+-,f-+-+·-1= ->-· ''" =tv.:i ·- V8
E...~
..B
... ~
..~..~
...~
...E...+.
. . ~.-+-+-11-1--+-~+-+-r-+-+-+- -- ·-+-~~+-1H+--1-t-1-·-;t-t-'+-t-+1+-+-+-1--..--1--1;-,,r--r-r--i--t-+--+-+-+,-
,_.:::_,.
:;-.;;:: ,~
:;;:..-:i...,.
;;:_ :::"°"
;::.._
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··:._...-"
·. _.·_,_
··...,.
:' -+-·+-+--+--+--!~+--+-+-· ···· ··· ........ ~. - - ··- - - --1-4·-l-~4-1--1--1--1--1--1-11-'-l-
1
"4.. -1--1--1-+--l-'-IF
fi:Fm"l'l~"'1
B:il'l"1ll'1'+1:=:.:.,= 1;1 ""ml'I-'·:·-"+-1- ·· +-1-+--+- - ··-1-1--r-·+-I ·f-+-~-1-·
· +:-4-1"- ·- ·- ! - - .• - f.-- -+-·~1-1--1-'-l-:+··,'·,-i~
,:;.+-···-·i-.-i ··=+' -'-1-f-"!--t-~
.. f- ····
ir.-m~11;;;tmi;;;.
~g~;+;;n~
11 :~
:nE m'l"
i ::;o'tll - ·+--+,-t-+..+·-+-+-H-1---1--1 ·r -+-1-+· 1-- _ _ i-- ·-·
. i ~- _ ·-···-t-··1--+-t-+--+-+-+-t-+-+-11-1--r-r--i--t-+--+-t,,.;
i;:::g±1~:::1rn""'l
l:i:r.:~~~gE""'m""mll":g~
.,..,
=: ·= :t--+.~:t,,.+-~- t - - · - : r--
7
_.._ ___ _,__,_....-..=..... ,__,__, _ _,_,~_,_.,_...~.._......................_.......,_.._.........-· ....··.....:......... =::
::· .....
. , ~; i;g iii~ gg E:: l;l .·.; · .·.· .. ... 1:: ••• • • .•
: : ]! !!!: gg g:; igj 'ii! :::; :-. ;::: ::;: : : ..
FIGURE 1-38 • Electrocardiogram taken during sinus rhytflm in the patient with ventricular tachycardia shown in Figure 8-37.
Note the lack ofT-wave inversions in the inferior as well as anterior and anterolateral leads.
The mechanism oftachycardia is typically reentry and almost all patients can have their arrhyth-
mia initiated at electrophysiologic study. The method of tachycardia induction is variable and,
although many patients have their arrhythmia initiated during rapid atrial or ventricular pac-
ing. it is common for VT to be initiated with premature atrial or ventricular stimuli. Almost
universal to this syndrome is the responsiveness of VT to intravenous verapamil treatment
(Figure 8-39). Almost all patients will have their tachycardia terminated when given 5 to 10 mg
of intravenous verapamil, and slowing usually precedes termination. Beta-adrenergic blockers
have been tested in only a few patients reported in the literature and appear to be relatively inef-
fective. Of note. VT is very uncommonly initiated during exercise testing, and most patients do
not give a history of onset of tachycardia during exertion. Even so. in our experience some of
these patients require intravenous isoproterenol in addition to programmed ventricular stimu-
lation for induction of tachycardia at electropbysiologic testing.
We prefer oral verapamil therapy if drugs are needed to treat these patients. We usually begin
with 240 to 360 mg/day, using sustained released formulations. Nonpharmacologic treatment
with endocardial radiofrequency catheter ablation should be considered for these patients (see
Chapter 18) (Figure 8-4.0).n.82
Left Bundle Branch Block/Right or Nonnal Axis

Unlike the syndrome of VT with right bundle branch block and left axis morphology that
occurs in patients without structural heart disease, patients with normal ventricular func-
tion and left bundle branch block VT form a more diverse group_i:urn Most patients have an
UIQO
VERAPAMIL 5 MG IV
llQOO
-
II
Ill
V1
HIS
FIGURE 8-39 • Termination of right bundle branch block, left axis deviation VT shortly after S mg of Intravenous verapamll was
given. (See text far demlls.}
inferior or right uis during tachycardia, but a normal uis has also been desaibed. The loca-
tion of tachycardia is usually in the right or left ventricular outflow tract but. again, anatomic
variations exist. In our experience and in most of the published patient series, sudden death
rarely occurs in these patients.
Noninvasive evaluation and cardiac catheterization in these patients reveals no evidence of

structural heart disease. The ECG during sinus rhythm is usually norm.al, which distinguishes
these individuals from those with arrhythmogenic right ventricular dysplasia. During VT, the
QRS duration is usually <140 ms and a more •typical" form ofleft bundle branch block pattern
may occur in some patients (Figure 8-36). When this happens, it is not surprising that the
arrhythmia is often misdiagnosed as SVT with aberrancy.
Several drugs have proved effective in the treatment of these patients. Success of certain agents
may depend on the clinical presentation; for example, eurclse-related arrhythmias more
commonly will respond to beta blockers or verapamil therapy. Endocardial catheter ablation
frequently eliminates VT in these patients7J,86,87 It is reasonable to prescribe radiofrequency
catheter ablation as first-line therapy in these relatively young individuals who otherwise will
have to undergo years ofantiarrhythmic drug therapy.
II
Ill
AVF
V1
V8
'/
9sec
0.3amp
CURRENT
FIGURE l-40 • Endocardlal radlofn!quency {Rf) catheter ablation of right bundle branch block, left axis deviation susmlned VT.
After 9 s of03 A of energy delivered to the site of tachycardia In tfle left ventricle, the arrhythmia terminates and sinus rhythm ls
restored, as noted by tfle last 3 ORS complexes in this tracing. This patient has had no further episodes of tachycardia and tachy-
cardia could no longer be initiated at electrophysiologic study. (Reproduced by permission from Page RL, et al. Radiofn!quency
catheter ablatton of Idiopathic recurrent ventrtcular tachycardia with rtght bundle branch block, left axis morphology. PACE.
1993;16:327.)
COMMENTARY
It is clear that sustained monomorphic VT is not a monolithic diagnosis. The origin of tachy-
cardia varies widely. depending in large measure on the underlying ventricular pathology.
However, obvious structural heart disease is not present in all patients. The consequences of
tachycardia depend on several factors, most importantly the degree of myocardial d}15function,
peripheral vascular adaptation, and tachycardia rate. Several types of therapy are available and
need to be tailored for each patient
REPBRENCBS
1. Bc:llwsm B. et al. Idiopa1hic recuJR11t rustained ventricular tachycardia reapom:ive to verapamil: an BCG-
electrophydologic entity. Am Htart J. 1984;108:1034.
2. Ohe T, et al Idiopathic summed leftventllcular tachycardia: dlnlcal and electrophysiologlc characterlstica. Circu-
lation. 1988;77:560.
3. Page RL, et al lla.diofre<iu.enc:y catheter ablation of idiopathic: rec:urnnt ventric:ular tachycardia with right bundle
branch block, le& uis morphology. PACB. 1993;16:327.
4. Galla.vudin L. Bxtrasystolie ventriculaire a. paroxyiimes tachycardiquea prolongea. Arch Mal Conr. l 922;15:298.
5. Parkinson], Papp C. Repetitive paroxysmal tachycardia. Br Httwt J. 1947;9:241.
6. Froment R, et al. Paroxysmal ventricular tachycardia: a clinical classification. Br Heart/. 1953;15:172.

7. Rahilly GT, et al. Clinical and electrophysiologic findings in patients with repetitive monomorphic ventricular
tachycardia and otherwise normal electrocardiogram. Am/ Cardiol. 1982;50:459.
8. Buxton AE, et al. Repetitive, monomorphic ventricular tachycardia: clinical and electrophysiologic characteristics
in patients with and patients without organic heart disease. Am J CardioL 1984;54:997.
9. Coumel P, et al. Repetitive monomorphic idiopathic ventricular tachycardia. In: Zipes DP, Jalife J, eds. Cardiac
Electrophysiology and Arrhythmias. New York: Grune & Stratton; 1985:457-468.
10. Morady F, et al. Long-tenn results of catheter ablation of idiopathic right ventricular tachycardia. Circulation.
1990;82:2093.
11. Klein LW, et al. Radiofrequency catheter ablation ofventricular tachycardia in patients without structural heart
disease. Cirr;ulation. 1992;85:1666.
12. Prystowsky EN, et al. Ventricular arrhythmias in the absence of structural heart disease. I Am Coll Cardiol.
2012;59:1733-1744.
13. Huizar JF, et al. Arrhythmia-induced cardiomyopathy. JAm Coll CardioL 2019;73:2328-2344.
14. Latchamsetty R, Bogun F. Premature ventricular complex-induced cardiomyopathy. J Am Coll Card BP.
2019;5:528-550.
15. Follansbee WP, et al. Nonsustained ventricular tachycardia in ambulatory patients: characteristics and association
with sudden cardiac death. Ann Intern Med. 1980;92:741.
16. Olshausen K, et al. Ventricular arrhythmias in idiopathic dilated cardiomyopathy. Br Hearl J 1984;51:195.
17. Holmes J, et al. Arrhythmias in ischemic and nonischemic dilated cardiomyopathy: prediction of mortality by
ambulatory electrocardiography. Am I CardioL 1985;55: 146.
18. Meinertz T, et al. Significance of ventricular arrhythmias in idiopathic dilated cardiomyopathy. Am J Cardiol.
1984;53:902.
19. Unverferth DV, et al. Factors influencing the one-year mortality of dilated cardiomyopathy. Am J Cardiol.
1984;54:147.
20. DeMaria R, et al. Ventricular arrhythmias in dilated cardiomyopathy as an independent prognostic hallmark. Am
J Cardiol. 1992;69:1451.
21. Bigger JT Jr, et al. Prevalence, characteristics and significance of ventricular tachycardia detected by 24-hour con-
tinuous electrocardiographic recordings in the late hospital phase of acute myocardial infarction. Am I Cardiol.
1986;58:1151.
22. Prystowsky EN. Antlarrhythmic therapy for asymptomatic ventricular arrhythmias. Am J CardioL 1988;61:102A.
23. Fananapazir L, et al. Prognostic determinants in hypertrophic cardiomyopathy: prospective evaluation of a
therapeutic strategy based on clinical, Holter, hemodynamic, and electrophysiological findings. Circulation.
1992;86:730.
24. Kammerling JM, et al. Characteristics of spontaneous nonsustained ventricular tachycardia poorly predict rate of
sustained ventricular tachycardia. Clin Res. 1986;34:312A.
25. Kennedy HL, et al. Long-term follow-up of asymptomatic healthy subjects with frequent and complex ventricular
ectopy. N Engl] Med. 1985;312:193.
26. Wu D, et al. Effects of atropine on induction and maintenance of atrioventricular nodal reentrant tachycardia.
Circulation. l 979;59:779.
27. Schwartz PJ, et al. Autonomic mechanisms and sudden death: new insights from the analysis of baroreceptors
reflexes in conscious dogs with and without a myocardial infarction. Circulation. 1988;78:969.
28. LaRovere MT, et al. Baroreflex sensitivity, clinical correlates and cardiovascular mortality among patients with a
first myocardial infarction: a proapective study. Circulation. 1988;78:816.
29. Sung RJ, et al. Effects of ~-adrenergic blockade on verapamil-responsive and verapamil-irresponsive sustained
ventricular tachycardias. J Clin Invest. 1988;81 :688.
30. Jouven X, et al. Long-term outcome in asymptomatic men with exercise-induced premature ventricular depolar-
izations. N Engl JMed. 2000;343:826-833.
31. Frolkis JP, et al. Frequent ventricular ectopy after exercise as a predictor ofdeath. N Engl JMed. 2003;348:781-790.
32. Verdile L, et al. Clinical significance of exercise-induced ventricular tachyarrhythmias in trained athletes without
cardiovascular abnormalities. Heart Rhythm. 2015;12:78-85.
33. Lerman BB, et al. Adenosine-sensitive ventricular tachycardia: evidence suggesting cyclic AMP-mediated trig-
gered activity. Circulation. 1986;74:270.
34. Woelfel A, et al. Reproducibility and treatment ofexercise-induced ventricular tachycardia. Am JCardiol. 1984;53:75 l .
35. Woelfel A, et al. Efficacy of verapamil in eurcise-induced ventricular tachycardia. Am J CardioL 1985;56:292.
36. Sung RJ, et al. Blectrophysiologic mechanism of exercise-induced sustained ventricular tachycardia. Am I Cardiol.
1983;5 l :525.
37. Wu D, et al Exercise-triggered paroxysmal ventricular tachycardia. Ann Intern Med. 1981;95:410.

38. Palileo EV, et al Exercise provo,able right ventri,ular outflow tnu:t tachy'ardia. Am Heart/. 1982;104:185.
39. O'Hara GE, et al. Incidence, pathophysiology and prognosis of exercise-induc:ed sustained ventri.c:ular tac:hy<:ardia
associated with healed myo~dial infarction. Am / CardioL 1992;70:875.
40. Mont L, et al Clinical and electrophysiologic characteristia of exercise-related idiopathic ventricular tac:h~dia.
AmJCardioL 1991;68:897.
41. Sokoloff NM, et al. Plasma norepinephrine in exercise-induced ventricular tachycardia. JAm Coll Cardiol. 1986;8:11.
42. Hong RA, et al. Life-threatening ventricular tachycardia and fibrillation induced by painless myocardial ischemia
during exercise testing. JAMA. 1987;257:1937.
43. Amsterdam EA, et al Exercise and sudden death. Cardiol Clin. 1987;5:337.
44. Wesley RC Jr, et al. Catecholamine-sensitive right ventricular ta.chy<:ardia in the absence of structural heart dis-
ease: a mechanism of exercise-ind~ed <:ardiK arrest. Cardiology. 1991;79:237.
45. M'Henry PL, et al. Comparative study of exercise-indu,ed ventri'ular arrhythmias in normal subje'ts and
patients with do'umented 'oronary artery disease. Am/ CardioL 1976;37:609.
46. Yang JC, et al. Ventricular ta.chy~ during routine treadmill testing. Arch Intern Med. 1991;151:349.
47. Milanes J, et al Exercise tests and ventricular tachycardia. West I Med. 1986;145:473.
48. Codini MA, et al. Clinkal significance and characteristics of exercise-induced ventricular tac:hy<:ardia. Cathet
CardioYasc Diagn. 1981;7:227.
49. Fleg JL, Lakatta EG. Prevalence and prognosis of exercise-induced nonsustained ventricular tachycardia in appar-
ently healthy volunteers. Am J CardioL l 984;54:762.
50. Busby MJ, et al Prevalence and long-term signifi'an'e of exercise-induced frequent or repetitive ventricular ecto-
pic beats in apparently healthy volunteers. I Am Coll CardioL 1989; 14: 1659.
51. Califf RM, et al. Prognostic value of ventricular arrhythmias associated with treadmill exercise testing in patients
studied with cardiac catheterization for suspected ischemic heart disease. I Am Coll CardioL 1983;2:1060.
52. Sami M, et al. Significance of exercise-induc:ed ventricular arrhythmia in stable coronary artery disease: a coronary
artery surgery study project. Am I Cardiol. l 984;54:1182.
53. Mo.kotoff DM, et al Exercise-induced ventricular tachycardia: clinical features, relation to chronic ventricular
ectopy, and prognosis. Chest. 1980;1:10.
54. Sriram CS, et al. Malignant bileaflet mitral valve prolapse syndrome in patients with otherwise idiopathic out
-of-hospital 'ardiac arrest. I Am Coll CardioL 2013;62:222-230.
55. Syed FF, et al. Sites of sua:essful ventri'ular fibrillation ablation in bileaflet mitral valve prolapse syndrome. Circ
Arrhythm Electrophysiol. 2016;9:1-ll.
56. Naccarelli GV, et al. Role of electrophysiologic testing in managing patients who have ventricular ta.chy<:ardia
unrelated to coronary artery disease. Am I CardioL 1982;50: 165.
57. Dessertenne F. La tac:hycardie ventriculaire a dewi: foyers opposes variables. Arch Mai Coeur. 1966;59:263.
58. Chorin E, et al. Female gender as independent risk factor of torsades de pointes during acquired atrioventricular
block. Heart Rhythm. 2017;14:90-95.
59. Thomas SHL, Behr ER. Pharmacologi'al treatment of acquired QT prolongation and torsades de pointes. BrI Clin
Pharmacol. 2015;81:420-427.
60. Tzivoni D, et al. Treatment of torsade de pointes with magnesium sulfate. Circulation. 1988;77:392.
61. Morris SN, Zipes DP. His bundle electro~diography during bidirectional ta.eh~. Circulation. 1973;43:32.
62. Towbin JA, et al. 2019 HRS expert consensus statement on evaluation, risk stratification, and management of
arrhythmogenic cardiomyopathy. Heart Rhythm; 2019. doi:l0.1016/j.hrthm.2019.05.007
63. Prystowsky EN. Electrophysiologic-electropharmacologic testing in patients with ventricular arrhythmias. PACE.
1988;11:225.
64. Akhtar M, et al. Wide QRS complex tachycardia: reappraisal of a common clinical problem. Ann Intern Med.
1988;109:905.
65. Hayes JJ, et al. Narrow QRS ventricular tac:hy<:ardia. Ann Intern Med. 1991;114:460.
66. Prystowsky EN, et al. Induction of ventricular tac:hy~dia during programmed electrical stimulation: analysis of
pWngmethods. Circulation. 1986;73(In:32.
67. Wellens HJJ, et al. Observations on mechanisms of ventricular tachycardia in man. Circulation. 1976;54:237.
68. Josephson ME, et al. Recurrent sustained ventricular tachy~: 1. Mechanisms. Circulation. 1978;57:431.
69. Wit AL, et al. Blectrophysiologic mapping to determine the mechanism of experimental ventricular ta.chy<:ardia
initiated by premature impulses: experimental approach and initial results demonstrating reentrant excitation. Am
I Cardiol. l 982;49:166.
70. Dillon SM, et al. Influen'e of anisotropic tissue s~e on reentrant circuits in the epi~dial border zone of
subKUte 'anine infarcts. Circ Res. 1988;63:182.
71. Rosen MR, Reder RF. Does triggered activity have a role in the genesis of cardiac arrhythmias? Ann Intern Med.
1981;94:794.
72. Al-Khatib SM, et al. 2017 AHA/ACCIHRS guideline for the management of patients with ventricular arrhythmias
and the prevention of sudden cardiac death. Heart Rhythm. 2017; doi:l0.1016/j.hrthm.2017.10.036
73. Cronin EM. 2019 HRS/EHRNAPHRS/LAHRS expert consensus statement on catheter ablation of ventricular
arrhythmias. Heart Rhythm. 2019; doi:l0.1016/j.hrthm.2019.03.002
74. Caceres J, et al. Sustained bundle branch reentry as a mechanism of clinical tachycardia. Circulation. 1989;79:256.
75. Lloyd BA, et al. Sustained ventricular tachycardia due to bundle branch reentry. Am Heart/. 1982;104:1095.
76. BeJhassen B, et al. Idiopathic recurrent sustained ventricular tachycardia responsive to verapamil: an ECG-
electrophysiologic entity. Am Heart J. 1984;108:1034.
77. German LD, et al. Ventricular tachycardia induced by atrial stimulation in patients without symptomatic cardiac
disease. Am I Cardiol. 1983;52:1202.
78. Ohe T, et al. Idiopathic sustained left ventricular tachycardia: clinical and electrophysiologic characteristics. Cin:u-
lation. 1988;77:560.
79. Kasanuki H, et al. Idiopathic sustained ventricular tachycardia responsive to verapamil: clinical electrocardio-
graphic and electrophysiologic considerations. Japan Circ J. 1986;50:109.
80. Lin FC, et al. Idiopathic paroxysmal ventricular tachycardia with a QRS pattern of right bundle branch block and
left axis deviation: a unique clinical entity with specific properties. Am J Cardiol. 1983;52:95.
81. Klein GJ, et al. Recurrent ventricular tachycardia responsive to verapamil. PACE. 1984;7:938.
82. Page RL, et al. Radiofrequency catheter ablation of idiopathic recurrent ventricular tachycardia with right bundle
branch block, left axis morphology. PACE. 1993;16:327.
83. Buxton AB, et al. Right ventricular tachycardia: clinical and electrophysiologic characteristics. Circulation.
1983;68:917.
84. Vetter VL, et al. Idiopathic recurrent sustained ventricular tachycardia in children and adolescents. Am J Cardiol.
1981;47:315.
85. Lerman BB, et al. Adenosine-sensitive ventricular tachycardia: evidence suggesting cyclic AMP-mediated trig-
gered activity. Circulation. 1986;74:270.
86. Morady F, et al. Long-term results of catheter ablation of idiopathic right ventricular tachycardia. Circulation.
1990;82:2093.
87. Klein LS, et al. Radiofrequency catheter ablation of ventricular tachycardia in patients without structural heart
disease. Cin:ulation. 1992;85:1666.
Atrial Fibrillation
Atrial fibrillation (AF) is a very common arrhythmia that has been the subject of an enormous
amount of research into its mechanism and treatment over the past 20 years. Nonetheless, treat-
ment decisions can be nuanced and complicated regarding whom to treat and how to treat with
choices of pharmacologic versus nonpharmacologic therapies. This new chapter has been added to
our second edition that will explore these areas leaving ablation of AF to be detailed in Chapter 17.
CLASSIFICATION
AF is characterized by rapid, typically more than 400/min., disorganized atrial activation that
varies both spatially and temporally. On the surface electrogram this can appear as a wavy base-
line without any distinct P waves (Figure 9-IA) or as a tracing that at times gives the appear-
ance of a flutterlike rhythm (Figure 9-18). However, true atrial flutter has an atrial rate like a
metronome with clocklike regularity. and careful measurement of the flutterlike appearance in
the AF tracing shows the atrial rate is irregular. With rare exception ofdissociated atria, AF and
true atrial flutter do not coexist. The ventricular rate is usually irregularly irregular unless the
patient has heart block.
A widely accepted classification follows: 1·J

Paroxysmal-Self-terminating episodes usually lasting less than 12-24 hours but up to 7 days;
Persistent-episodes lasting more than 7 days and often requiring pharmacologic or electrical
cardioversion;
Long-standing persistent-continuous AF for at least a year;
Permanent-AF that could not be c.ardioverted into sinus rhythm or a decision made by the
patient and phf5ician not to pursue sinus rhythm as a treatment option.
This classification system has problems since many patients have had episodes of both par-
oxysmal and persistent AF. In such cases, we tend to characterize patients by their dominant
presentation. So, for patients who typically have self-terminating ep:lsodes but over the years
have had an occasional cardioversion, we would designate them as paroxysmal. Further, the use
of' paroxysmal as a monolithic category is likely too simplistic. Some patients almost never have
episodes lasing more than 6-12 hours, while others often have them for days. It is possible that
triggers and substrate mechanisms differ between such patients.
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FIGURE ~1 • ECG rhythm strips of atrial fibrillation. Panel A, minimal ifany atrial activity noted; Panel a, coarse
atriaI actlvtty at times with a ftuttertlke appearance. (See text for detalls.l
EPIDEMIOLOGY
AF is estimated to affect up to 5 million Americans and 4.5 million Europeans.14 Its incidence
and prevalence increase with age. Approximately 1% of the population less than 60 years of age
has AF, but more than one-third of AF patients are at least 80 years old. A family history of AF is
not uncommon, but its significance is not clear if the onset of AF in the parent was in their 70s
or older. However, there are data on genetic abnormalities in AF.5.6 The actual prevalence of AF
is likely much. more than reported in large epidemiological studies because many patients have
"silent" AF and are not included in such studies. Examples are patients where AF is detected on
pacemaker or defibrillator interrogations that show intracardiac electrogram recordings of AF,
and on long-term electrocardiographic (ECG) monitoring done for other purposes.
ETIOLOGY
A primary etiology is not clear in most patients with AF. One should always investigate for a
potentially reversible problem such as hyperthyroidism or binge drinking. In some patients,
typically younger ones, AF may be caused by another arrhythmia (tachycardia-induced tacliy-
cardia), and cure of the primary arrhythmia may lead to no recurrence of AF (Figure 9-2).1-7
Typically, there are predisposing factors present such as hypertension, heart failure, coronary
disease, and valvular disease, and modifiable risk factors such as obesity and obstructive sleep
CHAPTER 9 • Atrial Fibrillation 215
11QO
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FIGURE •2 • AV reentry (AVRT) degenerating Into atria! flbrlllatlon. AVFIT with retrograde conduction over a
left-sided accessory pathway Is noted In the tlrst S QRS complexes but then atria! fibrillation Is Initiated as can
be seen by the disorganized atrial activity, best noted In the high right atria! (HRA) electrogram. Simultaneous
recordings for ECG leads~ II, Ill, Vl, V2, and V6; and electro grams from the HRA. His bundle (HBE), proximal (PCS),
mid (MCS) and distal coronary sinus (IXS), and right ventride (RV).
apnea.1•3 Atrial dilatation detected by echocardiography may be accompanied by changes in

atrial conduction and refractoriness. 1 There are also patterns implicating the autonomic ner-
vous system, fur example, onset predominantly with eurcise (sympathetic), or during sleep or
postprandial (parasympathetic). Yet, correlation does not equal causation. How these diverse
abnormalities interplay with genetic predisposition to allow the emergence of AF in an individ-
ual remains to be elucidated.
MECHANISM
The mechanism of AF is related to anatomic and electrophysiologic abnormalities in the atria,
and extrinsic influences such as the autonomic nervous system.1•3 It is useful to consider AF
triggers and maintenance separately. accepting some overlap.
AFTriggers
In 1948 Scherf et al.8 proposed an ectopic focus theory for AF. This received almost no atten-
tion fur decades, supplanted by the reentry mechanism of Moe et al.9 Development of both
pharmacologic and nonpharmacologic treatments typically targeted reentrant mechanisms, for
example, the maze surgical procedure and the early catheter ablation techniques. However, the
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FIGURE t-3 • Initiation of AF by rapid flrfng In a pulmonary vein {PV). A premature atriaI complex (PAC) fol-
lowed by rapid ectopy from the fll/ Initiates AFlb. The cattleter recording the fll/ ectopy Is positioned In the fll/.
(Reproduced with perml.sslon from Pry.stowsky EN, Halperln J, Kowey P. AtTlal fibrlllatfon, Atrlal flutter and atrlal
tachycardia. In: Fusts V, Willsh RA. Harrington RA. eds. Hurst:'s the Heart. 14th ed. New York: McGraw-Hill; 2017.)
key observation of Haissague.rre et al10 that pulmonary veins {PV) can serve as triggers for AF
(Figure 9-3) and isolation ofPVscan prevent AP changed the paradigm. AF can even continue
to occur in a PV after it has been isolated from the left atrium (Figure 9-4). Triggers can also
arise from the superior vena cava, ligament ofMarshall, musculature of the coronary sinus, left
atrial appendage and right atrium, as well as less common sites. 1•3.i•
AF Maintenance: Substrate
Persistent AF is considered by many to be facilitated by atrial substrate changes that allow the
perpetuation of the arrhythmia. Observations in animal models and humans in long-standing
AF include loss of myofibrils with increase in interstitial fibrosis, disruption of cell-to-cell gap
junctions, and enlargement of the atria.1 Such anatomic and electrophysiologic alterations of
conduction and refractoriness may lead to reentry as proposed by Moe,9 or possibly rotors or
spiral wave reentry.1 It is known that "AF begets AF," and the longer a patient is in AF, the less
likely that sinus rhythm can be restored and maintained. While triggers may have started this
journey to permanent AF, atrial structural changes sealed the deal
In summary. it is too simplistic to dichotomize AF into a problem of triggers or substrate, and

better to consider both possibilities in any given patient
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Isolated from the LA. Note the continuation of rapid ectopy In the PV but sinus rhythm In the pattent. (Reproduced with permission
from Prystowsky EN, Halperin J, Kowey P. Atria Iflbrlllation, Atrial flutter and atrial tachycardia. In: Fuster V, Walsh RA. Harrington RA.
eds. HutJt's the Heart. 14th ed. New York: McG~il~ 2017.)
CLINICAL PRESENTATION
Symptoms are many and variable and may relate to the arrhythmia itself or some of its severe
consequences, for example, stroke and heart failure. Common symptoms are palpitations, dys·
pnea. and fatigue, or none at all. Lightheadedness, syncope, and chest pain are less common
presentations. Patients often do not relate to the terms health care personnel utilize. They may
deny palpitations, but then tell you they feel a funny sensation in their chest like fish fiopping
around; dyspnea is not a term they use. so ask about shortness of breath. Often the symptoms
are vague such as "not feeling right"' or "cloudy thinking:" So, it is important to be thorough in
the history taking and allow patients to tell their story using their terms before concluding what
they are experiencing. It is not uncommon for patients with long-standing .AF to state they have
no problems, only to feel much better when sinus rhythm is restored.
Stroke is the most common thromboembolic event associated with .AF and is discussed later
in the chapter.1 Patients may present with heart failure symptoms resulting from a tachycardia·
induced cardiomyopathy.1-:),1z.15 The LV dysfunction develops as a result of rapid ventricular
rates over time, often months, and typically the patients' other symptoms are minimal. The lac.k.
of symptoms before heart failure likely explains why these patients do not seek medical atten-
tion earlier and is a good historical point in differentiating AF as the cause and not result of
heart failure. It is known that reduced LV function can occur even without prolonged periods of
rapid ventricular rates, possibly due to the negative hemodynamic consequences ofloss of atrial
contractility and variability in ventricular cycle length. In our experience, absence of delayed
enhancement on cardiac magnetic resonance imaging predicts a likely return of normal or near
normal LV function after rate control and restoration of sinus rhythm.
Several studies reported that AF is associated with a substantial reduction in quality oflife.1•1"' 15
Two studies evaluated the outcomes of catheter ablation and antiarrhythmic drugs on quality of
life in patients with AF.16.17 In CABANA, 16 patients receiving antiarrhythmic drugs or catheter
ablation had clinically important improvements in AF symptoms. However, catheter ablation
compared with drugs provided incremental quality of life benefits and symptomatic benefits.
In CAPTAF,'7 catheter ablation demonstrated greater improvement in quality of life compared
with antiarrhythmic agents. These newer observations from prospective randomized trials
should be considered when deciding on therapeutic options for patients.
PATIENT EVALUATION
The workup begins with a thorough history. The onset and time course of AF should be
noted, as well as the frequency and duration of episodes, whether cardioversion was needed,
and whether the pattern of AF changed over time. Determine whether there are any potential
reversible causes, for example, hyperthyroidism or alcohol abuse, and if symptoms of obstruc-
tive sleep apnea are present. Review what drugs the patient has received and at what doses,
and their effectiveness and side effects. Calculate the stroke risk score using the CHADS-VASc
system (Figure 9-5) to help decide the need for anticoagulation.
The physical examination is typically not very helpful. One may detect a cardiac murmur that
reveals a valvular etiology, but this is uncommon. Signs of atherosclerosis may be useful. On
the other hand, the echocardiogram is very important with special attention to atrial size and
left ventricular ejection fraction, size, and thickness. Right ventricular enlargement may lead to
A. Score B. Score
CHADS:z acronym CHA2DSz-VASc acronym
Congestive heart failure Congestive heart failure/LV dysfunction
Hypertension Hypertension 1
Aged ;i:75 years Aged ;i:75 years 2
Diabetes mellitus Diabetes mellitus
Stroke/TINTE 2 Stroke/TINTE 2
Maximum score 6 Vascular disease (previous Ml,
PAD, or aortic plaque)
Aged 65-74 years
Sex category (ie, female sex) 1
Maximum score 9
FIGURE 9·5 • Risk score using the CHAOS, (A) or CHA,DS,-VASc (B) scoring systems. (See text for details.)
...........................
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FIGURE 9-6 • Wearable event recorder showing the onset of AF.
the diagnosis of possible pulmonary problems. The ECG is also a valuable test and part of the
workup. Laboratory data include electrolytes and complete blood count. A chest radiograph
should be done if there is suspicion of pulmonary disease.
Short- and long-term wearable ECG monitors are invaluable in the workup and management
of AF. Many patients have asymptomatic episodes of AF and use of mobile outpatient cardiac
telemetry with 2417 recording capability can record the time and duration of symptomatic and
asymptomatic episodes that determine the patient's AF burden (Figure 9-6). Not infrequently
more than 1 arrhythmia is present, for example, AF and premature ventricular complexes, and
correlation of symptoms with the rhythm will allow the clinician to direct therapy accordingly.
In patients with very infrequent symptoms but in whom AF is suspected or has been recorded
in the past, an implantable loop recorder can provide valuable information (Figure 9-7). The
place of consumer purchased wearables, for enmple, wrist watches, remains to be determined.
AF Eplsodll 11
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1500
1200
900
600
200
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Panel A
FIGURE 9-7 • Initiation of AF captured by an Implanted loop recorder In a patient with very Infrequent episodes. Panel A.. The Ar-
is graphically depicted. Panel 8. The electrograms from the recording verify AF as the arrhythmia.
AF Epleode #'I
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Panel B
FIGURE~7 • (Conttnued}
TREATMENT
Management of AF can be discussed under 3 major areas not mutually exclusive (Figure 9-8).H
Whenever possible, eliminate potentially reversible causes, for example, hyperthyroidism. Pre-
vention of stroke resulting from thromboembolism from the left atrium, mostly from the left
atrial appendage (LAA), is a prime directive in the AF patient at risk for stroke. Rhythm con-
trol strives to maintain sinus rhythm by pharmac:ologic or nonpharmacologic means, typically
catheter ablation. Rate control is used to prevent rapid ventricular responses during AF that
can be quite symptomatic and ifleft unchecked for long time periods can result in tachycardia-
mediated cardiomyopathy. These 3 areas are discussed separately below, but 2 or 3 of them are
routinely involved in many patients.
Stroke Prevention
Not all patients with nonvalvular AF have the same stroke risk. and many &ctors have been
evaluated to identify those who need anticoagulation therapy. Anticoagulation strategies are
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FIGURE 9-1 • Schematic of treatment strategies in the management of AF. (See text for details.)
the same for patients who have atrial flutter. In the ACC/AHA/ESC 2006 AF management guide-
lines, the CHADS2 system was used to classify stroke risk (Figure 9-5).1*This is an acronym for
congestive heart failllle (C); hypertension (H); age 75 or greater (A); diabetes mellitus (D); and
prior stroke or TIA (S2), which was given 2 points. The adjusted stroke rate per 100 patient-years
was 2.8, 4.0. 5.9. 8.5,12.5, and 18.2 for a score of 1, 2, 3, 4, 5, and 6, respectively.1 Anticoagulation
was recommended for a score of 1 or more. However, the predictive accuracy of this system is
not very good with a c-statistic 0.570.19
In an effort to improve the accuracy ofthe risk stratification schema, additional factors were added
including v.iscular disease (V). age 65-74 years (A). and female gender (sex category; S). Thus
was born the CHA2DS2-VASc system, with a 1Dtal of 9 possible pointsP Anticoagulation was
recommended for a score of 2 or above. Yet the predictability of this system is only slightly better,
with a c-statistic 0.578.1 Obviously there are other factors important in the development ofan LAA
thrombus that require more study, possibly the LA scar burden or morphology of the LAA.
The 2019 AHA/ACC/HRS Focused update on AF management clarifies the definition of val-
vular AF to mean moderate-to-severe mitral stenosis or a mechanical heart valve.20 The type
of AF, that is, paroxysmal or persistent, has no bearing on the anticoagulation decision. Female
gender is no longer a separate risk factor, but instead of changing the acronym, it now states as
a Class I recommendation that oral anticoagulation be given with a CHA2DS2-VASc score of
~ in men and ~3 in women.20 In nonvalvular AF, it is reasonable to omit anticoagulation with
a score of 0 in men and 1 in women (Class Ila indication); and for a score of 1 in men and 2 in
women, oral anticoagulation may be considered (Class lib).
Direct-acting
Apixaban Factor Xa inhibitor • 5mg bid
• 2.5 mg bid with ~2 of the following: ~80 yrs;
serum creatinlne ~1.5 mg/dl; bodyweight ~60 kg
Rivaroxaban Factor Xa inhibitor • 20 mg once/day
• 15 mg once/day with CrCI 15-50 mLJmin
Edoxaban Factor Xa inhibitor • 60 mg once/day
• Should not be used with CrCI >95 mUmin
Dabigatran etexilate Thrombin inhibitor • 150mg bid
Warhlrin Vitamin K antagonist • 2-1O mg/day
• Dose adjusted to keep INR 2-3
Figure 9-8 shows pharmacologic options that include one of the direct-acting oral anticoagu-
lants (DOAC) that target specific clotting factors: dabigatran (direct inhibition of thrombin);
apixaban, rivaroxaban, and edoxaban (factor Xa inhibitors); or use of warfarin (Table 9-1).
Warfarin is required in valvular AF. In nonvalvular AF, a DOAC is preferred over warfarin
when acceptable to use, for they are renal-dosed (Class I recommendation). 20 This is not sur-
prising because they are much easier to use by the patient, have a noninferior or superior effi-
cacy against stroke, and the rates of major bleeding are comparable to or lower than those for
warfarin. 1
An alternative to oral anticoagulants is a percutaneous closure device introduced into the

LAA.21 Thus far, it appears comparable for stroke reduction with warfarin, but trials are lacking
comparing it with DOACs. The 2019 guidelines state that these devices may be considered in
those patients with increased stroke risk who have contraindications to long-term anticoagu-
lation (Class Ilb recommendation). We often recommend surgical exclusion of the LAA at the
time of cardiac surgery in patients with a known history of AF. It is important that the surgeon
check, typically using transesophageal echocardiogram (TEE), to be sure that there is no LA-
LAA continuity, which can lead to clot formation and stroke later. The 2019 guidelines give this
a Class Uh recommendation.20
RATE VERSUS RHYTHM STRATEGIES

The two principal treatment strategies for patients with AF are controlling the ventricular rate
when AF occurs but making no attempt to restore and maintain sinus rhythm (rate control),
or as a main goal to keep the patient in sinus rhythm (rhythm control) (Figure 9-8). Even if
a rhythm control strategy is chosen, it still is important to control the heart rate if AF recurs,
so the treatment plans can have overlap. The decision to choose a primary treatment strategy
is multifactorial and should be individualized for each patient. Rhythm control is clearly indi-
cated when the patient is still quite symptomatic even with good rate control. Likewise, rate
control might be preferred in elderly patients who are asymptomatic in AF. It is important to
remember that anatomic and electrophysiologic changes in the atria with persistence of AF for
years may make it difficult if not impossible to restore and maintain sinus rhythm.1 Thus, in a
patient with minimal symptoms now but who may need sinus rhythm in the future, for exam-
ple, with ventricular hypertrophy that could worsen over time, a rhythm control strategy may
be preferred. Let's examine some studies that compare these treatment approaches.
The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial

enrolled 4060 patients with a mean age of 69.7 years who were randomized to rate or rhythm
control.22 Patients had to be at least 65 years old or have other risk factors for stroke or death.
Mean follow-up was 3.5 years and over two-thirds of the rhythm control group received either
amiodarone or sotalol. There was no significant overall mortality difference between the
2groups.
The Rate Control versus Electrical Cardioversion for Persistent Atrial Fibrillation (RACE) trial
randomly assigned 522 patients after cardioversion to rate or rhythm control therapies.23 Mean
age was 68 years with a mean follow-up of2.3 years. The primary endpoint was a composite of
cardiovascular death, heart failure, thromboemboli, bleeding, need for a pacemaker, or serious
drug side effects, and did not differ between treatment groups.
A meta-analysis of 10 studies that compared rate control with rhythm control using antiar-
rhythmic drugs demonstrated no difference in any clinical outcomes.24 An exploratory analysis
in patients younger than age 65 years showed an advantage in the prevention of all-cause mor-
tality for rhythm control.
AF is often a lifelong illness, yet the follow-up in AFFIRM and RACE was less than 4 years.
Caution should be used extending the results to longer durations of follow-up, as well as to
younger patients who were not represented in the trials. In fact, using a large population-based
database of patients (not a randomized prospective trial) given rate or rhythm control drugs,
the crude rates for mortality after 5 years of follow-up were 41.7% in the rhythm control group
and 46.3% in the rate control group.25 No difference was apparent in mortality during the first
4 years, but in those who survived 5 or more years mortality was statistically lower in the
rhythm control group.
While stroke has been studied in detail in patients with AF, other important neurologic conse-
quences have not received the same attention.26 Findings from a prospective database of about
37,000 patients concluded that AF was independently associated with senile, vascular, and
Alzheimer's dementia.27 Cognitive function and the prevalence of silent cerebral ischemia was
evaluated in control subjects and in those who had paroxysmal and persistent AF.28 Cognitive
performance was significantly worse in persistent and paroxysmal AF compared with controls,
and silent cerebral ischemia was also more prevalent. A meta-analysis of 14 studies concluded
that AF was significantly associated with the risk ofthe development of cognitive impairment.29
In summary, before deciding on a particular treatment strategy, the health care provider should
have a thorough discussion with the patient of the rate and rhythm therapeutic pathways and
be sure to tell them that years of AF may prevent sinus rhythm in the future. Some patients
with minimal symptoms may choose sinus rhythm as a "bridge to the future."u Further, the
health care provider should be flexible and willing to modify the strategy if the clinical situation
changes.
RHYTHM CONTROL
When a rhythm control strategy is chosen, either an antiarrhythrnic drug or nonpharmacologic
therapy, typically catheter ablation, is required to maintain sinus rhythm. Ideally, elimination
of all AF episodes would be the therapeutic goal, but this is hard to achieve, even with catheter
ablation. A more realistic goal for many patients is a marked reduction of the duration, fre-
quency, and symptoms of AF that allow a much better quality of life. Importantly, the need for
continued anticoagulation is based on stroke risk and not an apparent clinical resolution of AF.
The treatment algorithm in Figure 9-8 gives equal weight to antiarrhythrnic drugs and catheter
ablation as potential first-line therapies, which is the authors' opinion. This assumes that the
electrophysiologist has appropriate training in AF ablation and does enough volume per year to
maintain these skills. Many studies have demonstrated catheter ablation to have superior effi-
cacy over drugs regarding recurrence of AF. 13 The Catheter Ablation vs Antiarrhythmic Drug
Therapy for Atrial Fibrillation (CABANA) trial was a randomized study that included 2204
patients aged 65 years or more or younger than 65 years with 1 or more risk factors for stroke.30
The primary end point was a composite of death, disabling stroke, serious bleeding, or cardiac
arrest. The median follow-up was 48.5 months. The intention-to-treat analysis showed the pri-
mary end point occurred in 8% vs 9.2% of patients in the ablation vs drug group, which did not
reach statistical significance. As anticipated, AF recurrence was statistically less in the ablation
group. Thus, CABANA demonstrated superior efficacy regarding recurrence in AF and no dif-
ference in major safety outcomes, lifting ablation in our opinion to a first-line treatment option
in patients who are good candidates for it and do not want to pursue antiarrhythrnic drugs.
Catheter ablation is discussed in Chapter 17.
Amiodarone is the most effective drug to maintain sinus rhythm in patients with AF, but has
protean toxicity including pulmonary fibrosis. 1- 3 To minimize toxicity in using antiarrhythmic
drugs, the choice of a particular agent is mostly determined by its potential side effects in an
individual patient rather than presumed efficacy (Figure 9-8). 1·3.31 In fact, other than amiodar-
one, the efficacy of most of the other agents is not that different. For most patients, a specific
etiologic factor for AF initiation is not apparent, an exception being the occasional patient with
exercise-only AF, where beta blocker therapy seems most reasonable. So, as shown in Figure 9-8,
the drugs are listed in alphabetical order, not by presumed efficacy. Table 9-2 gives details on
dosing and some key side effects of the drugs.
In patients with no structural heart disease, initial drug choices have minimal noncardiac tox-
icity, and include dofetilide, dronedarone, flecainide, propafenone, and sotalol; amiodrone is
a second-line alternative. This does not mean one needs to try all the first-line drugs before
switching to amiodarone, but an attempt to use ones with different mechanisms such as flecain-
ide vs sotalol seems reasonable when possible. Safety of drugs in patients with coronary artery
disease has been shown for dofetilide, dronedarone, sotalol, and amiodarone (second-line).
For heart failure, both dofetilide and amiodarone are first-line choices, but in our experience
amiodarone is often preferred. Many patients with hypertension do not have significant ven-
tricular hypertrophy and should be considered in the no structural heart group regarding drug
selection. However, when substantial left ventricular hypertrophy (wall thickness> 1.5 cm) from
any etiology is present, there is an increased risk of ventricular proarrhythmia with most drugs,
and amiodarone appears to have the best safety profile in this group. Drugs such as quinidine,
Flecainide 50-200mg Every 12 h Sinus node or AV node dysfunction

Atrial flutter with 1:1 ventricular response
Propafenone 150-300 mg (immediate release) EveryB h Sinus node or AV node dysfunction
225-425 mg (extended release) Every 12 h Atrial flutter with 1:1 ventrlcular response
Amlodarone Loading dose: 400-600 mg/d For4wk Sinus node or AV node dysfunction
Maintenance dose: 200-300 mg Daily Lung, liver, or thyroid toxicity
Prolonged QT interval (torsade de pointes
ventricular tachycardia rare)
Dofetilide• 125-500 µg Every 12 h Prolonged QT interval with torsade de pointes
ventrlcular tachycardia
Dronedarone 400mg Every 12 h Sinus node or AV node dysfunction
Prolonged QT interval (torsade de pointes
ventricular tachycardia rare)
Sotalol.,. 40-160mg Every 12 h Sinus node or AV node dysfunction
Prolonged QT Interval with torsade de polntes
ventricular tachycardia
•Dosing based on renal fi.inction.

••Dosing may be~ 24 hourJ with renal dysfi.inction.
AV. atrioventrtcular.
procainamide, and disopyramide are rarely used in clinical practice, although some of us con-
tinue to use disopyramide in selected patients who cannot tolerate the other first-line agents.
The clinician should be aware of some specific safety issues with the use of antiarrhythmic
drugs. Dofetilide and sotalol can substantially prolong the QT interval and need to be used
with caution or not at all in patients at risk for torsade de pointes (TdP) ventricular tachycardia.
Patients should be given instructions to check with the pharmacist or physician before taking
any over-the-counter or prescription drugs to avoid a drug-drug interaction that could cause
TdP. Amiodarone and dofetilide can also increase the QT interval but the risk of TdP is very
low. Propafenone and tlecainide may alter the atrial electrophysiologic properties during AF
resulting in atrial flutter, which if slow enough could lead to 1:1 atrioventricular conduction
with a rapid ventricular response and possible syncope or cardiac arrest. To minimize this from
happening, a beta blocker, verapamil, or diltiazem should be prescribed along with these agents.
When using amiodarone, periodic safety surveillance is recommended. Some of us routinely
evaluate liver and thyroid function as well as obtaining a chest radiograph every 6 months.
There are few studies on the safety of outpatient initiation of most antiarrhythmic drugs, with
the possible exception of amiodarone. Yet, hospital admission solely for the purpose of moni-
toring drug safety and efficacy is costly and very inconvenient to most patients. If there is any
question of safety, the agent should be started in-hospital. Dofetilide requires in-hospital ini-
tiation, but for the other drugs we offer some general guidelines for outpatient drug initiation.
Flecainide and propafenone can be given to patients in sinus rhythm without heart disease
maximizing safety by prescribing an AV nodal blocker first; start with a lower dose and obtain
an ECG several days after each dose titration. Sotalol may be administered to patients in sinus
rhythm with no or minimal heart disease who have a normal QT interval and electrolyte status.
Begin with a lower dose and uptitrate as needed obtaining an ECG within a few days of each
new dose. Amiodarone and dronedarone may be started in sinus rhythm or AF. Amiodarone
typically is given at a loading dose of 400 to 600 mg daily for about a month, and we often
get periodic ECG recordings either by an ECG in the office or an event recorder given to the
patient for the loading period to check for any potential bradycardia (not uncommon) or tachy-
cardia (relatively rare) proarrhythmia.
RATE CONTROL
Controlling the ventricular rate during AF is important to the patient not only for symptom
relief but to prevent a tachycardia-mediated cardiomyopathy.1- 3 This is true whether the pri-
mary treatment strategy is rhythm or rate control. Pharmacologic as well as nonpharmacologic
methods are available to accomplish this goal (Figure 9-8; Table 9-3). Intravenous drugs may
be the best initial approach for very symptomatic patients with rapid ventricular rates who are
not in hemodynamic distress requiring cardioversion (Table 9-3). However, most patients can
be started as an outpatient with an oral agent to achieve adequate rate control with uptitration
of the dose as needed. Unfortunately, there is no overall agreement on what defines optimum
rate control.32 One suggestion is 60-80 per minute at rest and between 90 and 115 per minute
with exercise. 3 Further, methods to evaluate rate control vary widely including follow-up ECGs,
exercise testing, Holter monitors, and combinations ofthem. 32 Our approach takes into account
jS-Adrenergic Blockers
Atenolol 25-100mg/d
Blsoprolol 2.5-10.0 mg/d
Carvedilol 3.125-25 mg (bid)
Metoprolol succinate 5<>-400 mg/d (may be bid)
Metoprolol tartrate 25-100 mg (bid)
Nadolol 10-240mg/d
Propranolol 1<>-40 mg (3 or 4 times/day)
Calcium Channel Antagonists
Digoxin 0.125-0.250 mg/d
Diltiazem' 120-360 mg/d
Verapamll1 120-480 mg/d
Intravenous Agents
Digoxin2 0.25 mg initial
Diltiazem• 0.25 mg/kg
Esmolol• 500µg/kg
Verapamll 5 0.075-0.150 mg/kg
'Can use divided doses and extended-te/ease forms.

'Additional doses a/lo~ but 1.5 mg maximum within 24-hour period.
'Bolus over2 minutes; dose ronge: 5 to 15 mg per hour.
•Bo/us over 1min.; then 50 to 300 µg/kg/mln.
'Bolus over2 min.; ifno response. an additional 10 mg afttr 30 minutes and then a 0.005 mgllcglmin infusion.
Control
HRTrend Chart- HR Min: 13 at 05:15, HR Max: 182 at07:15
200
50
0 02:00 04:00 08:00 08:00 10:00 12:00 14:00 16:00 18:00 20:00 22:00
Panel A
Meroprolol XL 50 mg/day
HR Trend Chart - HR Min: 43 at 03:45, HR Max: 147at18:15
150
100
50
0
02:00 04:00 06:00 08:00 10:00 12:00 14:00 16:00 18:00 20:00 22:00
PanelB
FIGURE 9-9 • Use of mobile continuous outpatient telemetry to adjudicate rate control in patient with AF. (See text f'or dmils.}
the importance of controlling heart rate for each patient during their own daily activities/1
while attempting as best as possible to •mimic• the heart rates during the day ifthe person was
in sinus rhythm. Using mobile cardiac monitoring. the patient's 24-hour heart rate trends are
sent to the office daily. and adjustments in medications are done to achieve adequate rate con-
trol An example ofthis is shown in Figure 9-9. In the control state, the mean heart rate during
the day is often over 100/minute, and the variations in rate are quite wide. We often find that
wide swings in heart rate are quite symptomatic. Long-action metoprolol was given and the
heart rate over the next couple ofdays was well-controlled and the variations in rate were much
less. Some patients require multiple dose changes and additional agents to achieve rate control
When large doses ofa drug are needed to control rate, but then cause significant side effects, it
may be better to use 2 different agents at moderate doses to achieve rate control with minimal
side effects, for example. a beta blocker and calcium channel bloclctr.
Selecting the initial oral agent to manage rate control often is physician or patient preference, but
there are some general issues to consider.2 In patients with heart failure and depressed ventricu-
lar function, a beta blocker is preferred over verapamil or diltiazem. However, younger patients
and those who are very active often cannot tolerate beta blockers. Calcium channel blockers are
favored in patients with asthma and chronic obstructive pulmonary disease, but when possible
should be avoided in heart failure with a reduced ejection fraction due to their negative inotropic
effects. In older patients, problems with leg edema and constipation may limit their use. Digitalis
may be useful in patients with heart failure and ventricular dysfunction. However, there are data
suggesting an increased mortality in patients with AF receiving digoxin compared with those
not taking it.u and so we advise caution using this drug when other options are available.
AV junctional. ablation to create heart block with insertion of a permanent pacemaker is an

effective rate-control strategy for selected patients (Figure 9-8).H An example ofthis is demon-
strated in Figure 9-10. The patient had troubling symptoms in the presence of ma:ximally tol-
erated AV nodal blockers, had failed drugs to maintain sinus rhythm. and was not a candidate
for catheter ablation (Figure 9-IOA); after AV junctional ablation (Figure 9-lOB) the patient
remained in AF but the rate was regular and controlled and symptoms resolved. However, this
approach creates a new disease, complete heart block, which has important consequences.
Patients may become pacemaker-dependent without an adequate escape rhythm. The constant
Patient 1: No Pacing
I ' I I .
Panel A
Patient 2: Permanent Pacing
1' f j' j' r

I
f
.. I
PlnelB
FIGURE 9-10 • AVjunction;ll abliltion with pacem;iker implant to control ventTicul;ir rate during Ar-. Panel A i5
before ablation and Panel 8 after ablation. (See text f'Or de1ails.}
right ventricular pacing produces an abnormal left ventricular activation and contraction
sequence, and some patients develop a pacing-induced cardiomyopathy.J.S& When the latter
occurs, an upgrade to a biventricular pacing system typically improves left ventricular func-
tion. The use of His bundle padngin such situations is not well-studied but seems reasonable.
In summary, rate control with drugs should be the therapy of choice over AV junctional abla-
tion. While the latter can lead to an excellent outcome regarding symptom control. it has sub-
stantial downside risk over time. Fwther, it does not change the need for anticoagulation that
is based on the patient's risk of stroke.
BRADYCARDIA-TACHYCARDIA SYNDROME
The bradycardia-tachycardia syndrome (BTS) describes patients with AF who have periods
of very slow and fast rates, both of which can be quite symptomatic. One variety may occur
in a patient who does not have marked sinus bradycardia, but who has long and symptomatic
pauses after termination of AF (Figure 9-11). This patient presented with near syncope due to
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N-7
FIGURE 9-11 • Bradycardia-tachycardia syndrome in a patient with long symptomatic pauses after termination of Ar-. {See text f'or
details.) The episode shown occurted during sleep without symptoms.
the pause but had no symptoms during AF, and was diagnosed with extended outpatient mon-
itoring (see Chapter 10). The post-conversion pause is due to overdrive suppression of sinus
node automaticity; and antiarrhythmic drugs to maintain sinus rhythm likd.y will increase the
duration of the pause if AF recurs. Thus, to ensure safety; either a pacemaker is implanted
before starting antiarrhythmic agents, or catheter ablation is given with the hope AF does not
recur, but at least the pause will not get worse.
Another type of BTS is shown in Figure 9-12. This patient had marked sinus bradycardia
that surprisingly was minimally symptomatic (Figure 9-12, upper panel). However, the rapid
ventricular rates during AF were very symptomatic (Figure 9-12, bottom panel). Ifa rate con-
trol strategy is selected, the sinus rate would likely be slower and symptomatic. One possible
choice for rhythm control is dofetilide that has few effects on sinus rate in OW' experience. A
better approach would be to consider catheter ablation to minimize AP recurrences in a can-
didate for ablation, but insertion ofa pacemaker with subsequent drug therapy is a reasonable
alternative.
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P-48
FIGURE,.., 2 • Bradycan:lla-tachytardla syndn>me In a patient with marked sinus bradycardla and rapid ventrlcular responses
during Ar-. (See text for detallsJ
CARDIOVERSION
Cardioversion is used to restore sinus rhythm by electrical or pharmacological. means. Appro-
priate anticoagulation is required to minimiu stroke risk regardless of the method of cardio-
version, and the niles are the same for AF and atrial flutter (AFl).20
1. For patients in whom the duration of AF or AFl is :<?48 hours or unknown, administration
of warfarin with an lNR of 2 to 3, a direct thrombin inhibitor, or a factor Xa inhibitor for at
least 3 weeks before and at least 4 weeks after cardioversion is recommended regardless of
the CHA2DS2-VASc score (Class I). Continuation of anticoagulation after 4 weeks depends
on a patient's stroke risk as noted earlier in the chapter.
2. For patients with AF or AFl <48 houri duration who have a CHA2DS2-VASc score of~2 in
men and ~3 in women, administration of heparin, a factor Xa inhibitor, or a direct thrombin
inhibitor is reasonable as soon as possible before the cardioversion with long-term anticoag-
ulation post cardioversion (Class lla).
3. For patients with AF or AFI <48 hours' duration who have a CHA2DS2-VASc score of 0 in
men and 1 in women, administration of heparin, a factor Xa inhibitor, a direct thrombin
inhibitor or no anticoagulation at all may be considered before cardioversion, without post
cardioversion anticoagulation (Class lib).
An alternative strategy is the use of transesophageal echocardiography (TEE) to evaluate for LA

thrombi before cardioversion in patients who require adequate anticoagulation but who have
not had it for the 3 weeks as needed (Figure 9-13).35 H no LA thrombus is seen on TEE and
anticoagulation is achieved before TEE is done, cardioversion may proceed with at least 4 weeks
of anticoagulation after cardioversion (Class Ila).2G
Direct current cardioversion requires a shock synchronized to the QRS complex to be given
through electrode pads on the chest. The adhesive gel pads are usually placed posteriorly just
FIGURE t-13 • Thrombus In the leftatrlal appendage shown bytransesophageal echocardlography.

left to the spine and anteriorly over the stemurn.36 If sinus rhythm is not restored, an alternative
patch placement should be considered, for example, anterior-lateral. Biphasic waveforms are
preferred37 with adequate anesthesia so the patient does not feel the pain of the shock. We prefer
an initial shock of 200 Jfor its efficacy, but there is a theoretical additional advantage since the
higher energy is more likely to be above the lower limit of vulnerability to induce ventricular
fibrillation if the shock falls on the T wave. 1
Pharmacologic cardioversion is less effective than direct current cardioversion.3 Successful

cardioversion depends on the duration of AF, being substantial with AF <1 week using oral
propafenone, flecainide, dofetilide, or intravenous ibutilide.1•3 A single dose of propafenone
600 mg or flecainide 300 mg is often used. For longer duration AF, even for months, dofetilide
has a reasonable chance to restore sinus rhythm. 38 For patients with very infrequent episodes
of persistent AF who do not want to take an antiarrhythmic drug daily, an alternative approach
is "pill-in-the-pocket." These patients self-administer either propafenone or flecainide for out-
patient conversion after safety of the approach has been demonstrated during observation in
hospital.39 An AV nodal blocking agent should be administered concomitantly to minimize the
chance of 1:1 ventricular conduction if drug conversion of AF to atrial flutter occurs.I In our
experience, very few patients are candidates for such an approach.
POSTOPERATIVE ATRIAL FIBRILLATION

Approximately one-third of patients after open-heart surgery have AF.4{) Anticoagulation should
be considered despite the increased risk of bleeding to reduce stroke risk. i,40 Beta blockers are
typically given preoperatively to prevent AF with modest benefit.I Patients without a history ofAF
before surgery typically will not need long-term antiarrhythmic drugs, and AF even without drug
therapy usually resolves within 4-6 weeks in such patients. One study compared rate vs rhythm
control strategies for postoperative AF and demonstrated no difference in the absence of AF at
60 days.41 Thus, ifthe patient is adequately anticoagulated and rate controlled with minimal symp-
toms of AF, it is probably best to avoid antiarrhythmic agents and reassess them during follow-up.
REFERENCES
1. Prystowsky EN, Halperin J, Kowey P. Atrial fibrillation, Atrial flutter and atrial tachycardia. In: Fuster V, Walsh RA,
Harrington RA, eds. Hurst~ the Heart. 14th ed. New York: McGraw-Hill; 2017.
2. Prystowsky EN, Padanilam BJ, Fogel RI. Treatment of atrial fibrillation. JAMA. 2015;314(3):278-288.
3. January CT, et al. 2014 AHNACC/HRS guideline for the management of patients with atrial fibrillation: a report
of the American College Cardiology/American Heart Association Task Force on practice guidelines and the Heart
Rhythm Society. Circulation. 2014;130(23):el99-e267.
4. Chugh SS, et al. Epidemiology and natural history of atrial fibrillation: clinical implication. ] Am Coll Cardiol.
2001;37:371-378.
5. Ellinor PT, et aL Locus for atrial fibrillation maps to chromosome 6ql4-16. Circulation. 2003;107:2880-2883.
6. Darbar D, et al. Familial atrial fibrillation is a genetically heterogeneous disorder. ] Am Coll Cardiol.
2003;41:2185-2192.
7. Prystowsky EN. Tachycardia-induced tachycardia: a mechanism of initiation of atrial fibrillation. In: DiMarco JP,
Prystowsky EN, eds. Atrial Arrhythmias: State of the Art. American Heart Association Monograph Series. Armonk.
NY: Futura Publishing Company, Inc.; 1995:81-95.
8. ScherfD, Romano FJ, Terranova R. Experimental studies on auricular flutter and auricular fibrillation. Am Heart J.
l 948;36:241-251.
9. Moe GK. Abildskov JA. Atrial fibrillation as a self sustaining arrhythmia independent offocal discharge. Am Heart/.
l 959;58:59-70.
10. Haissaguerre M, et al. Spontaneous initiation of atrial fibrillation by ectopic beats originating in the pulmonary
veins. N Engl J Med. 1998;339:659-666.
11. Tsai CF, et al. Initiation of atrial fibrillation by ectopic beats from the superior vena cava: electrophysiological
characteristics and results of radiofrequency ablation. Circulation. 2000;102:67-74.
12. Packer DL, et al. Tachycardia-induced cardiomyopathy: a reversible form of left ventricular dysfunction. Am J
CardioL 1986;57(8):563-570.
13. Nerheim P, et al. Heart failure and sudden death in patients with tachycardia-induced cardiomyopathy and recur-
rent tachycardia. Circulation. 2004;110(3):247-252.
14. Wood M, et al. Clinical outcomes after ablation and pacing therapy for atrial fibrillation: a meta-analysis. Circulation.
2000;101:1138-1144.
15. Dorian P, et al. The impairment of health-related quality of life in patients with intermittent atrial fibrillation:
implications for the assessment of investigational therapy. JAm Coll Cardiol. 2002;36: 1303-1309.
16. Mark DB, et al. Effect of catheter ablation vs medical therapy on quality of life among patients with atrial fibrilla-
tion. The CABANA randomized clinical trial. JAMA. 2019;321(13):1275-1285.
17. Blomstrom-Lundqvist C, et al Effect of catheter ablation vs antiarrhythmic medication on quality oflife in patients
with atrial fibrillation. The CAPTAF randomized trial. JAMA. 2019;321(11):1059-1068.
18. Fuster V. et al. ACC/AHA/ESC 2006 guidelines for the management ofpatients with atrial fibrillation: a report of the
American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European
Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 1001 Guidelines for
the management of patients with atrial fibrillation). doi:l0.1016/j.jacc.2006.07.018
19. Olesen JB, et al. The value of the CHA2DS2-VASc score for refining stroke risk stratification in patients with atrial
fibrillation with a CHADS2 score 0-1: a nationwide cohort study. Thromb Haemost. 2012;107:1172-1179.
20. January CT, et al. 2019 AHA/ACC/HRS focused update of the 2014 AHA/ACC/HRS guideline for the manage-
ment of patients with atrial fibrillation. JAm Coll Cardiol. 2019;74:104-128.
21. Holmes DR. et al. Left atrial appendage closure as an alternative to warfarin for stroke prevention in atrial fibrilla-
tion. JAm Coll Cardiol. 2015;65:2614-2623.
22. Wyse DG, et al. The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) inves-
tigators: a comparison of rate control and rhythm control in patients with atrial fibrillation. N Engl J Med.
2002;347:1825-1833.
23. Van Gelder IC, et al. Rate control versus electrical cardioversion for persistent atrial fibrillation study group: a
comparison of rate control and rhythm control in patients with recurrent persistent atrial fibrillation. N Engl J
Med. 2002;347:1834-1840.
24. Chatterjee S, et al. Pharmacologic rate versus rhythm control strategies in atrial fibrillation: an updated compre-
hensive review and meta-analysis. Pacing Clin ElectrophysioL 2013;36(1):122-133.
25. Ionescu-Ittu R. et al. Comparative effectiveness of rhythm control vs rate control drug treatment on mortality in
patients with atrial fibrillation. Arch Intern Med. 2012;172(13):997-1004.
26. Prystowsky EN. A bridge to the future: maintenance of sinus rhythm in patients with atrial fibrillation. J Cardiovasc
ElectrophysioL 2018;29:1604-1606.
27. Bunch TJ, et al Atrial fibrillation ls independently associated with senile, vascular, and Alzheimer's dementia.
Heart Rhythm. 2010;7:433-437.
28. Gaita F, et al Prevalence of silent cerebral ischemia in paroxysmal and persistent atrial fibrillation and correlation
with cognitive function. J Am Coll Cardiol. 2013;62:1990-1997.
29. Kalantarian S, et al. Cognitive impairment associated with atrial fibrillation: a meta-analysis. Ann Int Med.
2013;158:338-346.
30. Packer DL, et al. Effect of catheter ablation vs antiarrhythmic drug therapy on mortality, stroke, bleed-
ing and cardiac arrest among patients with atrial fibrillation. The CABANA randomized clinical trial. JAMA.
2019;321(13):1261-1274.
31. Prystowsky EN. Proarrhythmia during antiarrhythmic drug treatment for supraventricular tachyarrhythmias: the
paradoxical risk of sinus rhythm for sudden cardiac death. Am J CardioL 1996;78:35-41.
32. Prystowsky EN. Assessment of rhythm and rate control in patients with atrial fibrillation. J Cardiovasc ElectrophysioL
2006;17:S7-Sl 0.
33. Turakhia MP, et al. Increased mortality associated with digoxin in contemporary patients with atrial fibrillation:
findings from the TREAT-AF study. J Am Coll CardioL 2014;64(7):660-668.
34. Curtis AB, et al. Biventricular versus right ventricular pacing in heart failure patients with atrioventricular block
(BLOCK HF) trial investigators. Biventricular pacing for atrioventricular block and systolic dysfunction. N Engl J
Med. 2013;368(17):1585-1593.
35. Klein AL, et al. Assessment of cardioversion using transesophageal echocardiography investigators: use of
transesophageal echocardiography to guide cardioversion in patients with atrial fibrillation. N Engl J Med. 2001;
344:1411-1420.
36. Botto GL, et al External cardioversion of atrial fibrillation: role of paddle position on technical efficacy and energy
requirements. Heart. 1999;82:726-730.
37. Page RL, et al Biphasic versus monophasic shod waveform for conversion of atrial fibrillation: the results of an
international randomized, double-blind multicenter trial/ Am Coll CardioL 2002;39:1956-1963.
38. Prystowsky EN, et al. Clinical experience with dofetilide in the treatment of patients with atrial fibrillation.
I Cardiovasc Electrophysiol. 2003;14:5287-5290.
39. Alboni P, et al. Outpatient treatment of recent-onset atrial fibrillation with the •pill-in-the-poclret" approach.
N Engl] Med. 2004;351:2384-2391.
40. McKeown PP, Gutterman D. Executive awnmary: American College ofChest Physicians guidelines for the preven-
tion and management of postoperative atrial fibrillation after cardiac surgery. Chest. 2005;128(suppl):IS-5S.
41. Gillinov AM, et al Rate control versus rhythm control for atrial fibrillation after cardiac surgery. N Engl I Med.
2016.doi:10.1056/NEJMoa1602002
Bradycardia: Causes of Pauses
George J. Klein, MD
Bradycardia o.r transient a.systole can result from a wide variety of disorders of the sinus node
and cardiac conduction system interacting with neural and humoral influences.1•2 Abnormali-
ties may be discovered as incidental electrocardiographic (ECG) findings during screening or
monitoring for other medical problems. Alternatively. they may be discovered after investiga-
tion for symptoms suggesting transient or persistent b.radycardia. There is little difficulty when
the abnormality is persistent and clearly related to presenting symptoms. Transient abnorm.al-
ities, on the other hand, may be very difficult to demonstrate. A sudden and transient loss of
consciousness o.r a feeling of impending unconsciousness (presyncope) are the major symp-
toms suggesting transient asptole. However, a wide variety of symptoms possibly reflecting
chronic or intermittent hypoperfu.sion of the central nervous system or other organ systems
may be caused by intermittent or chronic bradycardia, including dizzy or lightheaded spells,
fatigue, cognitive disturbances, dyspnea, and so on. The diagnostic difficulties are compounded
in the elderly, who frequently have multiple chronic medical disorders and conduction system
abnormalities that may be difficult to relate to symptoms.
DIAGNOSIS
The asymptomatic patient with unexpected ECG abnormalities is discussed in more detail in
Chapter 11. In general, intervention is rarely indicated, although a reasonable search. for silent
cardiac disease with follow-up is usually warranted. The assessment of the patient presenting
with symptoms suggesting bradyeardia or conduction disorders can be guided by 3 general prin-
ciples. First, a broad approach. is necessary to understand the problem in its clinic.al context.
Symptoms suggesting bradycardia are frequently nonspeeific, with a wide variety of potential
causes. A "'reflex" focus on the cardiac conduction system without clinical correlation is inap-
propriate. Secondly, transient symptoms are an exercise in monitoring. The goal is to acquire
ECG information with direct correlation between these 2 variables-symptoms and data-the
desired end point. Ifa clear precipitating factor is described, it can be useful to try to reproduce
the situation observing the patient and monitoring the ECG. Thirdly, it may be impossible to
obtain ECG data while the symptom is occurring. In such. eases, inferences can be made using
the presence of abnormalities detected even though they have not been associated with symp-
toms. For example. the detection oftransient third-degree atrioventrieular (AV) bloc.k. suggests
that the patient's presenting light-headed spell was related to AV block. even though the episode
recorded was not associated with symptoms. These inferences sometimes require considerable
clinical judgment. In general, the more striking the abnormality, the more confident the clini-
cian is in making the inference that it is causing the symptoms.
From a broad point of view, symptomatic bradycardia requires pacing regardless of the mech-
anism unless a primary reversible issue is recognized and treated. On the other hand, there
should be a high burden of proof of future adverse effect to recommend permanent pacing in
the asymptomatic patient.
History and Physical Examination

A careful history taken from the patient or a good witness often provides a focus for subsequent
investigations. The witness is especially important when the symptoms relate to presyncope or
syncope, where the patient may be unable to provide important details. Transient bradycardia
may cause a plethora of symptoms that are often nonspecific and an open mind is required. The
physical examination should be broad-based and should include attempts to reproduce symp-
toms if they are related to a specific physical activity. Careful carotid sinus massage during ECG
monitoring may be part of the physical examination after freedom from significant carotid
disease is determined at very least by auscultation.
Exercise Testing
Exercise testing may reveal chronotropic incompetence associated with sinus node dysfunction
or it may reveal AV block or bundle branch block when the heart rate increases. It is, of course,
particularly useful when the patient's symptoms are related to exercise.
Ambulatory Monitoring
Ambulatory monitoring is the cornerstone for the investigation of suspected bradycardia as it
provides the opportunity to monitor the patient during everyday activities and record the ECG
during the occurrence of symptoms. The continuous 24-h Holter record is most frequently
used and most useful when symptoms occur daily or almost daily. For patients with less fre-
quent symptoms, a wide variety of event recorders are more useful. These can be applied by the
patient and activated when symptoms appear or they can record in a continuous-loop mode
and provide ECG data prior to the time the device is activated by the patient. The latter devices
require some competence and commitment from the patient, but they can be used by a close
companion or relative if the patient is incapable oflearning how to use them. Automatic activa-
tions based on predetermined criteria or auto triggers are frequently present.
The ambulatory ECG may reveal abnormalities even if symptoms do not occur. Relating
asymptomatic abnormalities to clinical symptoms is obviously inferential and must be done
cautiously. The spectrum of arrhythmias in overtly normal individuals includes bradycardia of
40/min or less (especially during sleep), Wenckebach AV block, sinus arrhythmia with 3 second
pauses or greater and sinus pacemaker shifts with slight changes in P-wave morphology and
heart rate.
Electrophysiologic Testing
Although hardly ever needed today for suspected bradycardia, electrophysiologic testing may be
considered when the patient's symptoms suggest a bradycardia but persistent attempts to obtain
ECG documentation while symptoms occur have failed. The most optimistic expectation is
CHAPTER 10 • Bradycardia: Causes of Pauses 237
to provoke a bradycardia that convincingly reproduces the patient's spontaneous symptoms.

A more realistic aim is to uncover abnormalities of sinus node function or atrioventricular
conduction that support bradycardia as an etiology but do not provide proof. This can provide
a rationale for a therapeutic "trial" of permanent pacing if problematic symptoms potentially
causing injury suspected to be related to bradycardia persist without a firm diagnosis. 3 It must
also be appreciated that a normal electrophysiology study does not rule out transient brady-
cardia.4 Details of electrophysiologic testing are given in Chapter 16, with key points briefly
reviewed below.
Conduction intervals5
Intracardiac recordings can subdivide ECG intervals more specifically into intracardiac com-
ponents. The PA interval is measured from the earliest onset of the P wave on the ECG to the
first rapid deflection of the atrial electrogram at the His bundle recording. It reflects right intra
atrial conduction (normal usually 30 to 40 ms with a little variability). It has minimal clinical
utility although grossly abnormal values would be expected with extensive atrial disease.
The atrial-His (AH) interval is measured from the rapid deflection on the atrial electrogram at
the His bundle site to the onset of the His deflection. This approximates AV node conduction
time (normal limits, 60 to 120 ms). The His-ventricle (HV) interval is measured from the onset
of the His deflection to earliest recorded ventricular activation. This approximates His-Purkinje
conduction time (normal limits, 35 to 55 ms). Incremental atrial pacing (pacing the atrium pro-
gressively faster) tests the conduction system in a dynamic way and assesses "margin of safety»
for conduction. Incremental atrial pacing generally results in progressive prolongation of the
AH interval followed by block proximal to the recorded His deflection (i.e., Wenckebach cycle
length). The Wenckebach cycle length is usually between 350 and 500 ms and is very dependent
on autonomic tone. The HV interval typically is constant, and block below the His at a cycle
length >350 ms is usually considered abnormal.
Sinus Node Recovery Time (SNRTJ

Spontaneous termination of a naturally occurring rapid heart rhythm results in a pause of vari-
able duration due to overdrive suppression of the sinus node and subsidiary pacemakers. In the
bradycardia-tachycardia syndrome (BTS), this interval is prolonged and results in symptoms.
The sinus node recovery test is an attempt to measure this phenomenon in a systematic and
reproducible way in the laboratory.6.7
Although intuitively the SNRT is a measure of overdrive suppression of automaticity, the test is
also affected by conduction and refractoriness around the sinus node, autonomic tone, and the
site ofpacing. Overall, it can be said to reflect "sinus node function." The test is considered to be
very specific for sinus node dysfunction (95%-100%), although it can be normal in the presence
of known sinus node dysfunction (sensitivity, 60%-80%).
Sinoatrial Conduction Time (SACT)

Sinus node dysfunction may result from block of the sinus impulse to the atrium (sinus node
exit block). This provided the rationale for measurement of the sinoatrial conduction by both
direct recording and the indirect method. 8 In the latter, premature atrial stimuli are introduced
throughout the sinus cycle and SACT is calculated from extrastimuli that result in reset of the
sinus node. The SACT depends on assumptions that are debatable and subject to substantial
error. It is rarely used today.
Autonomic testing
Sinus node dysfunction may be caused by intrinsic sinus node abnormality, abnormal auto-
nomic innervation or reflex responsiveness, or combinations of the above. There have been 2
general approaches to assessing the contribution of autonomic abnormalities.
First, attempts have been made to assess responsiveness to standard agonists and antagonists.6
Normalization of inappropriate bradycardia with atropine or an exaggerated response to atropine
indicates that parasympathetic stimulation is contributing to sinus bradycardia, whereas a blunted
response implicates intrinsic sinus node dysfunction. An exaggerated response to edrophonium
suggests inappropriate responsiveness to normal parasympathetic stimulation. Similarly, a blunted
response to isoproterenol suggests poor responsiveness to normal sympathetic stimulation. The
intrinsic heart rate (IHR)9 is perhaps the most standardized test and is obtained by "totar auto-
nomic blockade at rest, historically after atropine (0.04 mg/kg) and propranolol (0.2 mg/kg). The
IHR adjusted for age has been determined as IHR =118.1 - (0.57 x age) with 95% confidence lim-
its of 14% for age 45 years and under and 18% for age greater than 45. An abnormal IHR suggests
intrinsic abnormality of the sinus node in the absence of autonomic influence.
The second approach is the use of physiologic or phannacologic interventions aimed at assessing
reflex responsiveness using a provocation known to initiate a series of changes. The response to
standing involves decrease in vagal tone and increase in sympathetic tone. Carotid sinus massage
(following precautions to evaluate carotid stenosis) assesses baroceptor response, with the end result
being an increase in parasympathetic tone. A prolonged pause (greater than 2.5-3.0 s) suggests an
exaggerated response to normal parasympathetic drive or excessive parasympathetic drive.10.u The
Valsalva maneuver assesses responsiveness to sympathetic stimulation (strain phase) and parasym-
pathetic stimulation (post strain phase). Passive tilt testing has been used clinically,1a-14 although the
physiologic responses to this maneuver are incompletely understood. Basically, passive tilt results
in loss of parasympathetic tone and increase in sympathetic tone with pooling of blood volume in
the lower torso. With continuation of tilt, normal subjects will maintain a relatively constant heart
rate and blood pressure, while some will experience slowing of sinus heart rate and even asystole
(cardioinhibitory response) and concomitant diminished blood pressure (vasodepressor response).
The usage of tilt testing has declined due to issues of sensitivity and specificity.15
CLASSIFICATION OF CAUSES OF BRADYCARDIA

Bradycardia may be classified broadly as spurious bradycardia, sinus node dysfunction, atrio-
ventricular conduction disturbance, or neutrally mediated ("reflex") bradycardia.
Spurious Bradycardia
Spurious bradycardia refers to bradycardia or pauses mimicking sinus node or atrioventricu-
lar conduction disease clinically or electrocardiographically. A common example results from
closely coupled ventricular ectopic activity not perceived as a pulse (pulse deficit). Closely
coupled atrial premature depolarizations may not conduct to the ventricles (blocked atrial
extrasystole) and may mimic sinus arrest {Figure 10-1). Technical difficulties with recording
system or leads may result in brief"flat lines" that can mimic asystole (Figure 10-2). Ventricular
extrasystoles may have very low voltage in a monitored lead and simulate a pause. Rarely, His
bundle extrasystoles may fail to conduct to either atria or ventricles but can still result in epi-
sodic AV block due to concealed conduction into the AV node.16•17 (See Chapter 2.) This may
CHAPTER 10 • Bradycardla: Causes of Pauses 239
FIGURE 1~1 • Pause due to blocked atrial extrasystole. In this example. the blocked P wave Is evident In the deformed ST segment
of the cycle prior to the pause.
FIGURE 1~2 • Pseudo pause related to recording device malfunctlon. The upper channel shows a bizarre miniaturization of the
QRS prior to a very straight line. In the lower panel, there ls no signal on the flrst beat of recavery In the upper channel while a QRS
Is slmuhaneously pre5ent on the lower channel. There may be a sudden DC shift In the recording lead. None of the above ls co~
patible with physiological events.
be suspected clinically if manifest junctional extrasystoles are observed in conjunction with

episodic AV block. but the diagnosis must be confirmed by His bundle recording.
Sinus Node Dysfunction

The rerm sick sinus wuJromtl refers to a constellation of ECG findings attributed to dysfunction
of the sinus node and subsidiary pacemakers that results in symptomatic bradycardia or asystole.
The term sinus node dvgimction refers to similar ECG abnormalities without symptoms. Several
manifestations of sick sinus syndrome are recognif.ed, although there may be considerable overlap
in individuals.
Sinus bradycardla
By definition, a sinus rate less than 50-60/min is considered bradycardia. However, only
·inappropriate" sinus bradycardia is considered to be sinus node dysfunction. A resting sinus
rate of 40/min may be physiologic during sleep or in the well-conditioned athlete but is
inappropriate in an individual during moderate activity. '"Chronotropic incompetence" refers
to a failure to increase sinus rate under appropriate phf5iologic circumstances as judged by
comparison with normal age- and sex-matched individuals performing the same activity.
Sinusanest
The term sinus arrest refers to an a.systolic pa.use. Pauses up to 2 seconds occur relatively frequently
in overtly normal individuals; hence. an "abnormal" pause is frequently arbitrarily defined here
as greater than 2 seconds. Nonetheless. pauses of 4-5 seconds especially during heightened vagal
tone are not uncommon in overtly normal and asymptomatic individuals. The lengthy pause in
Figure 1~3 was recorded from a patientwith intennittentligbtheaded spells. including during this
-r:- .
II
> t~.
II
FIGURE 1C.-J • Pause due to sinus arTeSt.

FIGURE 1H • Pause compatible with sinus node exit block. The calculation i5 hampered by some 5inu5 arrhythmia, but the asy:s-
tolic pause closely approximates 2 sinus cycles {dotted red line at midpoint between 2 cycles, blue lines).
recording. It may be terminated by a sinus cycle or a subsidiary pacemaker, frequently junctional as

in the individual in Figure 10-3. These pauses occur sporadically and the length of the pause is not
an exact multiple of the P..P interval. suggesting that the mechanism is a failure of automaticity of
the sinus node. Because the actual mechanism. (i.e., failure of automaticlty or conduction) usually
cannot be determined from the ECG, some prefer the term sinus pause instead of arrest.
Sinus node exit block

Analysis of the sinus pause may suggest normal automaticity with intennittent exit block of the
impulse from the sinus node to the surrounding atrium. A sudden pause where the length of
the pause is an exact multiple of the P-P interval. suggests Mobitz type 11 sinus node exit block
(Figure 10-4). A progressive shortening of the P-P interval prior to the nonconducted P wave
suggests Mobitz type I sinus node exit block (Figure 10-5). A definitive distinction between
sinus arrest and exit block frequently cannot be made without recording the sinus node elec-
trogram during the event. Practically, the distinction is not important
Bradycardia-tachycardia syndrome
As the name suggests, patients with this variant have episodes of both bradycardia and supraven-
tricular tachycardia (Figure 10-6). The most common tachycardia is atrial fibrillation. Pauses
may be observed after abrupt cessation of tachycardia, presumably due to overdrive suppres-
sion of the sinus node and subsidiary pacemakers. Additionally, tachycardia may be initiated in
the course of bradycardia or sinus arrest. possibly due to increased dispersion of refractoriness
or early after depolarizations occurring with slower heart rates.
Atrial fibtlllatlon
Lone atrial fibrillation, inability to cardiovert at.rial fibrillation, and atrial fibrillation with a
relatively slow ventricular response in the absence of drugs are frequently included in the spec-
trum. of sick sinus syndrome in spite of the fact that the sinus node may not be the most prom-
inent focus of abnormality with these arrhythmias.
Pacemaker shift
Slight changes in P-wave morphology with associated change in heart rate are frequently
observed in asymptomatic individuals and reflect a shift in location of the dominant pacemaker
in the sinus node region or to a lower site along the crista terminalis (Figure 10-7). This can1'
be considered within the realm. of "normal"' unless the alternate pacemaker site is associated
with marked bradycardia.
FIGURE 10-5 • Pause compatlble with sinus node exit block of the Wenckebach type. The rhythm appears to show atrlal extrasy.s-
toles but the P waves are identical, suggesting both originate in the sinus node. The a110ws show the postulated sinus pacemaker
flrtng times, which would flt with the ob$ervattons.
Symptoms
The cardinal symptoms of sick sinus syndrome are presy:ncope and syncope. However. cogni-
tive dysfunction, fatigue, and other symptoms poten1ially related to hypoperfusion of organ
systems can result Finally, symptoms may be related to peripheral embolism associated with
atrial fibrillation.
FIGURE 10-6 • Bradycardla-tachycardla syndrome. Atrlal flbrlllatton tennlnates and a long pause follows. This Is tennlnated with a
sinus beat but a PAC lmmedlately relnltiates atrial flbrlllatlon.
++ ·+ >++ ... + ·+ ... ++

+:: ... f+;:+;_ ,:H: ;:+;_ ,=H:t
ij :~+ ~rt th rt tH
:th H
r u+tH
p: +-
........
........... T'T" ~ - ... _ . "T
n+ j t, ..
... ,,
.~
,I"" >++1 r• .........

......_ 1
f:I
/ ~ t
..I .~ ..: +_A .' -.+- ~ + H
..........- -t ~ ""-' -'1
.:~1 H~'..t+-
_......,, '\;"""' H -t
l~ ~
~ ·~
~
LL
+-
J
...- 1-
l~+ :~+- ~rl hf ~i id

t Mt1 MMt
FIGURE 10-7 • Sinus pacemaker shift. In this asymptomatic individual, there is a sudden slight prolongation of the cycle length
accompanied by a change in the P-wave morphology, caused by a shift in the site of the primary pacemaker. This shift is probably
to a lower site along the crlsta termlnalls, perhaps related to Increased parasympathetic tone. A pacing site with negative P waves
in the inferior leads has been called "coronary sinus rhythm.•
Incidence and Etiology111

Sick sinus syndrome is observed predominantly in the middle-aged and elderly. It accounts for
the majority of pacemaker implants for bradycardia in North America. Sick sinus syndrome
is associated with coronary heart disease, hypertension, and virtually any condition affecting
the heart but is frequently observed in the absence of any clinically identifiable heart disease.
Acute myocardial infarction may be associated with sinus node dysfunction that may or may
not resolve with time. Finally, many drugs may cause sinus node dysfunction, usually aggravat-
ing preexisting sinus node dysfunction. These drugs include digitalis glycosides, beta blockers,
calcium antagonists, antiarrhythmics, sympatholytic antihypertensives, miscellaneous agents
such as lithium carbonate and cimetidine, and many others.
Therapy
Initial therapy is based on ECG abnormalities demonstrated or strongly suspected to be related
to symptoms. Permanent pacing is the mainstay of therapy for sick sinus syndrome. Occasion-
ally, suppression of tachycardia with antiarrhythmic drugs in patients with TBS will also prevent
bradycardia, although this strategy should be carried out with caution. Dual chamber (DDD)
pacing is generally used in symptomatic patients with sinus node dysfunction. Atrial demand
(AAI) pacing is adequate when there is no evidence of significant AV conduction disease (nor-
mal QRS, normal PR interval, atrial pacing with 1:1 conduction attainable at 120/min or greater)
although the use of this pacing modality is relatively infrequent and regional. Ventricular
demand (VVI) pacing is indicated with chronic atrial fibrillation and reasonable in patients with
infrequent bradycardia. The high incidence of systemic embolization in sick sinus syndrome is
probably related to atrial fibrillation (discussed elsewhere).
Atrioventricular Block
Atrioventricular conduction disturbance can be associated with any process affecting the heart
rendering a detailed list of etiologies not very useful. Congenital AV block and AV block associ-
ated with surgery for congenital heart disease predominate in the young. Idiopathic fibrosis and
calcification of the AV conduction system is predominantly a disease of the elderly. Ischemic
and valvular heart diseases are also relatively common causes of conduction disease. Medi-
cations in therapeutic doses can result in clinical AV conduction disease, usually in patients
with preexisting latent dysfunction. Digitalis gl.ycosides, calcium. channel blockers, and beta
blockers a.ffed the AV node, while antiarrhythmic drugs can exacerbate block in the AV node
or His-Purldnje system, depending on the agent used
The ECG has traditionally provided the starting point for classifying patterns of AV block.1'.20
The ECG can usually provide accurate inferences on the site of AV block, namely the AV node,
His bundle, or bundle branches. Recording of the intra.cardiac intervals during AV block may be
required .infrequently to pinpoint the site of block in ambiguous cases although the great majority
of pacing decisions are made on the basis of clinical symptoms and ECG recordings. Both the
type of AV block and the site of block. influence prognosis and the decision to pace. Block in
the AV node (Figure 10-8) is usually associated with a more stable junctional escape rate than
block in the His bundle or bundle branches. which is associated with less stable escape pace-
makers and more unpredictable asystole.
Rrst-degree AV block
First-degree AV bloc.k. defined as PR interval greater than 0.2 s, can result from intraatrial
delay, AV nodal delay, infra-nodal delay (His bundle or bundle branches), or combinations
of the above. The AV node conduction time is the predominant influence on the PR interval
and is almost invariably prolonged in first-degree AV block. Of note, no P waves are actually
"blocked"' and some prefer the term first-degree amduction delay.
PR
RV
RA
~
105 95
~~
AH A
r ')
1-soo ms-t
FIGURE 1H • Apparent Mobitz type 2 block due to failure of conduction over the AV node. The surface QRS complex and PR
Interval are nonnal. There has been gradual PR prolongation (not shown) but no prclongatlon of the PR Interval In the beats lmme-
dlately prior to the nonconducted P wave. The non conducted P wave Is associated wtth an atrial deflectlon without a subsequent
His deflection denoting block In the AV node. The PR and AH Intervals following the block cycle are sltghtly shorter than the pre-
ceding conducted ones, p!O\tldlng a clue that the level of block ls In the AV node. There Is also an Increase In the P..P Interval prior
to the blocked P wave, suggesting an Increase In vagal tone as a possible mechanism for block.
Second-degree AV block
Second-degree AV block is usually classified as Mobitz type I or II. The descriptor "high-grade"
or "advanced.. AV block is sometimes added with Mobitz type II block and a slow ventricular
response (greater than 2: 1 AV conduction ratio) or apparently complete AV block where there
appears to be intermittent conduction over the AV node.
Mobitz type I AV block (Wenckebach block) is associated with prolongation ofthe PR intervals
prior to the blocked cycle and shortening of the PR interval (Figure 10-8) in the first conducted
cycle after block.1' In "classic"' Wenckebach periodicity, the R-R interval shortens prior to the
blocked cycle, because maximum prolongation of the PR interval occurs between the first and
second cycle of the sequence. The site of block in the majority of Mobitz type I sequences is the
AV node. Mobitz type I block is often physiologic, with high vagal tone often seen in athletes
and during sleep.
Mobitz type II block requires a constant PR interval prior to and following the blocked cycle.
The site of block is generally the His-Purkinje system (Figure 10-9). It is impossible to designate
fixed 2: 1 AV block as Mobitz type I or II because this requires seeing at least 2 conducted cycles
prior to block. Maneuvers to alter sinus rate will usually clarify this. Atropine will increase sinus
rate and improve AV nodal conduction but will worsen His-Purkinje block. Vagal maneuvers
will decrease sinus rate and prolong AV nodal conduction and tend to improve block at or
below the His. Appearance or worsening ofblock during exercise strongly suggests block below
the AV node (Figure 10-10). Enhanced sympathetic and deaeased parasympathetic tone occur
with exercise and facilitate AV node conduction.
Site of block in the AV node is favored by a Mobitz type I pattern, a narrow QRS, and a pro-
longed PR interval of conducted beats. Site of block in the His bundle or bundle branches is
favored by a Mobitz type II pattern, bundle branch block or intraventricular conduction delay,
and a relatively normal (<.24 s) PR interval ofconducted cycles.
v, _)\_ J
'""'
RA
_J"
t r f AH•60 r f
AH AH AH AH AH V
H
FIGURE 1o-t • Atrloventrlcular block due to failure of conduction In the Hls-fasclcular system. The surface ECG shows lntraven-
tJlculer conduction delay and a canstant PR lrrterval of conducted QRS complexes. The noncanducted P wave Is associated with a
normal Aand Hdeftectlon without a subsequent QRS, denoting block below the level of the recorded His potentlal. 1, 3, V1, surface
ECG leads; HB, His bundle electro gram; RA. high right atrial electrogram.
II
V5 ~~~~~~~~~~~~~~~
Panel A
II
PanelB
FIGURE 10-10 • Panel A shows 2:1 AV block with a relatlvely normal PR of 180 ms of the conducted beats. This suggests subnodal
AV block. This was verlfled during exercise testing In Panel B with more advanced AV block associated with the lnaeased sinus rate.
The relatlvely narrow QRS suggests the site of block In the His bundle.
Third-degree AVblock
Third-degree or complete AV block results in atrioventricular dissociation. The site of bloc.k.
can usually be inferred by the characteristics of the escape pacemaker emerging distal to the
block site. Block in the AV node is characterized by the following:
• A narrow QRS escape pacemaker (i.e., supraventricular morphology)
• Escape rate of 40/min or greater
• Acceleration of the escape rate after atropine and exercise
Block in the His bundle or bilateral bundle branch block is characterized by the following:
• A wider (110 ms) QRS escape pacemaker
• Escape rate frequently of 40/min or less
• Failure to accelerate significantly after atropine
Junctional pacemakers are more stable and less prone to overdrive suppression and swlden
asystole than are distal pacemakers.
Congenital AVblock'"
Congenital AV block is observed in approximately I per 20,000 live births. It occurs in associ-
ation with overt congenital heart disease (endocardial cushion defect. corrected transposition)
or without congenital heart disease. The latter has been associated with maternal lupus and
other collagen disease.22 Congenital AV block is usually at the level of the AV node and is felt to
be related to a developmental failure of the atrium to contact the AV node or failure of the AV
node to contact the His bundle. Padng is usually indicated for symptoms (presyncope, syncope,
poor exercise tolerance). The decision to pace asymptomatic individuals is considerably more
controversial, but usual criteria have included resting heart rate less than 40/min with fail-
ure to increase rate substantially with exercise, occurrence of ventricular ectopy with exercise,
demonstrated block below the His bundle, and prolonged juncti.onal recovery tlme (corrected
juncti.onal recovery time greater than 200 ms).
Decision to pace In the patient with AVblock'
The decision to pace is related to symptom status, the degree of block, and the site of block.
Pacing is indicated in the symptomatic individual regardless of the site of block. In the asymp-
tomatic individual, pacing is indicated in both second- and third-degree AV block at the level
of the His bundle or bundle branches because of the potential for sudden asystole.?J Pacing
may be indicated in third-degree AV block at the AV node level for symptoms or individual
considerations.
Electrophysiologic testing for bifascicular block with the intent of predicting symptoms is gen-
erally not helpful. The incidence ofprogression to complete heart block is low (196-3% per year)
and not predicted with sufficient predictive accuracy to be clinically useful. Alternating bundle
branch block (F~ 10-11) is associated with severe subnodal conduction disease and pacing
is generally indicated, all things being equal
FIGURE 10-11 • Alternattng bundle branch block. There Is sinus rhydtm with a relattwly normal PR Interval and spontaneous
transition from right to left bundle branch block.
n"----"--"
II
FIGURE 10-12 • ParolC)'Smal AV block. A stngle PAC Is followed by a long run of noncondueted Pwaves with the pause tamlnated
by ajunctlonal escape or possibly by a sinus beat Ifwe consider the Pwave of the first beat tennlnatlng the pause to be conducted.
Paroxysmal AVblock24
Paroxysmal AV block is a specific type of AV block associated with severe conduction dis-
ease and may result in sudden death. Although the manifestations are somewhat variable. the
cardinal feature is prolonged AV block after an extrasy5tole (Figure 10-12) with termination
after another escape or ectopic beat A potential mechanism is phase 4 (pause-dependent) AV
block where spontaneous loss of resting membrane potential leads to failure to depolarize when
stimulated after the pause. However, patients can have even slower sinus rates without ectopy
and without heart block, for example during sleep, suggesting other potential mechanisms for
block. Pacing is indicated as soon as possible after the diagnosis is established.
Role ofelectrophysiologic testing
Most decision malting in patients with AV block is determined by clinic:aI and ECG variables.
Eleclrophysiologic testing is indicated to determine the site of block in second- or third-degree
block if this is equivocal and if the information is necessary for a clinical decision. It may
be useful in third-degree AV nodal block to determine the properties of the jWlctional escape
pacemaker if the decision to pace is equivocal. Finally, it may be useful if symptoms of pre-
syncope or syncope are suspected to be related to AV block, but clinical documentation is not
available.
Neurally-Mediated, Vagal Bradycardia

Both sinus arrest and AV block can occur in the absence of resting sinus or AV node dysfunc-
tion as a result of autonomic stimulation. Asymptomatic sinus bradycardia, sinus pause, and
AV block are frequent during monitoring, especially during sleep or those situations known
to cause vagaI stimulation such as nausea and vomiting. This is rarely an indication for pacing
even if the bradycardia or pause is impressive. Although the vagus c:an affect heart rate and AV
node function differentially, the hallmark or "'fingerprint"' ofa vagaI response is the occurrence
of both sinus slowing and AV block (Figure 1~13).
Various syndromes have been described, including carotid sinus hypersensitivity. vasodepressor
(neurally mediated) syncope, cough syncope, swallow syncope, glossopharyngeal neuralgia syn-
cope, mic:turition syncope, and defecation syncope. These entities have in common various recog-
nized precipitating factors triggering a reflex that culminates in a vasodepressor response and/or
bradycardia (cardioiDhibitory) mediated at least in part by the parasympathetic nervous system.
3:59:51-4 HR=75
85 " J_ J _' 30 LLL~_LLl_J __
' I i '
!
j ! i
T l
I I !
. 1 -1-f
. '
&:41:0IM SVPB HR=H
FIGURE 10-13 • AV block of the Wenckebach type In an asymptomatic lndlvldual. lhere Is only sllght prolongation of the PR Inter-
val prior to the blocked P wave but the give away is the simultaneous transient slowing of the sinus cycle length.
The c:ardioinhibitory but not the vasodepressor response is attenuated or inhibited by atropine.
There is characteristically at least some component of a vasodepressor response even with rel-
atively dominant cardioinhibitory response. The most common and best-studied syndromes
are the hypersensitive carotid sinus syndrome and vasodepressor (vasovagal. neurally medi-
ated) syncope. In addition, an ill-defined syndrome of persistent. inappropriate hypervagotonia
has been described, where resting abnormalities of sinus node and AV node conduction are
reversed by atropine.
Carotid sinus hypersensltlvity10,1 r,s
Pressure on the right o.r left carotid sinus (after clinical or laboratory exclusion ofcarotid artery
disease) produces a reflex slowing of the sinus rate and decrease in blood pressure mediated
by activation of carotid baro.receptors. An "'exaggerated" reflex is gene.rally defined arbitrarily
as cardiac a.systole of 3 seconds or more or a drop in blood pressure of 30 to 50 mmHg. An
abnormal reflex is more frequently observed in the elderly and in association with hyperten-
sion, coronary artery disease. o.r in the presence of beta blockers. An abnormal response may
be observed in asymptomatic individuals. The classic presentation in symptomatic patients is
presyncope or syncope produced by maneuvers that stimulate the carotid baroreceptors, such
as stretching the neck while shaving. reaching for a high object, or wearing a tight collar. Prob-
ably more frequently, there are no obvious precipitating factors prior to symptoms. The diag-
nosis of carotid sinus syndrome depends on the demonstration of the abnormal reflex with a
convincing reproduction of symptoms or, more frequently. exclusion of other potential causes
of the symptoms.
The carotid sinus response usually results in both a cardioinhibitory (bradyc:ardia) component
and a vasodepressor component, with the former more frequent The cardioinhibitory com-
ponent but not the va.sodepressor component is bloclctd by atropine. Patients with recurrent
symptoms may .require permanent pacing. and atrioventricular pacing may be preferable to
ventricular pacing. Prior to institution of permanent pacing. it may be useful to demonstrate
that temporary pacing prevents syncope (cardioinhibitory component dominant) during

carotid sinus stimulation.
Vasodepressor (vasovagal, neurally mediated) syncope 1a.14

The classic "faint" has long been recognized as a clinical entity. Classically, symptoms will begin
in childhood or adolescence and may recur for many years. The precipitating event is often
an emotional upset, physical pain, a hot, uncomfortable environment, or prolonged standing.
There is frequently a prodrome of visceral symptoms such as nausea, cold sweat, or epigas-
tric distress followed by presyncope or syncope. The episode may be attenuated or aborted by
supine posture. The patient is observed to be pale, clammy, and pulsdess with dilated pupils
during syncope.
It is now appreciated that this classic presentation may be only the tip of the iceberg. Passive
upright tilt and/or isoproterenol infusion may expose an individual's susceptibility to develop
vasovagal symptoms or reproduce syncope. While individuals with no tendency to a vaso-
vagal response maintain heart rate and blood pressure with this maneuver while those with a
tendency to a vasovagal response can experience a slowing of the heart rate and hypotension
accompanied by presyncope or syncope with potentially reproduction of a unique prodrome.
The cardioinhibitory but not the vasodepressor component is prevented by atropine or pacing.
Initiation of the reflex is thought to occur via cardiac receptors activated by aggressive cardiac
contraction in the presence of a decreased afterload. The response may be attenuated or elimi-
nated by prior treatment with beta blockers. Unfortunately, the test is not perfectly sensitive nor
specific pinpointing the cause of syncope to a vasovagal response. For example, a patient with
a tendency to a vasovagal response exposed by this test may have syncope of another cause.
Confidence in a true positive is increased by reproduction of the patient's usual pre-syncopal
symptoms.
COMMENTARY
Clinical corrdation of documented ECG abnormalities with symptoms is the crux of assess-
ing bradycardia. Invasive dectrophysiologic testing has contributed greatly to our understand-
ing of bradycardia and remains helpful in selected individuals but is generally not required
clinically. Institution of pacing therapy in asymptomatic individuals requires a high burden of
clinical proof of impending harm and is generally unwise. It is important to have a high index
of suspicion for "neurally mediated" or "reflex" bradycardia, since pacing will generally not
prevent associated vasovagal symptoms.
REFERENCES
1. Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AlWHRS 2008 Guidelines for Device-Based Therapy of
Cardiac: Rhythm Abnormalities: Executive Summary: A Report of the American College of Cardiology/American
Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002
Guideline Update for Implantation of Cardiac Pacemaki:rs and Antiarrhythmia Devices) Developed in Collaboration
With the American Association for Thoracic Surgery and Society of Thoracic Surgeons./ Am Coll Cardiol 2008;
51(21):2085-2105. doi:l0.1016/j.jacc.2008.02.033
2. KU$umoto FM, Schoenfeld MH, Barrett C, et al. 2018 ACC/AHAIHRS Guideline on the Evaluation and Man-
agement of Patients With Bradycardia and Cardiac Conduction Delay./ Am Coll Cardiol 2019;74(7):e51-e156.
doi: 10.1016/j.jacc.2018.10.044
3. Rattes MF, Klein GJ, Sharma AD, Boone JA, Kerr C, Milstein S. Efficacy of empirical cardiac pacing in syncope of
unknown cause. CMA/.1989;140(4):381.
4. Fujimura 0, Yee R, Klein GJ, Sharma AD, Boahene KA. The diagnostic sensitivity of electrophysiologic testing in
patients with syncope caused by transient bradycardia. N Engl JMed. l 989;321(25): 1703-1707.
5. Josephson ME. Josephson's Clinical Cardiac Electrophysiology: Techniques and Interpretations. 5th ed. LWW; 2016.
6. Benditt DG, Sakaguchi S, Goldstein MA, Lurie KG, Gornick CC, Adler SW. Sinus node dysfunction: pathophysiol-
ogy, clinical features, evaluation, and treatment. Cardiac Electrophysiology: From Cell to Bedside. 1995;2:1215-1247.
7. Benditt DG, Strauss HC, Scheinman MM, Behar VS, Wallace AG. Analysis of secondary pauses following termi-
nation of rapid atrial pacing in man. Circulation. 1976;54(3):436-441.
8. Strauss HC, SaroffAL, Bigger Jr JT, GiardinaEG. Premature atrial stimulation as a key to the understanding ofsinoa-
trial conduction in man: pre5entation of data and critical review of the literature. Circulation. 1973;47(1):86-93.
9. Jose AD, Collison D. The normal range and determinants of the intrinsic heart rate in man. Cardiovasc Res.
1970;4(2):160-167.
10. Davies AB, Stephens MR, Davies AG. Carotid sinus hypersensitivity in patients presenting with syncope. HeaTt.
1979;42(5):583-586.
11. Strasberg B, Sagie A. Erdman S, Kusniec J, Sclarovsky S, Agmon J. Carotid sinus hypersensitivity and the carotid
sinus syndrome. ProgCardiovasc Dis. 1989;31(5):379-391.
12. Wuman MB, Yao L, Cameron DA, Wald RW, Roseman J. Isoproterenol induction of vasodepressor-type reaction
in vasodepressor-prone persons. Am J Cardiol. 1989;63(1):58-65.
13. Milstein S, Buetikofer J, Lesser J, et al. Cardiac asystole: a manifestation ofneurally mediatedhypotension-bradycardia.
J Am Coll Cardiol. 1989;14(7):1626-1632.
14. Almquist A, Goldenberg IF, Milstein S, et al. Provocation ofbradycardia and hypotension by isoproterenol and
upright posture in patients with unexplained syncope. N Engl/ Med. 1989;320(6):346-351.
15. Kapoor WN, Smith MA, Miller NL. Upright tilt testing in evaluating syncope: a comprehensive literature review.
Am/ Med. 1994;97(1):78-88.
16. Langendorf R. Concealed AV conduction: the effect of blocked impulses on the formation and conduction of
subsequent impulses. Am Heart/. 1948;35(4):542-552.
17. Anderson GJ, GreenspanM, Kimbiris D. Conceal.edjunctionalbigeminyinducingpseudo 2: 1 AV block./ Electrocardiol.
1981;14(1):91-96.
18. Kerr CR, Grant AO, Wenger TL, Strauss HC. Sinus node dysfunction. Cardiol Clin. 1983; 1(2):187-207.
19. Kastor JA. Atrioventricular block. N Engl J Med. 1975;292(9):462-465.
20. Kastor JA. Atrioventricular block (second of two parts). N Engl/ Med. 1975;292(11):572-574.
21. Friedman D, Duncanson L, Glickstein J, Buyon J. A review of congenital heart block. Images Paediatr Cardiol.
2003;5(3):36-48.
22. Chameides L, Truex RC, Vetter V, Rashkind WJ, Galioto Jr FM, Noonan JA. Association of maternal systemic
lupus erythematosus with congenital complete heart block. N Engl J Med. 1977;297(22): 1204-1207.
23. Strasberg B, Amat-Y-Leon F, Dhingra RC, et al. Natural history of chronic second-degree atrioventricular nodal
block. Circulation.1981;63(5):1043-1049.
24. Lee S, Wellens HJJ, Josephson ME. Paroxysmal atrioventricular block. Heart Rhythm. 2009;6(8):1229-1234.
doi:l0.1016/j.hrthm.2009.04.001
25. Wenger TL, Dohrmann ML, Strauss HC, Conley MJ, Wechsler AS, Wagner GS. Hypersensitive carotid sinus
syndrome manifested as cough syncope. Pacing Clin Electrophysiol. 1980;3(3):332-339.
PART
Clinical Presentations
Chapter 11 Electrocardiographic Abnormalities in Asymptomatic Individuals
Chapter 12 Narrow QRS Tachycardia
Chapter 13 Wide QRS Tachycardia
Chapter 14 Undiagnosed Syncope, Dizzy Spells, Palpitations
Chapter 15 Sudden Cardiac Arrest/Sudden Cardiac Death
Electrocardiographic
Abnormalities in
Asymptomatic Individuals
George J. Klein, MD
We are often confronted by electrocardiographic (ECG) abnormalities that are discovered inci-
dentally during screening o.r during the course of investigating an unrelated problem. These are
more frequent in the elderly. reflecting to some degree an increasing prevalence of subclinU:al
heart disease. Appropriate advice to the patient requires balancing a knowledge of the natural
history of the specific abnormality and potential favorable or harmful effects of a contemplated
intervention. An intervention in an asymptomatic individual should be undertaken only with
clear information supporting the potential benefit of further investigation and treatment over
the natural history of the finding.
It is also obvious that virtually any cardiac abnormality can be reflected in some way in the
ECG. For this reason, the scope of this brief section is to summarize the common abnormalities
in the domain of the cardiac electrophysiologist. The section is focused to answer the following
bottom-line question, namely: Do we leave it alone or do we need to move on to the next step.
whether further diapostic testina or treatment?
BRADYARRHYTHMIAS
Sinus Node Dysfunction
Sinus node dysfunction is said to be present when the ECG criteria of sick sinus syndrome
(severe inappropriate bradycardia, sinus pause, chronic atrial fibrillation with a slow ventricular
response, alternating tachycardia. and bradycardia) are present in the absence of symptoms.1
The diagnosis must be made with caution, because sinus bradycardia to 40/min or less and
sinus pauses to 3 s or greater can be observed in normal individuals during sleep and at rest2
There are no data to support the utility of permanent pacing in patients with asymptomatic
sinus node dysfunction.3 Patients followed for asymptomatic sinus node dysfunction may of
course ultimately develop symptoms requiring pacing or need other drug therapy potentially
aggravating bradycardia but mortality is dependent on the presence and severity of coexistent
disease.
The decision to pace becomes more complex in the patient with sinus node dysfunction who
has vague or nonspecific symptoms (fatigue, personality change, memory impairment, dizzy
spells), which could potentially be due to bradycardia. The relationship of these symptoms to
bradycardia may be established by ambulatory monitoring or treadmill testin~ but frequently
the link is difficult to clarify and the decision to pace is guided by clinical judgment. A trial
of pacing would be useful, especially if a more prolonged period of temporary pacing were
possible.
Atrioventricular Block
The risk of syncope or death in patients with atrioventricular (AV) block depends both on
the presence of concomitant heart disease and the site of block. In asymptomatic individuals,
first-degree AV block and Mobitz type I second-degree AV block are relatively common,4 the
latter usually reflecting vagal tone. Pacing is not indicated. The situation is more complex with
Mobitz type II second-degree AV block. Knowledge of the site of the block is helpful, as AV
nodal block is generally benign, while block at the His-Purkinj e level is more likely to progress
and become symptomatic.5 The level of block can frequently be approximated by ECG criteria,
with intracardiac electrophysiologic assessment useful for equivocal cases (Chapter 10}. Pacing
is arguably justified in asymptomatic patients with proven infranodal block, but the decision in
an individual is open to clinical judgment.
Complete AV block is uncommon in asymptomatic individuals4 and acquired AV block is

almost invariably associated with symptoms. More difficult therapeutic decisions arise in the
pediatric or younger patient with complete congenital AV block.6.7 The level of block in these
individuals is usually at the AV node, and the escape pacemaker may be stable and responsive
to autonomic influences. Although many of these patients may remain asymptomatic through-
out their lives, some will develop syncope and sudden death. Efforts to predict this outcome
have not led to unequivocal guidelines, but several risk factors have been suggested that gener-
ally indicate a more sluggish and unpredictable escape pacemaker. These include the following:
1. Mean heart rate <50/min while awake with little variability on ambulatory monitoring
2. Absence of heart rate increase during exercise
3. Associated ventricular arrhythmias
4. Exit block of the junctional escape rhythm
5. WideQRS
6. Prolonged QT interval
7. Associated heart disease
8. Prolonged junctional recovery time at electrophysiologic testing
These observations have not been rigorously evaluated in large numbers of individuals in ran-
domized trials but are supported by smaller studies and are intuitively reasonable. They may
assist in the clinical decision to institute pacing until more clear-cut guidelines are available.
Bundle Branch Block

The prevalence of bundle branch block (see Chapter 3) in asymptomatic individuals depends
on the population tested, but it is generally in the range of 0.1 % to 2%.4 Bundle branch block
may be an isolated abnormality or may be a marker of coexistent heart disease. Mortality is
most related to the accompanying heart disease and is not known to be increased in the other-
wise healthy individual. A key issue is potential progression to complete heart block, and this is
too infrequent and unpredictable to justify prophylactic pacing. 11,9
CHAPTER 11 • Electrocardiographic Abnormalities in Asymptomatic Individuals 257
Bifascicular block with or without prolongation ofthe PR interval would intuitively suggest more
severe conduction system abnormalities than simple bundle branch block. Nonetheless, the risk
of progression to complete heart block is in the range of 1% per year,10 arguably too low to justify
pacing in the asymptomatic individual Bifascicular block may indicate coexistent heart disease,
but the increased mortality in this group is generally not related to bradycardia and there is no
firm evidence that prophylactic pacing prolongs survival.5•11- 13 Electrophysiologic testing is gener-
ally not helpful in this context. A prolonged HV interval is frequently a marker of more extensive
disease but does not reliably predict progression to complete heart block.5
In summary, the finding of bundle branch block in an asymptomatic individual merits clinical
assessment to uncover potential associated heart disease but not prophylactic pacing.
TACHYARRHYTHMIAS
Atrial Ectopy and Supraventricular Tachycardia
The prevalence of atrial extrasystoles in normal populations may be as high as 3%4 by 12-lead
ECG and 50%2 or greater by 24-h ambulatory monitoring. Atrial ectopy may be a manifestation
of occult heart disease, pulmonary embolism, or thyrotoxicosis, but the ubiquity of the finding
in otherwise normal persons makes it very nonspecific. Treatment is not indicated. Nonsus-
tained supraventricular tachycardia (SVT) is also relatively common14 in normal populations
and similarly has poor specificity as a marker for occult disease.
Sustained SVT other than atrial fibrillation is rarely seen in the absence of symptoms. Interest-
ingly, some patients may have incessant SVT (Chapter 6) and be totally unaware of their rapid
heartbeaL This may lead to cardiomyopathy and congestive heart failure in some individuals.
The general strategy is to assess exercise tolerance and ventricular size and function. Patients
with impaired ventricular function should be treated, while those with normal ventricular
function may be followed carefully with serial assessment of ventricular performance.15
Atrial Fibrillation (AF)

AF is mentioned only briefly here for the sake of completeness as an important arrhythmia
whether the patient is symptomatic or not. AF is discussed extensively in Chapter 9. The indi-
vidual found to have AF as an incidental observation of course merits assessment to determine
the presence and extent of coexistent cardiac and medical disease, the need to restore sinus
rhythm or pursue rate control, and the advisability of anticoagulation.
Ventricular Ectopy and Tachycardia

Ventricular ectopy (see Chapters 2 and 8) is very common and may be found in 40% to 75%
of normal individuals, with complex ectopy in 5% to 10%.7 The only justification to treat an
asymptomatic individual is to improve survival. Consequently, treatment with antiarrhythmic
drugs should be preceded by a demonstration of increased mortality in the population in ques-
tion and proof that treating this group reduces mortality.
In the asymptomatic individual with minimal or no cardiac abnormality, the finding of ventricu-
lar ectopy or even ventricular tachycardia (VT) carries no demonstrable increased risk of sudden
death.16.17 Although LV function and associated heart disease are the main drivers of mortality,
frequent ectopy and nonsustained VT are associated with some increased risk of sudden death in
patients after acute myocardial infarction and those with dilated cardiomyopathy11-20 and proba-
bly any cardiac abnormality associated with severe left ventricular dysfunction.21-u This increased
risk appears to be additive to the contribution of left ventricular dysfunction. This information
has provided an intuitive rationale for the suppression of ectopic activity with antiarrhythmic
drugs in these individuals. The difficulties with this strategy are as follows:
1. Ventricular ectopic activity lacks specificity for identifying the potential victim of sudden
death. This subjects many individuals to the unnecessary cost, inconvenience, and potential
hazards of therapy.25
2. It is not c:lear whether ventricular ectopy causes sudden death or is merely a marktr for the
individual prone to have this complication by other mechanisms. Even ifventricular ectopy
is causative, it is not certain that elimination of ectopy is an adequate end point of therapy.
3. Finally, reduction of mortality with antiaJ.Thythmic drugs in the individual with ectopy has
not been demonstrated. Indeed, therapy with mexiletine26 in 1 trial was associated with a
trend toward increased mortality in the treated group while encainide and Becainide in the
Cardiac Arrhythmia Suppression Trial (CAST)27 and moricizine in CAST IP were associ-
ated with increased mortality compared with controls. This raises the possibility that proar-
rhythmia may be a dominant &ctor limiting the usefulness of the drugs tested to this date
in this context.
There are inadequate data to make definitive recommendations regarding antiarrhythmic ther-
apy in so-called high-risk patients with ventricular ectopy. Nonetheless, it would seem that
prophylactic antiarrhythmic therapy of these patients requires more spedftc identification of
the patient at risk for sudden death, perhaps using multiple clinical and laboratory variables
in addition to promising indicators provided by signal averaging techniques or programmed
electrical stimulation. Finally, it must be demonstrated that antiarrhythmic therapy directed at
the suppression of ectopy improves survival. Specific drugs and sped& end points remain to
be identified to this day.
It is also appreciated that very frequent (generally at least 5% of total heart beats) ventricular
ectopy may result in deterioration of ventricular function and even result in heart &ilure in prone
individuals.29.1° Thus. the finding of high-frequency ventricular ectopy merits further study that
includes at least ECG even in an asymptomatic individual without known heart disease.
ARRHYTHMIAS DURING SLEEP31.l2

Sleep is associated with vagal predominance. Sinus arrhythmia is frequent; sinus bradycardia
to <40/min and sinus pauses >2 or 3 seconds are not unusual in normal individuals during
sleep (Figure 11-1). Similarly, atrioventricular Wenckebach is relatively common and may be
FIGURE 11·1 • A long sinus pause In the context of a relative sinus bradycardla during sleep. This finding In the otherwise-well
~ptornatic individual is not an indication f'or pacing.
considered physiologic. It is arguable that virtually no bradycardia in an asymptomatic indi-

vidual exclusively or predominately during sleep should be acted upon in the majority of indi-
viduals. Ventricular arrhythmias are not a predominant feature during sleep in either normal
individuals or patients with ischemic heart disease.
The sleep apnea syndrome33·34. is characterized by hypoventilation, somnolence, and possibly

cor pulmonale with occurrence of obstructive apnea during sleep. It is also observed in heart
failure. Sleep apnea may result in extreme bradycardia, ventricular ectopic activity, or atrial
fibrillation. A high index of suspicion for sleep apnea is always warranted even with asymp-
tomatic arrhythmias.
VENTRICULAR PREEXCITATION
Although preexcitation syndromes are extensively discussed in Chapter 7, it is reasonable to
briefly discuss here the approach taken if preexcitation is discovered incidentally as an asymp-
tomatic abnormally. A short PR interval in the absence of ventricular preexcitation is of no sig-
nificance in the asymptomatic individual and probably reflects part of the spectrum of normal
atrioventricular nodal physiology. On the other hand, the Wolff-Parkinson-White pattern is
associated albeit rarely with sudden death usually related to the occurrence of atrial fibrillation
with a rapid ventricular response over an accessory atrioventricular pathway (the so-called
Kent bundle). Patients resuscitated from ventricular fibrillation35 are invariably found to have
inducible atrial fibrillation with a rapid preexcited ventricular response and a shortest R-R
interval (SRR) between preexcited beats <250 ms. with the majority actually <220 ms.
The latter finding raises the possibility of screening asymptomatic subjects, most specifically
by elective induction of atrial fibrillation. Although other risk factors have been suggested, it
is fair to say that the key and most relevant risk is simply a sufficiently rapid rate during atrial
fibrillation. This would suggest that targeting the group at risk (SRR <250 ms) for prophylactic
therapy would be a reasonable strategy to prevent sudden death. There are some serious logistic
difficulties to this strategy.
First, the prevalence of the Wolff-Parkinson-White pattern is on the order of 0.1% to 0.3%
of the general population, providing a prevalence in the United States in the range of 0.5
to 1 million individuals. On the other hand, the incidence of sudden death in asymptomatic
individuals is exceedingly low, in the order of 1 per 1000 years of patient follow-up at the most
pessimistic estimate.36
Secondly, the prevalence of a rapid ventricular response (SRR <250) when atrial fibrillation is
induced in the asymptomatic individual is too high (approximately 20%-30%) to make this a
specific marker for targeting interventions.37 Testing with isoproterenol has never been vali-
dated since the original threshold values for sudden death risk were derived in a baseline state.
It would not be expected to be useful because it unfortunately brings many more asymptom-
atic patients into the 250 ms range and thus further reduces the poor specificity of this EP
marker.38-41 In other words, a high percentage of asymptomatic individuals are at theoretical
risk, but the occurrence of ventricular fibrillation as the first symptom in the asymptomatic
individual is rare and sporadic. Some natural history studies and those comparing cathe-
ter ablation with no treatment in asymptomatic WPW42...,. exaggerate the malignancy of the
disorder by using broader end points such as documentation of atrial fibrillation with a rapid
rate. However, a careful examination of these studies verifies the actually rarity of sudden death
in the truly asymptomatic subject.45
Thirdly, catheter ablation is dearly the treatment of choice in symptomatic individuals with
WPW.46 This has certainly reduced our threshold for similar therapy in the asymptomatic
individual. Nonetheless, complications still occur,46.47 and it is fair to say that potentially seri-
ous complications such as inadvertent AV block, cardiac tamponade, vascular complications,
etc., still occur in the range of 1%. Many electrophysiologists in the current era may in fact
not have had a great deal of experience with WPW ablation, especially in the septal region
where the risk of permanent AV block is a significant consideration. This must be added to
the equation.
These facts certainly make it difficult to recommend mass screening with a view to catheter
ablation in the general population as a broad health priority. Nonetheless, patients are found to
have WPW incidentally and this necessitates some risk assessment. Some individuals may wish
no investigation on being told the "odds" of future problems but many will wish to pursue some
investigation or at least be required to pursue some investigation (professional athlete, pilot,
etc.) even though the risk of ventricular fibrillation is very low.
Noninvasive testing may be helpful in approximating the ventricular response in the event of
atrial fibrillation. Perhaps the most useful is diligently looking for intermittent loss of the delta
wave4s.49 on ECGs. This makes intuitive sense since the loss of preexcitation suggests the acces-
sory pathway has a low margin of safety of conduction over the accessory pathway, much like
intermittent LBBB suggests that the left bundle is not entirely robust. The patient found to
have sudden or intermittent normalization of a prominent delta wave is at very low risk indeed
of a sufficiently rapid preexcited ventricular response AF to result in VF. There are reports of
patients with intermittent preexcitation subsequently presenting with atrial fibrillation with a
relatively rapid response, 50 but presentation with VF is rare. Intermittent loss of preexcitation
may be observed with multiple 12-lead ECGs, ambulatory ECG, or exercise testing. Patients
with dear intermittent preexcitation have infrequently been reported to present subsequently
with atrial fibrillation with a relatively rapid response (observed on at least 1 occasion by 2 of
the authors) and this may constitute a subset of patients with catecholamine responsiveness.
Nonetheless, there are very few (if any?) reported cases of such individuals subsequently pre-
senting with actual cardiac arrest.
From a technical point, caution should be exercised in diagnosing intermittent loss of preex-
citation in patients with minimal preexcitation, because apparent loss of the delta wave may
represent only a slight shift in ventricular fusion and not true block in the accessory pathway.
This is especially true with exercise testing where AV node conduction is enhanced with exer-
cise. Only loss of a dear delta wave with concomitant prolongation of the PR interval should be
considered as accessory pathway block (Figures 11-2 and 11-3). In addition, junctional rhythm
in a patient with WPW is expected to have no delta wave because most patients with WPW
have atrioventricular pathways and the junction, of course, is distal to the accessory pathway
input (Figure 11-4). A change in atrial rhythm may result in more or less preexcitation of the
fused beat and this should not be confused with intermittent block in the accessory pathway
(Figure 11-5).
CHAPTER 11 • Electrocardlographtc Abnormalities In Asymptomatic Individuals 261
FIGURE 11·2 • The upper ECG was initially recorded by the refefring physician. The lower tracing was recorded when he was
seen in consultation shoniy after. The initiill ECG is of course preexcited while the sea>nd is cleilrly nonnal. This suggests tnilt the
accessory pathway has a low margin of safetyfor conduction and thus suggesu a very low risk ofsudden death due to AF with
preexcltatlon.
Noninvasive pharmacologic: tests have also been proposed to approi:imate accessory pathway
refractoriness.si-ss This is based on the notion that the most robust short ERP pathways will
be relatively resistant to the blocking effects of a membrane active drug such as proc:ainamide.
Loss of preexcitation after intravenous proc:ainamide and other drugs has generally correlated
with a long refractory period of the accessory pathway and a slow ventricular response during
atrial fibrillation. In general, loss of preei:c:itation at lower doses appears to be most specific.
Although intuitively reasonable, this is not currently mainstream. A robust randomized clinical
trial with long-term outcomes has never been done to assess this strategy and is unlikcly to be
forthcoming.
The management of the asymptomatic individual with preexcltation still engenders some con-
troversy. Nonetheless, most should agree that some assessment is reasonable. The key factor
FIGURE 11-J • The 12-lead ECG showsanterograde preexcltatlon over a left lateral accessory pathway. The second, foul1tl,and
eighth cycles demon SUate block t:Ner me aCCe$SOry pathway (l.e~ preexcltatlon Is absent and the PR lnteMil has lengthened}.
in our view is a fair discussion with the patient without hyperbole or pressure balancing the
natural history of the abnormality against the risks of an electroph}15iological assessment and
ablative strategy. Individuals may then make informed choices based on their own specific
circumstances.54
INHERITED ARRHYTHMIA SYNDROMES

We have elected to group several of these under this heading, admittedly a little arbitrarily,
because of their commonalities. Their commonality lies in a genetic causality and a potential
for sudden death due to ventricular arrhythmia as their initial manifestation without any obvi-
ous structural abnormality.55 Virtually any cardiac disorder including coronary artery disease
and cardiomyopathy may present with sudden death but we will focus on long QT syndrome
(LQTS), Brugada syndrome, arrhythmogenic right ventricular cardiomyopathy (ARVC). early
repolarization, and c:atecb.olaminergic polymorphic ventricular tachycardia (CPVT). It is
appreciated that ARVC is in. reality a cardiomyopathy and indeed, Brugada syndrome is also
probably a localized cardiomyopathy, but both often manifest at least initially by arrhythmia
with no obvious myocardial disorder.
In this section, we will emphasize the first level of management of the asymptomatic in.dividual
found to have an ECG suggestive of 1 of these by serendipity. A more complete discussion of
these entities is in. Chapters 8 and 15. The ECGs may be "classical" but are frequently more
ambiguous. Once a diagnosis is established, risk stratification can be difficult because the prob-
ability of a fatal event still remains relatively very low while sensitive and specific risk factors
are not available. "Shotgun" genetic testing may create more problems than it solves because of
frequent variants of unknown significance and is best preceded by a phenotype diagnosis or
family screening after a proband with a genetic abnormality is uncovered.ss It is probably fair to
say also that such individuals are usually better served by specific dedicated clinics or at least by
individuals with a specitic interest and expertise in their management.5'
CHAPTER 11 • Electrocardlographtc Abnormalities In Asymptomatic lndlvlduals 263
FIGURE 11-4 • The upper 12~ead ECG shows preexc113tlon over a right accessory pathway. The lower ECG ls recorded from the
same Individual during a transient junctional rhythm. This Is now nonnal as would be expected In a patient with an atJloventrlcular
pathway and has no bearing on the anterogracle refractory properties of the accessory pathway.
LONG QT SYNDROME
........................................................................................................................................................
The fundamental feature of LQTS is a measured corrected QT interval of 450 ms (men) or
470 ms (women) either at rest or during signature states such as exercise, tachycardia, or brady-
cardia.s7'°' Notably, a normal QTc at baseline or at a single point in time does not preclude
LQTS. It is thought that borderline QTc in general carries lower risk and those above 500 ms
in particular carry more risk. Additionally; a QTc beyond the normal range is found in many
cardiac disease states in a hospitalized patient population and ma:y be of prognostic significance
but such patients are generally not considered as LQTS and rarely have a known culprit LQT
mutation. A patient is considered to have LQTS if the ECG repeatedly shows QTc 500 ms or
greater in the absence ofdrugs or conditions known to prolong QT or if there is an unequivocal
mutation known to cause QT.
N N B B l I~
1 .,... .) \ I .J l/ I/
2Smm/sec
1Omm/mV
I II\ /\
2 A ~"I / v v / \ ,/\
I
25 mm/sec
1Omm/mV
I I I
Bradyca.n:fia 15-Feb-2017 06:35:45 53BPM

FIGURE 11-5 • The latter part of this monitoring ttadng shows sinus rhythm with ob'lltous preexcltatlon.The tlrst 2 cycles how-
evet' show a nam:iwer QRS and are seemingly not preexctted. However, the ftrst 2 cycles show a rower atrlal rhythm, probably a cor-
onary sinus rhythm, and this would favor conductfon over the AV node over a right pathway. Close Inspection of ttie lower tracing
shows that preex:clt!ltlon has not been lost. The degree of QRS fusion has merely shifted to more connlbutlon from the AV node
due to the site of supraventrlcular Input. This should not be Interpreted as Intermittent preexdtation.
Bizarre repolarization abnormalities may be seen with some gene mutations. Macroscopically
visible T wave altemans is not frequently seen but considered to indicate higher risk. Notched
Twaves may be seen with LQT2 but are ofcourse not specific. Sinus pauses may be seen in LQT3.
The presenting symptoms in LQT include cardiac arrest. "seizure,.. or sudden loss ofconscious-
ness. Note that palpitations are generally not a presenting symptom. Patients without symptoms
may be evaluated for an incidental finding on the ECG or during testing family members with
an affected proband. The discovery of a prolonged QTc is thus the portal of entry to this diag-
nosis and a few simple points relating to the measurement are worthy ofemphasis.60.41 Defining
the onset of the QT interval is not usually problematic but the termination is frequently more
ambiguous. The usual method is illustrated in Figure 11-6 where the downslope of the T wave
is extended to the baseline and the juncture is designated as the end of the T.
Measurement by inspecting the standard ECG in paper format at 25 mm/second can be very
inaccurate as a small measurement error can result in significant change in the QT interval. The
QT interval ideally is best measured on a larger screen, enlarging the ECG and expanding the
sweep speed as in Figure 11-7, using as many ECG leads as possible, preferably simultaneous.
ECG interpretation systems will often have multiple formats that are worth reviewing. One
of us (GJK) has found the "superimposed median" format in the MUSE system very useful in
judging the end of the QT, as demonstrated in Figure 11-8. The ECG computer will provide a
QT number that may or may not be accurate. This particular fonnat allows one to see where
the computer called the end of the T wave and allows the reader to visually validate and correct
accordingly. The value of this technique is shown in Figure 11-9 where the raw12-lead shows a
low-amplitude T wave with a wavy repolarization segment. causing some ambiguity in defining
I I
RR=793
I I
0Tc=405rns
\
\
\
\
(\ / \ '--
-
-1 "--
I --- ~
\
\
\
-- '-. ~
- V4
'·
0T=361
I I
FIGURE 11-6 • Traditional measurement of the QT Interval with the end of the QT designated as the Juncture of the downslope of
the T wave with the horizontal baseline.
the end of the T wave. The enlarged. simultaneous multiple-lead format provides more confi-
dence in one"s measurement and diagnosis.
There are provocative tests and drug challenges to diagnose LQTS, but the exercise stress test
is probably the most frequently used and useful diagnostic screening test61 The QT interval
! , . ..
! . . I• . '
..,,
- V1
-
1/
I I
I I
V4
-- V\
'"' ...-
!'\
-- h .
'
- - ,_, 7,... N- ,..__ ,_

t-
1--../"
1 ·-
,- '" '- ~
h.,: "- ~
\. ,...., uc
V2 vs
.
""- /' /\ r'l
I
- ~
- ~ /'-
- V3 V6 - 1--
I
FIGURE 11·7 • The 12-lead ECG Is enlarged and the frontil plane leads allowed to flll the entire screen. This enhanced •resolution•
results in more certainty for one's measurement
I II Ill
aVR aVL aVF
V1 V2 113
V4 V6 Ye
FIGURE 11-e • Superimposed median format for assessing QT end Is shown wtth the frontal leads summated on me left and
precordlals on the rtght. The blade fine Indicates wt.ere the computer shows the end of the QT Interval. The blue tine Indicates wt.ere
the reader has designated ttie end of the QT Interval by Inspection. In this partlcular Instance, the reader felt ttlat the computer
overestimated the QT Interval sllghdy.
Vt
II
vs
Panel A
FIGURE 11 "9 • Panel A. The raw 12-lead shows a flat.. undulating Twave especially in the frontal plane leads mmplicating measure-
ment ofthe QT Interval. Panel 8.The superimposed median format provtcles a venk:al llne to show wt.ere the computer select\!d
the end of me T wave. The fromal plane on the left shows no dear dellnea'don of the end ofthe Twave wt.lie the precordlal ECGs on
the right show a relative distinct end to the T wave Indicated by a blaclcvertkDItine. Vlsual Inspection of this suggests thatthe com-
putet' designation Is probably 10 to 20 ms longer than It should be, lead Ing one to correct the mmputer lntl!fpretatlon sllghtly In this
lnstllnce. Asmall undulatlon aftef the T wave meywell be Uwave also suggested In the raw 12-lead ECG.
I II Ill
aVR aVL aVF
V1 V2 \IS
V4 VS V8
Panel B
FIGUAE11-9 • (Continued)
shortens with exercise in normal individuals and the corrected QT remains more or less in
the normal range and this relationship is perturbed to some degree with LQTS. In LQTl in
particular, the QT may fail to shorten with increasing heart rate (Figure 11-10) during exercise
and hence the QTc continues to increase with advancing heart rate. This is easiest to appreciate
toward the beginning of exercise and right after recovery, in part because the tracings are free of
noise and the rates are not fast enough to obscure the end of the T wave.
Many LQT subtypes have been identified with genetic mutations identified for moste.u None-
theless, the 3 most common (probably>90%) are LQTl, LQT2, and LQT3, with the overwhelm-
ing majority LQTl (Figure 11-11). Stereotypically; most events will occur during exercise in
LQTl, at rest or with sudden loud noise in LQT2, and during rest or sleep in LQT3 although
there can be substantive overlap.
Risk stratification's,66 in the asymptomatic individual considered to have LQTS is difficult Cer-
tain genotypes such as mutations in the cytoplasmic loops of LQTl are considered to have
higher risk. Individuals with QTc >500 ms and especially >600 ms are considered at higher
risk. Management can also be challenging. There are obvious decisions to implant implantable
Ill
PllnelA
PllnelB
FIGURE 11-10 • Panel A. Although the Issue Is confounded a ltt:tle by RBBB and a prolonged QRS, the QT at rest appears to be
abnonnal and the QTc prolonged. Panel B. At a low worlcload of exercise, the heart rate Increases but the QT falls to shorten, further
lnaeaslng the QTc. This lndMdual had a genetically proven LQT1.
LQT1
ai~
II
LQT2
(~l1cr)
Iii .
FIGURE 11-11 • The 3 most ccmmon LQT subtypes with thelr"typlcal' ECG character1stlc:s and associated channel defect. There
Is probably considerable overlap and the ECG pattern ls better Interpreted as the "flrst approxlmaUon•to the LQT subtype. LQT1
resembles a normal T wave In general but with a longer QT. LQT2 Is associated with more undulating repolarizatlon pattern with
blfid, notched, or low-amplitude T waves. LQT3 ls typlcally associated with a lone lsoelectric segment
cardioverter-defibrillators (ICDs) in patients resuscitated from cardiac arrest or who have sei-
zures or syncope unresponsive to beta bloclctrs. Other than that, there is no such thing as zero
risk in the asymptomatic LQT patient and management is accordingly variable and individual-
ized. All are agreed on patient education emphasizing the importance of avoiding medications
that may trigger events such as ~blockers and diuretics. Fortunately. beta blockers are highly
effective in preventing arrhythmic events, especially in LQTI.67.68
~.~9.~T. qr..~.!.~ .~.~9.~J~~~~~.....................................................................................................

Short QT syndrome is diagnosed when the QTc is less than 330 ms. Patients with a QTc between
330 and 360 ms may be diagnosed as such with clinical symptoms (sudden death in absence of
other causes, VF, syncope suggestive of VT) or a pathogenic mutation. Cutoff values remain
somewhat controversial. Gain of function mutations have been found in potassium and calcium
channel genes. In part because ofits rarity, there is no meaningful risk stratification. There is no
suggestion of increased mortality in asymptomatic patients followed prospectively.
.~.~~.~~.~.~ .~!~.~~~.M~J~~.1. ~~.1.~ .~~.~.~~.~~.~I~.~~.~~~.~~)~.2:~.~-.~~·············································

The Brugada syndrome is inherited typically in an autosomal dominant fashion with multiple
responsible genes reported generally coding for sodium, calcium, or potassium currents. Genetic
abnormalities are found in the range of only 30% in patients with a positive phenotype and testing is
consequently most useful for screening family members when the proband has a known genotype.
It is characterized clinically by VF or polymorphous VT (often nocturnal), syncope, and sud-

den death. However, it is far more often suspected in an asymptomatic individual having ECGs
with a typical pattern or "suspicious" for the pattern, the great majority of whom will remain
asymptomatic.
The typical Brugada pattern is illustrated in Figure 11-12 (upper frame, type 1) and Figure 11-13,
namely 2 mm or more of convex ST elevation in leads VI or V2 occurring spontaneously or
with provocative drug testing with intravenous class 1 drugs such as ajmaline or procainamide.
Types 2 and 3 have a more concave "saddle back" ST elevation, type 3 of lesser elevation than
type 2. Such patients are considered to have the true Brugada syndrome only if type 1 pattern
is inducible by class 1 antiarrhythmic drugs or if it is seen at other times. Intermittency of the
pattern has been described and transitions from 1 type to another at different times can occur.
The pattern may attenuate or accentuate during exercise. The QRS in the right precordial leads
may be fragmented and late potentials may be observed on signal averaged ECG. First-degree
AV block, left axis deviation, atrial fibrillation, and LBBB type PVCs have been associated with
Brugada syndrome although these, of course, are not rare in the general population.
It is interesting that the positive ECG may be very regional and may only be seen in a single
lead. It is therefore useful to "explore" the right precordial area with additional leads or "high
leads" if an individual has a lead or 2 with suspicious type 2 or 3 pattern. This is exemplified
in Figure 11-14. The asymptomatic patient had the ECG taken for atypical chest pain. The
top panel shows Vl and V2 with relatively slight, hardly notable, ST elevation. Nonetheless,
the "high leads" just slightly superior to the normal Vl and V2 show a larger area of typical
Brugada 1 pattern. It is the practice of some clinics to perform high leads routinely in the
suspected individual, at least initially. Alternatively, 1 may proceed to intravenous class 1 drug
challenge6z.77 as typified in Figure 11-15 in another individual with a suspicious ECG.
Risk stratification in the asymptomatic individual is problematic after a diagnosis is made,

largely because the great majority of asymptomatic individuals will have a benign prognosis.78
Such individuals are generally advised to avoid drugs potentially increasing risk of an event,
a list of which can be found online (Brugadadrugs.org). The list is updated at intervals and
graded according to perceived risk. These individuals are also advised to avoid excessive alco-
hol intake and treat fever early on with antipyretic drugs. The use of EP testing to risk stratify
remains controversial. Counterintuitively, a family history of sudden death has not been shown
to be an independent predictor of increased risk.73
CATECHOLAMINERGIC POLYMORPHIC VENTRICULAR TACHYCARDIA (CPVT) 79.so

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is diagnosed in the individ-
ual with a normal heart and exercise-induced PVCs or VT or in the individual found to have
a pathogenic mutation as a result of family screening related to a clinically affected proband.
. r 1
•
A.
-
.....
.., Type1 -
-
,
'
-
. ' 1
'
\.
I ~
I' -- """ ... ,.

.,. ---
I
•
.- ,,,,, -
I
I"- r'\..
~
-
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w
---
Type2 ~
I
I I
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I
l
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I[
'I
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I
I
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--
r\..
... __._....
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-
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- -
-
-
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Type3
-
I I I I I I I I
FIGURE 11-12 • The 3 typlal pattemueen In Vl orV2.
The most common variety is autosomal dominant with the abnormality in the gene encoding
for the ryanodine receptor (RyR2}. Other genes and overlap syndromes are involved in an area
very much in evolution. The affected individual usually has a normal ECG at rest possibly
with PVCs but with increase in PVCs and VT observed during exercise or other catechola-
mine stress. Monomorphic VT, polymorphic VT, and VF can be observed but the characteristic
"bidirectionalD VT (Figures 11-16 and 11-17) is the hallmark of the syndrome. Bidirectional
PVCs and VT are not specific for CPVT, being seen in LQT7, digo:rin toxicity, other disease,
aVR
II aVL
i
Ill aVF
II
FIGURE 11-13 • Atyplcal Brugade 1 pattem In an asymptomatic patient who presented to en emergency department with atypl-
cal chest pain and was sent to the catft lab for Intervention. The coronary arteries were of course normal.
V4
aVL
aVF
PanelA
Panel B
FIGURE 11-14 • V2 in this individual (Panel A) was considet'ed to•resemble"a Brugada 2 pitttem andV1 a potential BNgada 1
pattet"n, with borderllne ST elevatlon. •High• precordlal leads are shown In Panel 8 and show unequtvcc:al type 1 BNgada pattem
In these leads. Such ECGs record lnterspaces dlrectly superior to the usual V1 and V2 leads to get a better coverage of the basal and
higher RV regions. In this tracing, V1 elecirode Is moved 2 lnterspaces superior to the usual V1 position (relabelled as V1 + 2 lntel'-
costal spaces [ICSD, V2 electrode Is moved 2 lnterspaces superior to the usual V2 position (relabelled es V2 + 2 ICS), V3 Is moved
1 ICS above the usual V1 position {relabelled as V1 +1 ICS), V4 electrode Is moved 1 ICS above the usual V2 position (relabelled as
V2 + 1 ICS), VS electrode is moved to the usual Vl position and V6 electrode is moved to the usual V2 position.
272
PllnelA Panel B
FIGURE 11-15 • Panel A shows an arguable Brugada type 2 pattem In lead V2. Panel B shows the unequivocal transformation to
a type 1 pattern after Intravenous procalnamlde.
FIGURE 11-16 • The ECG shows a classical bldlrectlonal tachycardia In a patient with cllnlcal CPVT.
FIGURE 11·17 • Bldlrecttonal couplets In an asymptematlc lndMdual subsequently diagnosed as CPVT.
or overtly normal individuals. Exercise-related atrial arrhythmias and atrial fibrillation also
accompany with some frequency.
The issue from the context of an asymptomatic individual arises when such an individual is
found to have bidirectional PVCs as an incidental finding during general screening or related to
another context. Patients with heart disease and frequent ventricular ectopy will also be found
to have bidirectional PVCs. Clearly, the finding in itself is not specific.
CPVT will rarely be diagnosed in an asymptomatic individual with only bidirectional eaopy
or very brief runs of VT but it is reasonable to screen further with exercise testing or Holter
monitoring Oooking for escalation of ventricular arrhythmia related to heart rate increase) if
there is clinical suspicion.
8 17
EARLY REPOLARIZATION (J WAVE) SYNDROMES ,..
..................................................................................................................................................
Early repolarization (ER) "'pattern" is diagnosed by expert consensus as elevation of the Jpoint
~ 1 in ~ contiguous inferior or lateral leads of the 12-lead ECG. The ER "syndrome" on the
other hand requires the pattern to be associated with otherwise unexplained VF or polymor-
phic VT. It is thought to be related to increased dispersion of refractoriness between epi and
endocardium and is considered to have similar electrophysiology to the Osborn wave associ-
ated with hypothermia. The pattern has clearly been associated with idiopathic VF and sudden
death as exemplified in the patient relating to Figure• ll-18 and 11-19.
The pattern is associated with an increase in mortality in some studies and is seen disproportion-
ately frequently in patients with unexplained VF. Nonetheless, similar patterns are observed in
FIGURE 11-18 • Ayoung man Investigated for cardiac arrest of unknown etiology with no evidence of heart disease. J waves are
present most notably in the lateral precordial leads.
the range of 1%-1396 ofthe general population with higher prevalence in children. men. athletes,
African Americans, and Southeast Asians. It is thus clear that the ECG pattern in asymptomatic
individuals is very common and is highly nonspecific (Figura 11-20 and 11-21).
A horizontal or descending ST segment after the Jpoint elevation is less frequent and has been
suggested to carry a worse outcome. Greater ST elevation or higher amplitude Jwave are more
likely to be associated with VF but the absolute increment in risk is far too small to be prac-
tically useful Genetic testing is not useful in asymptomatic individuals since the inheritance
science of the syndrome is at early stages of understanding. Unfortunately. useful risk strati-
fication is not possible at this point and the great majority of individuals with this syndrome
should be merely reassured with only a rare minority investigated further on the basis of some
clinical suspicion.
ARRHYTHMOGENIC CARDIOMYOPATHY (ARVC) ,aa 65

...................................................................................................................................................................................................................................................................
Arrhythmogenic cardiomyopathy (ARVC, ARVD) is an inherited cardiomyopathy predomi-
nately but not exclusively affecting the right ventricle with a clinical presentation that is dom-
inated by the potential for ventricular arrhythmias and sudden death. There is variability in
pathophysiology, presentation, and prognosis in this "famiJ:Y' ofdisorders depending largely on
the specific genetic abnormality or abnormalities. In an asymptomatic individual, suspicion is
FIGURE 11-19 • Spontaneous cardiac arrest In the patient of Figure 11-18 heralded by rise In amplltude of the J waves.
~ l~ i-RH-fFh i.aVR q-ii - 1~ 1:+ I;t.-r 1 ~ ~ff- If_ f V4 ··-

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FIGURE 11-20 • An asymptomatic lndlvfdual without he.art disease showing J waves on a routine ECG, arguablyveryslmllarto
l"""I" -!:...--µ.:; I' - --i---
the patient with the cardiac arrest of Agure 11-19.

raised when LBBB type ventricular arrhythmia is observed or when QRS and ST abnormalities
are present over the anterior precordial leads. specifically V 1 to V3.
The signal averaged ECG (SAECG) (Figure 11-22) available on some ECG carts allows con-
siderable amplification of the QRS while filtering out the attendant noise by eliminating non-
recurring signals (namely artifact) to reveal late potentials. ie.• low-voltage signals after the
termination of the QRS.89 This can be thought of as equivalent to the epsilon waves detected
electrocardiographically; essentially late potentials that are the representation of slow conduc-
tion to an abnormal area of muscle with low voltage. The detection of at least 1 criterion for
late potentials has excellent sensitivity for ARVC (69%) while maintaining specificity (95%).89
I I<, ! I I
1
,_ 111 _ _,__f-+:;-+-
; ~··1-'"-+=j=-r-
~ __,_,a1 ,..v...F-+-...;-.-1 1,_.!-f":'"c. ;1"'1,:,,
-1" H-+--+vpf f-+-i--+-.-ll+,-+--l-ii-..~v8 _ ,_ ·-- ~!=+''"-+-+
" i-1-f-+11 .
~ ~- I I +
r
A I
·- 1_._ "- . I -1-

I I I I ' I I I I I ·· I I I 1 I' • I I I I'
FIGURE 11-21 • Another asymptomatic indMdual with what could be called J waves of smaller amplitude but wider distribution.
Analysis Fitter: 40-250 Hz Number of Beets Averaged : 205

Std. QRS Duration (unftltered) : 120 ms Number of Beets Detected : 239
Total QRS Duratlon(ftltered) : 149 ms Noise Level (Std. Deviation) : 0.27 uV
Duration of HFLA signals <40 uV : 82 ms
RMS Voltage In terminal 40 ms 8 uV
Mean Voltage In terminal 40 ms : 6 uV
A
1000mmlmV
0~
01· Hz 100 uV
20 m
x
1+I ----1,.;vJ__
y :-W---
z
90
80
70
~ ~~ = 30
20
I,~ ~
40-250
10
1000m I I
~ 0
VM
FIGURE 11·ll • Signal aveJaged ECG of a pa'dentwtth ARVC as recortied by a standard ECG cart The late potential ls In solid black.
All 3 parametef's are abnorma~ I.e. to~I QRS duration (>110 rnsec}, duration of the high-frequency, low-amplitude sign al {>38 msec),
and root mean square (RMS) volttlge of the tefmlnal 40 msec (< 2011}.
The ECG parameters included in the 2010 task force document"' include:
1. Inverted T waves in precordial leads Vl, V2, and V3(Figura11-23and11-24) in individuals
>14 years of age in the absence of complete right bundle branch block. (Major criterion)
2. Inverted T waves in leads Vl and V2inindividuals>14 years of age in the absence of com-
plete right bundle branch block. (Minor criterion)
3. Inverted T waves in leads Vl, V2, and V3 in individuals >14 years of age in the presence of
complete right bundle branch block. (Minor criterion)
4. Epsilon waves, i.e., reproducible low-amplitude signals situated between the end of the
QRS and the onset of the T wave in leads Vl to V3 (Figures 11-25and11-26). (Major
criterion)
S. Terminal activation duration of QRS (TAD) :<!:55 mssio (Figure 11-24) measured from the
nadir of the S wave to the end of the QRS in precordial leads Vl to V3 in the absence of
complete right bundle branch block. (Minor criterion)
6. Nonsustained or sustained VT ofleft bundle branch block morphology with superior access
bracket (major criterion) or inferior axis (minor criterion).
7. Greater than 500 ventricular atrasystoles ofleft bundle branch block type over 24 hours of
monitoring. (Minor criterion)
8. A late potential (Figure 11-22) by signal averaged ECG (minor criterion) by at least 1 of 3
criteria including: 1. filtered QRS duration greater than or equal to 114 rnsec, 2. duration of
terminal QRS less than 40 11V :<!:38 msec, 3. root mean square voltage of terminal 40 msec
S20 µV.
FIGURE 11 ·21 • Twelve-lead ECG in an individual with AP.VC. Three f'eatures compatible with ARVC are present induding a PVC
wfth LBBB morphology, T-wave lnve~lon In the right precordlal leads, and an abnonnalVl, V2 morphologywtth prolonged terml-
nal activation delay. The lattef ls better appreciated In the enlargement of the right pn:!cordlal leads In the next figure.
FIGURE 11-24 • Enlarged V1, V2 leads from the ECG of Figure 11-23.The tefmlnal activation delay or"TAD" measured from the
nadir of the S wave to the end of the ORS is 70 msec {normal :SSS msec). In addition, the ORS is "fractured•and quite abnormat
virtuauy•split.•
AvR
2 Avl
3 AvF
, ... u,.... ,.
FIGURE 11-15 • Very abnonnal ECG In a young man wtth severe ARVC and recurrent VT. The QRS has low voltage throughout.
There Is a very large term Ina I acttvatlon seen wldely In ttie right precordlal le.ads separated from the terminal QRS by a small
lsoelectrlc component, by definition an epsilon wave. Technlcally speaking, late activation within the tefmlnal QRS Is not an epsllon
wave by definition although both are related to the same pathophyslology, namely late activation of abnormal muscle.
FIGURE 11-26 • Twave lnwfsion over right precordlal leads In another lndMdual wtth ARVC wltti a more sub1fe epsllon wave
(arrow). V3 is also abnormal showing a split ORS.
Allhough not spedflc:ally listed in the table ofthe task force document, a fractionated or "fractured"
QRS in Vl-V3 is frequently cited as suggestive of ARVC. This would include multiple spikes of
variable voltage included Jn the QRS in lieu ofa •clean" rS complex ofnormal duration. In addition,
more than 1 type ofLBBB PVC or VT suggests ARVC.'1
The issue of ARVC is frequently raised Jn patients with outflow tract PVCs. 92.9' Idiopathic PVCs
(Figure 11-27) are statistically considerably more probable than those related to ARVC in gen-
eral but a normal ECG otherwise (absence of T inversion, epsilon waves, or fractured QRS) fur-
ther favors the diagnosis of idiopathic PVCs. ARVC is unlikely in a completely normal 12-lead
ECG with no signal in the family history of ARVC. Even patients with genetically proven ARVC
but with a relatively normal ECG have a relatively benign prognosis."
.. " ' t '~· ' •t • ., • • f' ""!• • •!• t ~
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1 .... l'!ll ·.• I
. 1111 , 1111 1111 ; :~'ii. :1 1 1 1

: . 1 :11 ••1! Ii 1
::11: . .:' 11t ~·1:
1
n·1rn ·w:1·::1 t ... 1<1', tr:t..::· ·~ :'.!' ' ! , . 1 1- :1 ..: :.:~:::!~ rs: ] 1-1 1
• •, :1 11'1-·;v
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I
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r:i:- .•-
.'I. ,I I !I
i .i:f i '.,f ~~ ' ~:tt'! · fr l ~jl:''' ' J: ·- rl1 ... · ..:, -f.i-:·, ;-: 4:tt '!::, , @f.'=! 'I •I •':Ii :l
I;:; ., ,.;; .- ~ ;t · 11T:,. · : 0
, ~~ .... ~!Ji ·u ·, ·v ·· 1i • 1 .
1
L
.: .1! ~ 1 • ::·~Ji::t - Ii' .. · : 8!hi ... ;;..''-[J ':;.-, ,t. · ~f :i!H:'f:t·l· ·::!J::· ·•. ~~ l:lJ: ! !! ; ..~ I : , ., ...
J; j:-f.P IJ.:l: ' 'i:.:1: . : :=l!i I 'it ::"U:U ' ~ .·: .. "'' " . : i ..l d: It::". '........ ,_ ·- iffi - " : :: : II i II ·~ l"'"'I~
FIGURE 11-27 • ECG from a young woman, totally asymptomatic, with frequent PVC of LBBB morphology. There was no
slgnal In the family of unexpected sudden death and the ECG was normal. Notably, the PVC has high voltage and Is relatlvely
narrow and the remainder of the ECG has none of the features suggesting ARVC. This Individual would be very unllkely to
haveARVC.
COMMENTARY
Uncovering a disease process in a preclinical stage is laudable and is indeed a cardinal goal of
the physician. There are abnormalities that clearly merit definite action and those that clearly
don't but the majority in between the obvious require clinical judgment. No clinician wants
to miss an important harbinger of trouble. Nonetheless, the great majority of individuals with
asymptomatic ECG issues deviating from the majority will not be affected by them and label-
ling a patient with a disorder creates needless anxiety, further investigation, and therapies.
One is unlikely to improve the symptomatic status of an asymptomatic individual and any
intervention must be made with the intent of preventing impending morbidity or mortality.
There should be reasonable evidence in the literature to support both impending harm as well
as a reasonable expectation that therapy will improve this. Because both these criteria are rarely
met, a conservative noninterventional approach is often appropriate.
REFERENCES
1. Rubenstein JJ, Schulman CL, Yurchak PM, Desanctis Rw. Clinical spectrum of the sick sinus syndrome. Circulation.
1972;46(1):5-13.
2. Brod.ky M, WuD, Dene. P, Kanakis C, Rosen KM. Arrhythmias documented by 24 hour continuous electrocardio-
graphic monitoring in 50 male medical students without apparent heart disease. Am J Cardiol. 1977;39(3 ):390-395.
3. Epstein AE, DiMarco JP, Ellenbogen KA, et al ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of
Cardiac Rhythm Abnormalities: Executive Summary: A Report of the American College of Cardiology/American
Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHAJNASPE 2002
Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices) Developed in Collabo-
ration With the American Association for Thoracic Surgery and Society of Thoracic Surgeons. /Am Coll Cardiol.
2008;51(21):2085-2105. doi:l0.1016/j.jacc.2008.02.033
4. Barrett PA, Thomas Peter C, Swan HJC, Singh BN, Mandel WJ. The frequency and prognostic significance of
electrocardiographic abnormalities in clinically normal individuals. Prog Cardiowuc Dis. 1981;23(4):299-319.
doi:l0.1016/0033-0620(81)90018-9
5. Surawicz B. Prognosis of patients with chronic bifascicular block. Circulation. 1979;60(1):40-42. doi:l0.1161/01.
CIR.60.1.40
6. Dewey RC, Capeless MA, Levy AM. Use of ambulatory electrocardiographic monitoring to identify high.-
risk patients with congenital complete heart block. N Engl J Med. 1987;316(14):835-839. doi:l0.1056/
NEJM198704023161403
7. Michaelsson M, Riesenfeld T, Jonzon A. Natural history of congenital complete atrioventricular block. PACE.
1997;20(8):2098-2101. doi: 1O.l l l l/j.1540-8159.1997.tb03636.x
8. Rotman M, Triebwasser JH. A clinical and follow-up study of right and left bundle branch block. Circulation.
1975;51(3):477-484. doi:l0.1161/01.cir.51.3.477
9. Fisch GR, Zipes DP, Fisch C. Bundle branch block and sudden death. Prog Cardiowuc Dis. 1980;23(3):187-224.
doi:l0.1016/0033-0620(80)90021-3
10. Dhingra RC, Wyndham C, Bauernfeind R, et al. Significance of chronic bifascicular block without apparent
organic heart disease. Circulation. 1979;60(1):33-39. doi:l0.1161/01.cir.60.1.33
11. McAnulty JH, Rahimtoola SH, Murphy ES, et al. A prospective study of sudden death in ~high-rislc" bundle-
branch block. N Engl JMed. 1978;299(5):209-215. doi:l0.1056/NEJM197808032990501
12. McAnulty JH, Rahimtoola SH, Murphy E, et al. Natural history of"high-risk" bundle-branch block: final report of
a prospective study. N Engl JMed. 1982;307(3):137-143. doi:10.1056/NEJM198207153070301
13. Peters RW. Scheinman MM, Modin C, O'Young J, Somelofski CA, Mies C. Prophylactic permanent pacemakers for
patients with chronic bundle branch block. Am JMed. 1979;66(6):978-985.
14. Clarke J, Shelton JR, Venning GR, Hamer J, Taylor S. The rhythm of the normal human heart. Lancet.
1976;308(7984) :508-512.
15. O'Neill BJ, Klein GJ, Guiraudon GM, et al. Results ofoperative therapy in the permanent form of junctional recip-
rocating tachycardia. Am J Cardiol. 1989;63(15): 1074-1079.
16. Morganroth J, Horowitz LN. Antiarrhythmic drug therapy 1988: for whom, how and where? Am J Cardiol.
1988;62(7):461-465.
17. Kennedy HL, Underhill SJ. Frequent or complex ventricular ectopy in apparently healthy subjects: a clinical study
of25 cases. Am J CardioL 1976;38(2):141-148.
18. Ikegawa T, Chino M, Hasegawa H, et al. Prognostic significance of24-hour ambulatory electrocardiographic mon-
itoring in patients with dilative cardiomyopathy: a prospective study. Clin Cardiol. 1987;10(2):78-82.
19. Meinertz T, Hofmann T, Kasper W, et al Significance of ventricular arrhythmias in idiopathic dilated cardiomyo-
pathy. Am J Cardiol. 1984;53(7):902-907.
20. Maron BJ, Savage DD, Wolfson JK, Epstein SE. Prognostic significance of24 hour ambulatory electrocardiographic
monitoring in patients with hypertrophic cardiomyopathy: a prospective study. Am J Cardiol. 1981;48(2):252-257.
21. Buxton AE, Marchlinski FE, Waxman HL, Flores BT, Cassidy DM, Josephson ME. Prognostic factors in nonsus-
tained ventricular tachycardia. Am J Cardiol. 1984;53(9): 1275-1279.
22. Rubennan W, Weinblatt E, Frank CW, Goldberg JD, Shapiro S. Repeated 1 hour electrocardiographic monitoring
of survivors of myocardial infarction at 6 month intervllls: arrhythmia detection and relation to prognosis. Am J
Cardiol.1981;47(6):1197-1204.
23. Bigger Jr JT, Fleiss JL, Rolnitzky LM, Groupab TMP-Ill. Prevalence, characteristics and significance of ventricular
tachycardia detected by 24-hour continuous electrocardiographic recordings in the late hospital phase of acute
myocardial infarction. Am J CardioL 1986;58(13):1151-1160.
24. Kostis JB, Byington R, Friedman LM, Goldstein S, Furberg C, Group BS. Prognostic significance of ventricular
ectopic activity in survivors of acute myocardial infarction. JAm Coll Cardiol. 1987;10(2):231-242.
25. Brugada P, Wellens HJJ. Arrhythmogenesis of antiarrhythmic drugs. Am J Cardiol. 1988;61(13):1108-1111.
doi: 10.1O16/0002-9149(88)90136-1
26. Group IR. International mexiletine and placebo antiarrhythmic coronary trial: I. Report on arrhythmia and other
findings. JAm Coll Cardiol. 1984;4(6):1148-1163.
27. Echt DS, Llebson PR, Mitchell LB, et al. Mortality and morbidity in patients receiving encainid.e, flecainid.e, or
placebo: the Cardiac Arrhythmia Suppression Trial N Engl J Med. 1991;324(12):781-788.
28. Investigators• CAST!. Effect of the antiarrhythmic agent moricizine on survival after myocardial infarction.
N Engl] Med.1992;327(4):227-233.
29. Yokokawa M, Kim HM, Good E, et al. Relation of symptoms and symptom duration to premature ventricular
complex-induced cardiomyopathy. Heart Rhythm. 2012;9(1):92-95.
30. Taieb JM, Maury P, Shah D, et al Reversal of dilated cardiomyopathy by the elimination of frequent left or right
premature ventricular contractions. J Interv Card Electrophysiol. 2007;20(1-2):9-13.
31. LowN B, 'fykocinski M, Garfein A, Brooks P. Sleep and ventricular premature beats. Circulation. 1973;48(4):
691-701.
32. Gillis RA, Raines A, Evans DE, Levitt B, Standaert FG. Sleep and ventricular premature beats. Circulation.
1974;50(4):863-864.
33. Guilleminault C, Connolly SJ, Winkle RA. Cardiac arrhythmia and conduction disturbances during sleep in 400
patients with sleep apnea syndrome. Am J Cardiol. 1983;52(5):490-494.
34. Miller WP. Cardiac arrhythmias and conduction disturbances in the sleep apnea syndrome: prevalence and signif-
icance. Am JMed. 1982;73(3):317-321.
35. Klein GJ, Bashore TM, Sellers TD, Pritchett ELC, Smith WM, Gallagher JJ. Ventricular fibrillation in the
Wolff-Parkinson-White syndrome. N Engl JMed. 1979;301(20):1080-1085. doi:l0.1056/NEJM197911153012003
36. Klein GJ, Prystowsky EN, Yee R, Sharma AD, Laupacis A. Asymptomatic Wolff-Parkinson-White. Should we
intervene? Circulation. 1989;80(6):1902-1905.
37. Leitch Jw. Klein GJ, Yee R, Murdock C. Prognostic value of electrophysiology testing in asymptomatic patients
with Wolff-Parkinson-White pattern. Circulation. 1990;82(5):1718-1723.
38. Wellens HJ, Brugada P, Roy D, Weiss J, Bar Fw. Effect of isoproterenol on the anterograde refractory period of
the accessory pathway in patients with the Wolff-Parkinson-White syndrome. The American journal ofcardiology.
1982;50(1):180-184.
39. German LD, Gallagher JJ, Broughton A, Guarnieri T, Trantham JL. Effects of exercise and isoproterenol during
atrial fibrillation in patients with Wolff-Parkinson-White syndrome. Am J Cardiol. 1983;51(7):1203-1206.
40. Yamamoto T, Yeh S-J, Lin F-C, Wu D. Effects ofisoproterenol on accessory pathway conduction in intermittent or
concealed Wolff-Parkinson-White syndrome. Am J Cardiol. 1990;65(22):1438-1442.
41. Szabo TS, Klein GJ, Sharma AD, Yee R, Milstein S. Usefulness of isoproterenol during atrial fibrillation in evalua-
tion of asymptomatic Wolff-Parkinson-White pattern. Am J Cardiol. 1989;63(3): 187-192.
42. Pappone C, Santinelli V, Rosanio S, et al Usefulness of invasive electrophysiologic testing to stratify the risk of
arrhythmic events in asymptomatic patients with Wolff-Parkinson-White pattern: results from a large prospective
long-tenn follow-up study./ Am Coll Cardiol. 2003;41(2):239-244. doi:l0.1016/S0735-1097(02)02706-7
43. Santinelli V, Radinovic A, Manguso F, et al. The natural history of asymptomatic ventricular pre-excitation: a
long-term prospective follow-up study of 184 asymptomatic children. I Am Coll Cardiol. 2009;53(3):275-280.
doi:l0.1016/j.jacc.2008.09.037
44. Santinelli V, Radinovic A, Manguso F, et al. Asymptomatic ventricular preexcitation. Cire Arrhythm Blectrophysiol.
2009;2(2):102-107. do!: 10.1161/CffiCEP.108.827550
45. Klein GJ, Gula LJ, Krahn AD, Skanes AC, Yee R. WPW Pattern in the asymptomatic individual. Gire Arrhythm
Blectrophysiol. 2009;2(2):97-99. doi:l0.1161/CIRCEP.109.859827
46. Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS guideline for the management of adult patients
with supraventricular tachycardia: a report of the American College of Cardiology/American Heart Association
Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. I Am Coll Cardiol. 2016;67(13):
e27-e115.
47. Hindri.cks G. The Multicentre European Radiofrcquency Survey (MERFS): complications of radiofrequency cath-
eter ablation of arrhythmias. Bur Heart]. 1993;14(12):1644-1653. doi:l0.1093/eurheartj/14.12.1644
48. Klein GJ, Gulamhusein SS. Intermittent preexcitation in the Wolff-Parkinson-White syndrome. Am I Cardiol.
1983;52(3):292-296. doi:l0.1016/0002-9149(83)90125-x
49. Brugada J, Keegan R. Asymptomatic ventricular preexcitation: between sudden cardiac death and catheter
ablation. Arrhythm BlectTophysiol Rev. November 2017. https://www.aerjournal.com/articles/asymptomatic-
ventricular-pre-excitation. Accessed June 27, 2019.
50. Gemma LW, Steinberg LA, Prystowsky EN, Padanilam BJ. Development of rapid preexcited ventricular response
to atrial fibrillation in a patient with intermittent preexcitation. J Cardiovasc BlectrophysioL 2013;24(3):347-350.
51. Wellens HJJ, Braat S, Brugada P, Gorgds APM, Bar FW. Use of procainamide in patients with the Wolff-Parkinson-
White syndrome to disclose a short refractory period of the accessory pathway. Am I CardioL l 982;50(5):1087-1089.
doi:l0.1016/0002-9149(82)90422-2
52. Fananapazir L, Packer DL, German LD, et al. Procainamide infusion test: inability to identify patients with
Wolff-Parkinson-White syndrome who are potentially at risk of sudden death. Circulation. l 988;77(6):1291-1296.
doi:l 0.1161/0 l.CIR.77.6.1291
53. Boahene KA, Klein GJ, Sharma AD, Yee R, Fujimura 0. Value of a revised procainamide test in the Wolff-Parkinson-
White syndrome. Am J Cardiol. 1990;65(3):195-200. doi: 10.1016/0002-9149(90)90084-E
54. Cohen MI, Triedman JK, Cannon BC, et al. PACES/HRS Expert Consensus Statement on the Management of
the Asymptomatic Young Patient with a Wolff-Parkinson-White (WPW, Ventricular Preexcitation) Electrocar-
diographic Pattern: Devdoped in partnership between the Pediatric and Congenital Blectrophysiology Society
(PACES) and the Heart Rhythm Society (HRS). Endorsed by the governing bodies of PACES, HRS, the American
College of Cardiology Foundation (ACCF), the American Heart Association (AHA), the American Academy
of Pediatrics (AAP), and the Canadian Heart Rhythm Society (CHRS). Heart Rhythm. 2012;9(6):1006-1024.
doi:l0.1016/j.hrthm.2012.03.050
55. Ackerman MJ, Priori SG, Willems S, et al. HRS/EHRA expert consensus statement on the state of genetic testing
for the channdopathies and cardiomyopathies: this document was devdoped as a partnership between the Heart
Rhythm Society (HRS) and the European Heart Rhythm Association (EHRA). Buropace. 2011;13(8):1077-1109.
56. Ahmad F, McNally EM, Ackerman MJ, et al Establishment of specialized clinical cardiovascular genetics pro-
grams: recognizing the need and meeting standards: a scientific statement from the American Heart Association.
Gire Genom Pncis Meli. 2019;12(6):e000054. doi:l0.1161/HCG.0000000000000054
57. Schartz P, Crotti L. Long and short QT syndromes. In: Cardiac Electrophysiology: From Cell to Bedside. 6th ed.
Philaddphia: ELSEVIER, Saunders; 2014:935-947.
58. Schwartz PJ, Crotti L, Insolia R. Long QT syndrome: from genetics to management. Gire Arrhythm Blectrophysiol.
2012;5(4):868-877. do!: 10.1161/CffiCEP.111.962019
59. Shah SR, Park K, Alweis R. Long QT syndrome: a comprehensive review of the literature and current evidence.
Curr Probl Cardiol. 2019;44(3):92-106. doi:10.1016/j.cpcardiol2018.04.002
60. Wong JA, Gula LJ, Klein GJ, Yee R, Skanes AC, Krahn AD. Utility of treadmill testing in identification and geno-
type prediction in long-QT syndrome. Gire Arrhythm Blectrophysiol. 2010;3(2):120-125.
61. Viskin S, Rosovski U, Sands AJ, et al Inaccurate dectrocardiographic interpretation oflong QT: the majority of
physicians cannot recognize a long QT when they see one. Heart Rhythm. 2005;2(6):569-574.
62. Obeyesekere MN, Klein GJ, Modi S, et al How to perform and interpret provocative testing for the diagnosis
of Brugada syndrome, long-QT syndrome, and catecholaminergic polymorphic ventricular tachycardia. Gire
Arrhythm Electrophysiol. 2011 ;4(6):958-964. doi: 10.1161/CIRCEP.111.965947
63. Itoh H, Crotti L, Aiba T, et al. The genetics underlying acquired long QT syndrome: impact for genetic screening.
Bur Heart J. 2016;37(18):1456-1464. doi:10.1093/eurheartj/ehv695
64. Roden DM, Thompson KA, Hoffman BF, Woosley RL. Clinical features and basic mechanisms of quinidine-
induced arrhythmias. I Am Coll Cardiol. 1986;8{1 Suppl A):73A-78A.
65. Towbin JA, McKenna WJ, Abrams DJ, et al 2019 HRS expert consensus statement on evaluation, risk stratification,
and management of arrhythmogenic cardiomyopathy. Heart Rhythm. May 2019. doi:l0.1016/j.hrthm.2019.05.007
66. Priori SG, Schwartz PJ, Napolitano C, et al. Risk Stratification in the long-QT syndrome. N Engl I Med.
2003;348(19):1866-1874. doi:l0.1056/NEJMoa022147
67. Wilde AAM, Acki:rman MJ. Beta-blocki:rs in the treatment of congenital long QT syndrome: is one beta-blocki:r
superior to another? I Am Coll Cardiol. 2014;64(13):1359-1361. doi:l0.1016/j.jacc.2014.06.1192
68. Vmcent GM, Schwartz PJ, Denjoy I, et al. High efficacy of ~-Blocki:rs in long-QT syndrome type 1. Circulation.
2009;119(2):215-221. doi:l0.1161/CIRCULATIONAHA.108.772533
69. Giustetto C, Di Monte F, Wolpert C, et al. Short QT syndrome: clinical findings and diagnostic-therapeutic: impli-
cations. Bur Heart]. 2006;27(20):2440-2447. doi:10.1093/eurheartj/ehl185
70. Gollob MH, Redpath CJ, Roberts JD. The short QT syndrome: proposed diagnostic: criteria. I Am Coll Cardiol.
2011;57(7):802-812. doi: 10.1016/j.jac:c:.2010.09.048
71. Patel Chinmay, Yan Gan-Xin, Antzelevitch Charles. Short QT syndrome: from bench to bedside. Circ Arrhythm
Electrophysiol. 2010;3{4):401-408. doi:l0.1161/CIRCEP.109.921056
72. Rudie: B, Schimpf R, Borggrefe M. Short QT syndrome - review of diagnosis and treatment. May 2014. https:I/
www.aerjoumal.com/articles/short-qt-syndrome-review. Accessed June 29, 2019.
73. Priori SG, Napolitano C, Gasparini M, et al Natural history of Brugada syndrome. Circulation. 2002;105(11):
1342-1347. doi:10.1161/hc:ll02.105288
74. Priori SG, Wilde AA, Horie M, et al. HRS/EHRA/APHRS expert consensus statement on the diagnosis and man-
agement of patients with inherited primary arrhythmia syndromes: document endorsed by HRS, EHRA. and
APHRS in May 2013 and by ACCF, AHA, PACES, and AEPC in June 2013. Heart Rhythm. 2013;10( 12): 1932-1963.
75. Antzelevitch C, Brugada P, Borggrefe M, et al. Brugada syndrome: report of the Second Consensus Conference.
Circulation. 2005; 111(5):659-670. doi:l0.1161/0l.Cm.oooo152479.54298.51
76. Berne P, Brugada J. Brugada syndrome 2012. Circulation. 2012; advpub. doi:l0.1253/cirtj.CJ-12-0717
77. Wolpert C, Echternach C, Veltmann C, et al Intravenous drug challenge using flec:ainide and ajmaline in patients
with Brugada syndrome. Hearl Rhythm. 2005;2{3):254-260. doi: 10.1016/j.hrthm.2004.11.025
78. Takenaka S. Kusano KF, Hisamatsu K, et al Relatively benign clinic:al course in asymptomatic: patients with Brugada-
type electrocardiogram without family history of sudden death. I Cardiovasc Electrophysiol. 2001;12(1 ):2-6.
doi:l0.1046/j.1540-8167.2001.00002.x
79. Sy RW, Gollob MH, Klein GJ, et al. Arrhythmia characterization and long-term outcomes in catecholaminergic
polymorphic ventricular tachycardia. Hearl Rhythm. 2011;8{6):864-871. doi:l0.1016/j.hrthm.2011.01.048
80. Napolitano C, Priori SG. Diagnosis and treatment of catecholaminergic: polymorphic ventricular tachycardia.
Heart Rhythm. 2007;4{5):675-678. doi:l0.1016/j.hrthm.2006.12.048
81. H.aissaguerre M, Derval N, Sacher F, et al. Sudden cardiac: arrest associated with early repolarization. N Engl JMed.
2008;358(19):2016-2023.
82. Macfarlane PW, Antzelevitch C, Haissaguerre M, et al. The early repolarization pattern: a consensus paper. I Am
Coll Cardiol. 2015;66(4):470-477.
83. Noseworthy PA, Tikkanen JT, Porthan K. et al. The early repolarization pattern in the general population: clinical
correlates and heritability./ Am Coll Ciirdiol. 2011;57(22):2284-2289.
84. Tildcanen JT, Anttonen 0, Junttila MJ, et al. Long-term outcome associated with early repolarization on elec:troc:ar-
diography. N Engl I Med. 2009;361(26):2529-2537.
85. Haruta D, Matsuo K, Tsuneto A, et al Incidence and prognostic: value of early repolarization pattern in the 12-lead
electrocardiogram. Circulation. 2011;123(25):2931-2937.
86. Wu S-H, Lin X-X, Cheng Y-J, Qiang C-C, Zhang J. Early repolarization pattern and risk for arrhythmia death: a
meta-analysis. I Am Coll Cardiol. 2013;61(6):645-650.
87. Klatsky AL, Oehm R, Cooper RA, Udaltsova N, Armstrong MA. The early repolarization normal variant electro-
cardiogram: correlates and consequences. Am I Metl. 2003;115{3): 171-177.
88. Marcus FL McKenna WJ, Sherrill D, et al Diagnosis of arrhythmogenic: right ventricular cardi.omyopathy/dyspla&ia.
Circulation. 2010;121(13):1533-1541. doi:l0.1161/CIRCULATIONAHA.108.840827
89. Karnath GS, Zareba W, Delaney J, et al Value of the signal-averaged electrocardiogram in arrhythmogenic: right
ventric:ular c:ardiomyopathy/dysplasia. Heart Rhythm. 2011;8(2):256-262.
90. Nasir K. Bo=a C, Tandri H, et al. Elec:trocardiographic features of arrhythmogenic: right ventricular dysplasia/
cardiomyopathy according to disease severity: a need to broaden diagnostic: criteria. Circulation. 2004;110(12):
1527-1534.
91. Cox MG, Nelen MR, Wilde AA, et al. Activation delay and VT parameters in arrhythmogenic right ventricu-
lar dysplasia/cardiomyopathy: toward improvement of diagnostic ECG criteria. I Cardio'Vasc Electrophysiol. 2008;
19(8):775-781.
92. Ainsworth CD, Skanes AC, Klein GJ, Gula LJ, Yee R, Krahn AD. Differentiating arrhythmogenic right ventricular
cardiomyopathy from right ventricular outflow tract ventricular tachycardia using multilead QRS duration and
axis. Heart Rhythm. 2006;3(4):416-423. doi:l0.1016/j.hrthm.2005.12.024
93. Ren L, Jia Y, Liu Z, et al differentiating arrhythmogenic right ventricular cardiomyopathy from right ventricular
outflow tract ventricular tachycardia with electrocardiographic indexes. Cardiology. 2013;123:85.
94. Bhonsale A, James CA, Tichnell C, et al. Risk stratification in arrhythmogenic right ventricular dysplasia/
cardiomyopathy-associated desmosomal mutation carriers. Circ A"hythm Electrophysiol. 2013;6(3):569-578.
doi:l O.l 161/CIRCEP.113.000233
Narrow QRS Tachycardia
George J. Klein, MD
The supraventricular tachycardias are classified by mechanism in Chapters 6 and 7, where the
specific entities are discussed in more detail This chapter is intended to provide a pract:U:al
diagnostic and therapeutic approach to the patient presenting with supraventricular tachycar-
dia of unknown mechanism. It will become evident that simple steps can narrow the diagnostic
possibilities and suggest appropriate therapy in most patients.M
DEFINITION AND CLASSIFICATION4

Supraventricular tachycardia may be defined as tachycardia in which the "atrium or atrioven-
tricular junction above the bifurcation of the His bundle is the origin or a critical link in the
perpetuation of tachycardia:" The QRS morphology is normal or "'aberrant," the latter gener-
ally being functional right or left bundle branch block. A few notable caveats can be added
at this point Ventricular tachycardia can be relatively narrow depending on mechanism and
site of origin. One needs to be especially cautious when only 1 lead or a limited lead array
is available. Preexcited tachycardia related to atrioventricular pathways will not resemble
bundle branch block but will be indistinguishable from focal VT originating near either AV
ring. Pr~xcited tachycardia over an atriofascicular pathway will resemble relatively typical
left bundle branch block because these most frequently insert into the distal right bundle
branch region.
A classification based on mechanism as presented in Figure 12-1 is useful for cataloging and
discussing tachycardia, but it is not adequate when a supraventricular tachycardia of unknown
mechanism presents itself.
A useful working classification should be simple and helpful for guiding therapy. In our sug-
gested classification, all the supraventricular tachycardias can be placed into 1 of 2 categories
based on the requirement of the atrioventricular (AV) node for the perpetuation of tachycardia
(Figure 12-2). The tachycardia is ·;ndependent• ofthe AV nodewhen the arrhythmia "generator"
is above the level of the AV node. The AV node-independent tachycardias are not influenced
by AV block and comprise all forms of atrial tachycardia, including atrial reentrant tachycar-
dia, atrial flutter, and atrial fibrillation. With rare exceptions,5 continuation ofsupraventricular
tachycardia in the presence of AV block classifies the tachycardia as AV node-independent
PanalB
PanelC PanelD PanelE
FIGURE 1:Z-1 • Classification of supraventricular tachycardia by mechanism. Mechanisms include AV node reentry (Panel A), AV
reentry utilizing an accessory pathway (Panel BJ, nonparoxysmal junctional tachycardia (Panel 0), atrial tachycardia due to atrial
reentry or abnormal automatlclty (Panel Q, and nodoventrlcu lar reentry (Panel E).The latter Is uncommon but utlllzes a nodoven-
trlcular accessory pathway as part of the clrcult, usually the retrograde llmb, and may be lndlstlngulshable from typlcal AVN RT elec-
trocardiographical ly. Atrial tachycardia also includes rhythms such as atrial flutter and atrial fibrillation.
Panel A PanelB
FIGURE 1 :z-:z •
Classification based on the requirement or lack of requirement of the AV node in the tachycardia mechanism.
Panel A represents AV node-independent tachycardia such as atrial flutter, atrial fibrillation, or ectopic atrial tachycardia. Panel B
represents AV node-dependent tachycardia such as AV reentry using the AV node for anterograde conduction and an acces-
sory pathway for retrograde conduction (as Illustrated) or AV node reentry. AV node reentry (not shown) Is, of course, also AV
node-dependent.
CHAPTER 12 . Narrow QRS Tachycardia 289
nn -:-::: tlr" nc ::-:· :::: :::; ~:r: r::'. rr:: :""T' ·::r 1:::· ·;·· ..... •: ....:. ••• •q: -......, T!" ::: ::: •:•· "'' '.::1 .,_,_, ":' ·::· "'"!''. "!'. ~1:: •t:! '"!'' ':""!! ~rr 1'.!"! -:::· ~::: '"":!' •:•: :n• •r•• ~ .. , rnt ~· • "!I :::• ;:•• ::1: ~
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FIGURE 11·3 • AV node-Independent tach)'l:ardla later detennlned to be due to atria! reentry at efec:trophyslology study. Tachy-
cardia Is unaffected by transient AV block (verttcal bars Indicate P waves). The atrial activation Is high to low Indicated by positive
P waves In the Inferior leads, ruling out the possibility of AV node reentry with block below tile level of the AV node.
(Figure 12-3). On the other hand, the tachycardia is "dependent'" on the AV node when the
AV node is a critical component of the tachycardia mechanism... AV node-dependent tachy-
cardias include those due to AV node reentry or AV reentry utilizing an accessory pathway.
AV node-dependent tachycardias cannot continue in the presence of AV block. with a caveat.
One may observe AV block with continuation of tachycardia in AV node reentry; but, in these
instances, the AV block is usually below the level of the AV node, at or below the His bundle
(Figure 12-4).
Most supraventricular tachycardias can be readily classified into AV node-dependent or AV

node-independent. This can be done by vagal maneuvers such as carotid sinus massage but
is facilitated by intravenous adenosine that provides a brief but intense prolongation of AV
node conduction time and refractoriness that is usually diagnostic, creating AV block with
continuation of atrial tachycardia or tennination or lengthening in the PR interval for AV
node-dependent tachycardias. Some focal atrial tachycardias will respond to adenosine as
well but the time course of adenosine effect on the AV node vs. the tachycardia will usually
not be the same. For example, AV block or PR prolongation will often be observed prior to
slowing or termination of a focal tachycardia. Focal junctional tachycardia (JT) is uncom-
mon in adults especially and not as extensively studied, but slowing and termination may
be observed with adenosine. JT al.so typically restarts soon thereafter without an extra-
systole. It is probably seen in adults most frequently acutely after slow AV node pathway
ablation and resolves spontaneously in this instance. It may arguably also be classified as AV
node-dependent, appreciating that this would not encompass those junctional tachycardias
originating in the His bundle.
1() 11 12 13 14
II
V1
V6
HRAp l ~ H
HISp
H H
HIS:M
HISd
esp
CS7-S
CS5-6
CS:M
CSd
RVAp
FIGURE 12-4 • AV node reentry with blodt below the His recording. The beginning of the tracing shOW5 SVT with 2 Pwaves f'or
every ORS. The nonconducted P wave is almost exactly in the center of diastole, inverted in the infet'ior leads and relatively narTOW.
The lntraardl•c recordings demonstrate that every second P wave Is associated with block to the ventrlcles dlstal to ttie recorded
Hdeflection. The atrial electrograms have a central activation sequence with the electrograms close together reflecting central
activation that favors a more simultaneous depolarization of the right and left atria (reflected also by the relatively narrow retro-
grade P wave). APVC converts ttie SVT to a 1:1 Ato Vrelatlonshlp at about twice the ventricular rate of the lnlttal SVT. This event Is
undoubtedly related to concealed retrograde conduction by the PVC into the distil bundle branches and His bundle, effectively
preexciting the His bundle and allowing it a longer time to recover refractoriness for the next anterograde wave.
HISTORY AND PHYSICAL EXAMINATION

As with all tachycardias, the clinical assessment can provide clues to the tachycardia mecha-
nism. The AV node-dependent tachycardias, such as AV node or AV reentry, involve a tachy-
cardia substrate present from birth and are, in essence, congenital abnormalities. Accordingly,
a long history of paroxysmal (sudden in onset) tachycardia since childhood or early adult-
hood would suggest these latter mechanisms. On the other hand, AV node-independent
tachycardias-such as atrial flutter, atrial fibrillation, or atrial tachycardia-are probably
"acquired,. in the majority of patients and frequently associated with organic heart disease,
hypertension, and other comorbidities..s.7 For example, the occurrence of supraventricular
tachycardia in a 60-year-old man with chronic obstructive lung disease should suggest AV
node-independent tachycardia, such as atrial tluttet; rather than AV (accessory pathway) reentry.
The AV node-independent tachycardias, such as those due to intra atrial reentry. are also
more likely after AF ablation, with congenital heart disease such as atrial septa! defect or after
CHAPTER 12 • Narrow QRS Tachycardia 291
operative repair of congenital lesions. An exception may be Ebstein's anomaly, which is associ-
ated with a higher than expected frequency of Wolff-Parkinson-White syndrome.
Other clues can be obtained from the history, although it must be appreciated that they are falli-
ble. Perception of irregularity suggests atrial fibrillation. The converse is less helpful, since even
atrial fibrillation can be perceived as regular if sufficiently rapid. Regular constant neck pul-
sations, presumably due to simultaneous atrial and ventricular contraction, suggest AV node
reentry. Sudden termination with maneuvers such as Valsalva, quiet breathing, squatting, or
lying down suggest AV node dependence.
The physical examination during tachycardia or otherwise is usually not helpful. Findings
of cardiac dysfunction or pulmonary disease are more common with AV node-independent
tachycardia. The hemodynamic status of the patient depends on such factors as ventricular
function, tachycardia rate, and peripheral vascular resistance and gives little clue to the tachy-
cardia mechanism. Consequently, patients with SVT may have profound symptoms and syn-
cope while a patient with VT may have minimal symptoms. Of course, the physical findings
of AV dissociation (cannon A waves, variable S1, variable pulse pressure) overwhelmingly with
rare exceptions point to a diagnosis of ventricular tachycardia.
ELECTROCARDIOGRAPH IC DIAGNOSIS
A good-quality 12-lead electrocardiogram (ECG) with rhythm strip using the lead best show-
ing P waves is very helpful. Identification of P waves may be facilitated in several ways:
1. A careful comparison with a previous 12-lead ECG may help identify P waves buried in the
QRS complex or ST segment.
2. Nonstandard ECG leads such as the Lewis lead may identify P waves. For example, position-
ing the right-arm lead in the upper sternum and the left-arm lead in the lower sternum may
provide a larger-amplitude P wave.
3. Positioning an esophageal lead8-10 will usually provide a good atrial electrogram. This lead
may also be used for programmed atrial stimulation.
4. Atrial activity may also be recorded using signal-averaged electrocardiography,11 and atrial
mechanical activity may be identified using echocardiography. 12
There are several points of focus to aid diagnosis using the 12-lead ECG:
1. The P-wave morphology may provide an approximation to the atrial activation sequence
and suggest a site of origin of atrial activation.13 For example, a negatively oriented P wave in
lead 1 suggests activation from left atrium to right atrium. The latter can be related to only
2 possibilities, AV reentry utilizing a left lateral accessory pathway or left atrial tachycardia.
Negative P waves in the inferior leads 2, 3, and AVF suggest activation beginning in the pos-
terior right or left atrium at or near the coronary sinus orifice. Unfortunately, the P wave can
be obscured by ventricular depolarization and repolarization or of low amplitude making
this a technically difficult exercise in some individuals.14 Very narrow P waves may originate
in the anterior septum due to cancellation of forces.
2. By long-standing definition, an atrial rate of 250 cycles per minute or faster is atrial flutter.
More recently, some have reserved the term flutter for macro reentrant atrial tachycardia
regardless of rate. The latter definition of course is only applicable after a mechanistic diag-
nosis is available and verified by EP testing while the traditional definition using rate alone
has the advantage of applicability by ECG. A ventricular rate of 150 to 160/min should sug-
gest the possibility of atrial flutter with 2-to-1 AV block. Otherwise, there is too much over-
lap in ventricular rates observed with different mechanisms for rate alone to be useful in
distinguishing them.
3. A change in rate with transition from normal QRS to a bundle branch block pattern points
to AV reentry utilizing an accessory pathway. The latter observation obviously suggests that
1 of the bundle branches is part of the reentrant circuit, with block in that bundle branch
prolonging circuit size. The change in circuit size will usually also prolong or shorten the
AH interval so that the net tachycardia cycle length may be variously affected. Atrioventric-
ular or the considerably less common nodoventricular reentry are the only supraventricular
tachycardias that incorporate ventricular and His-Purkinje tissue in the circuit, potentially
resulting in changes to the circuit with bundle branch block ipsilateral to the accessory
pathway.
4. Aphasic alternation in QRS amplitude (QRS altemans) during stabilized tachycardia has
been suggested by some to support the diagnosis of AV reentry using an accessory pathway.15
Our experience and that of others 16 suggests that QRS alternans is probably a function of
a faster tachycardia rate and not of a specific mechanism. However, QRS cycle altemans, a
regular alternating long-short R-R interval due to PR interval change during tachycardia,
points to AV node dependence and usually AV reentry.
5. Observations during spontaneous tachycardia termination may be helpful (Figures 12-5
and 12-6). In Figure 12-6, tachycardia terminates, with the last event being a P wave. This
strongly suggests that the AV node is part of the reentrant circuit (AV node-dependent), as
in atrioventricular reentry. This can occur by chance in any SVT, so it is most diagnostic if
reproducible. AV node-independent tachycardia, such as atrial tachycardia, will not termi-
nate in this way, because AV block would have to occur fortuitously on the very last atrial
cycle of the tachycardia.
6. The AV relationship is very helpful if P waves can be identified. If atrial tachycardia persists
in the presence of AV block, the tachycardia can be classified as AV node-independent.
With AV node-dependent tachycardia and only in AV node-dependent tachycardia, the posi-

tion of the P wave relative to the QRS can be helpful (Figure 12-7).17 The presence of a P wave
simultaneous or nearly simultaneous with the QRS (P on QRS) favors the diagnosis of AV
node reentry. If the P wave is clearly past the QRS complex, with the RP interval less than the
PR interval, a diagnosis of atrioventricular reentry utilizing an accessory pathway is prob-
able (Figure 12-8). In a more infrequent type of tachycardia, with the RP greater than the PR
interval (PJRT type), the mechanism is frequently AV reentry utilizing an atypical accessory
pathway with a long conduction time as the retrograde limb of a circuit. However, the mech-
anism could also be atypical AV node reentry with the slow AV nodal pathway serving as the
retrograde limb of the circuit. It could also be atrial tachycardia where the RP interval is longer
than the PR interval. Thus, the term long RP is merely descriptive and mechanistically not dis-
criminating between atrial tachycardia, AV node reentry, and AV reentry.
It is worth reemphasizing that the above criteria apply only when AV node-independent tachy-
cardia has been ruled out, because the P wave can obviously be anywhere in the cardiac cycle
Panel A
PanelB
FIGURE 12·5 • Value ofspontaneous tennlniftlon In detennlnlng mechanism. TennInation with the last event being ventricular
depolarization (no retrograde P) can occur with either AV node-dependent or independent tachycardia {Panel Al. However, a>nsis-
tent tennination with the last event being atrial depolarization (Panel 8) invariably indicates AV node-dependent tachycardia.
...........................................
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FIGURE 12-6 • ECG record of a patient with spontaneous termination of a brief run ofSVT with a 1:1 relatlonshlp between atrium
and ventricle. The last event is a P wave. This finding, especially if consistent. is highly suggestive of AV node-dependent tachyar-
dia that stops when atrial activation is blocked from reaching the ventricle. That is, the AV node must be part of the circuit.
PaMIA
PaMIB
PanelC
FIGURE 12·7 • Value of P wave position within the cardiac cycle. The P wave can be anywhere In the cycle during AV node-
Independent tachycardia. depending on rile PR Interval. (Consequently, the followlng guldellnes are helpful only If the tachycardia Is
known to be AV node-dependent.) The PR Interval Is greater than the RP Interval with the usual type of AV reentry, with the P wave
following the QRS complex (Panel A). Thi5 relationship may be seen with atypical AV node reentry, but the presence of a P wave
within or marginally bef'cre or after the QRS (Panel 8) occurs with AV node reentry. The RP interval is longer than the PR in AV reen-
o-y utlllzlng an unusual accessory pathway wtth a long conduction time (Panel Cl and, less f~quently, wtth the uncommon type of
AV node reentry (fast~low). Note that atrial tachycardia with 1:1 AV conduction also usually has a PR Interval shorter than rile RP
Interval with variable P-wave morphology dependent on the site of the atrlal focus.
depending on the PR interval in the latter. For example, a P on QRS can occur with an atrial
tachycardia conducting over a slow AV node pathway.
ACUTE MANAGEMENT
After reviewing the ECG, the key step is to classify the tachycardia as AV node-dependent
or independent if this is not already apparent. Maneuvers that suddenly depress AV nodal
conduction will allow this distinction. Carotid sinus massage or pressure has been used
for many years for this purpose. 1'"20 Up to 5 s of steady right or left carotid sinus pressure
is applied after significant carotid disease has been excluded historically, by the absence
of decreased carotid pulses or bruits and probably most accurately with ultrasound. It is
important to reemphasize that aggressive carotid stimulation may result in stroke if the
FIGURE 12-9 • ECG ttace during tac:hycardfa. A P wave can be seen In the ST segment In most leads (a"ows). The PR Interval ls
greater than the RP interval. The P wave in the fA>ntal plane leads 1, :z, 3 indicates a P wave vector from left to right and low to high,
m0$t compatible wtth a left posterolateral accessory pathway. This patient had orthodromlc AV reentry but me tracing alone does
not rule out a left atrial tachycardia.
latter is not assessed. This vagotonic maneuver may be enhanced by pretreating the patient
with an anticholinesterase drug such as edrophonium (Tensilon) 5 to 10 mg intravenously.
Head-down tilt and the post strain phase of the Valsalva maneuver are also vagotonic and
beta blockade may potentiate the vaga1 maneuvers. The observation of persistent atrial
tachycardia with temporary AV block provides a diagnosis of AV node-independent tachy-
cardia (Figure 12-9). whereas slowing or abrupt termination of tachycardia indicates AV
node-dependent tachycardia.
A transient but intense negative dromotropic effect can also be readily achieved with. the puri-
nergic compound adenosine.11...is This intervention has probably replaced vagotonic maneu-
vers for most of us due to its speed of action, reliability, and relative safety. Adenosine will
almost invariably expose AV node-independent tachycardia by transient slowing of cycle
length. related to AV prolongation and will generally terminate AV node-dependent tachy-
cardia (Figure 12-10}. Some focal atrial tachycardias will also terminate with adenosine. This
is usually distinguishable from AV node-dependent tachycardias because the time course of
the AV node effect is slightly different from the effect on the focal tachycardia. A direct rela-
tionship with PR prolongation and prolongation of the tachycardia cycle length is specific for
AV node-dependence. The calcium antagonist diltiazem or verapamil can be used in a similar
fashion iftachycardia is recurrent after adenosine or adenosine is relatively contraindicated (as
with. history ofsignificant asthma) or ifthere is reasonable certainly that one is not dealing with
ischemic or cardiomyopathic VT.
y...- y... ...... y.. '\.r V" ~

V1
v v v v v
CSp
A A A
csd
I I I I I I I I I I I I I I II I I I I I I I
FIGURE 12-9 • Use of arotid sinus massage In supraventrlcular tachycardia. This lntracardlac record demonstrates the occurrence
of transient AV block during carotid massage without influencing the atrial tachycardia (by definition, AV node-independent). 1, 2,
V, are ECG leads; CSP and CS., are proximal and distal coronary sinuselectrograms, respectively.
At this point, the task is simplified. An AV node-dependent tachycardia will have been tenninated
and an AV node-independent tachycardia will still be present ('.lible 12-1). Acute treatment strat-
egy for AV node-independent tachycardia ofany mechanism involves 2 steps. The first is slowing
of the ventricular response with drugs directed at the AV node (digitalis. calcium antagonists. beta
blockers). This step alone will sometimes result in conversion to sinus rhythm, possibly by improv-
ing hemodynamies. With rate slowing, therapy with membrane-active medication such as inlra-
venous procainamide may be instituted in an attempt to restore sinus rhythm. Atrial tachycardia
and atrial flutter in particular may be difficult to rate control so that early use of membrane-active
drugs and especially c:ardioversion in these instances is reasonable. Oral instead of intravenous
medication may be considered if the tachycardia is well-tolerated and more rapid reversion to nor-
mal rhythm is not a priority. It is useful to remember that intravenous amiodarone26 behaves as
essentially an alpha and beta blocker acutely so that it will generally not be useful ifearly reversion
to normal rhythm is desired. However, it may be useful acutely as an AV node blocking agent to
slow ventricular rate in AV node-in.dependent tachycardia. especially if there is any concem about
depressed LV function.
Elective cardioversion is appropriate at any time in the event of significant hemodynamic

deterioration or treatment failure. In the latter circumstance. it may be reasonable to load the
patient with antiarrhythmic medication prior to cardioverslon to prevent subsequent relapse.
Anticoagulation guidelines as per patients with atrial fibrillation are applicable for atrial flutter
but generally not for other atrial tachycardias (see Chapter 9).
v,
FIGURE 12-10 • Use of adenoslne to terminate AV node-dependent tBchycardla (AV l'ffntry In tills case). Note that tBchycardla
terminates with an atrial electrogram that blocks In tile AV node, 1.e~ not followed by His activation. Observe that the AH prolongs
in the few cycles prior to termination causing proportionate prolongation of the cycle length and proving that the AVN is part of
the circuit This ls usually observed with adenoslne even Ifthe tachycardia does not break with the drug, at least proving the mech-
anism. This direct relationship between AH prolongation and the cycle length would not be observed even If adenoslne terminated
an atria! tachycardia. Note also that atrial activation ls'"eccentrlc"wlth tile distal CS atria! activity coming flrst Indicating a left lateral
accessory pathway. 1, V1 are ECG leads; CSP and CS4 are proximal and distal coronary sinus. respectlvely; HB ls His bundle electro-
gram; and RA ls right crtrlal electrogram.
APPROACH TO CH RON IC THERAPY

The first decision after termination of the acute episode is whether or not chronic therapy
is required. Chronic therapy is not essential if episodes are well-tolerated with minor symp-
toms, if they are infrequent. and if the patient has reasonable access to a medical facility. This
decision is informed by patient preference and their comfort zone with respect to leaving the
issue untreated at least for a period of time. Patients with manifest preex:citation need further
TABLE 12-1 Acute pharmacological treatment of supraventricular tachycardia.

AV node-independent
Slow venttlcular response (digit.alls, beta blockers, allclum antagonists).
Restore sinus rhythm with membrane-active antlarrhythmlc drug such as Intravenous procalnamlde.
AV node-dependent
In general, direct lnltlal therapy at the AV node {adenoslne usually ftrst-llne but calcium antagonists, beta
blocker, dlgltalls also feasible).
Membrane-active drugs (procalnamlde, amlodarone) generally used after fallure d Initial therapy. May be
useful in nonparoxy.smal junctional tachycardia as well.
Mechanism unknown
Treat as AV nod~lndependent
assessment as a considerable percentage have the potential for the occurrence of atrial fibrilla-
tion with a rapid ventricular response.27
CHOICE OF CHRONIC THERAPY

Catheter ablation is covered in more detail elsewhere in this book but it fair to say it has become
the treatment of preference for most patients with recurrent SVT of any mechanism, individ-
ual patient considerations notwithstanding. Ablation in experienced hands is highly successful
with minimal probability of a serious adverse effect in most circumstances.
Antiarrhythmic drugs are currently infrequently used and mainly offered to those who do not
wish to have catheter ablation, when catheter ablation is not preferred for individual consid-
erations, or if it is unavailable as a medical option in the region. However, in AF the decisions
are more complex. Antiarrhythmic drugs are generally prescribed empirically. Those that pro-
long refractoriness in the AV node (beta blockers, calcium channel blockers, rarely digitalis)
have traditionally been the initial choice, probably for their general record oflong-term safety
and reasonable efficacy. Membrane-active drugs such as flecainide, propafenone, more rarely
procainamide or disopyramide are used usually in combination with the above when needed.
Sotalol can be used alone since it has beta-adrenergic blocking activity. The goal of the latter
is prevention of atrial tachycardia or prolongation of refractoriness over an accessory path-
way when this is a therapeutic target such as in the patient with preexcited atrial fibrillation.
Amiodarone of course has excellent efficacy for most SVTs, but it is not considered a preferred
long-term strategy in most circumstances for reasons oflong-term adverse effects.
Nonpharmacologic approaches such as operative ablation and antitachycardia pacemakers

have generally passed into obsolescence in the era of catheter ablation.
COMMENTARY
It is usually not necessary to know the exact mechanism of supraventricular tachycardia in
order to move forward with a treatment strategy. However, the concept of dividing supraven-
tricular tachycardias into AV node-independent versus AV node-dependent types has merit
in that the distinction can usually be made without intracardiac recordings or sophisticated
equipment and the information is very helpful in planning ablation or drugs when required
(Table 12-1). This is probably a key take-home message in this section. Adenosine has simpli-
fied the acute management of SVTs and ablative therapy has arguably become the preferred
treatment for long-term management where the procedure is available.
REFERENCES
1. Klein GJ, Prystowsky EN. Clinical Electrophysiology Review. 2nd ed. New York: McGraw-Hill Medical; 2013.
2. Klein GJ. ECG and Intracardiac Tracings: A Toolkit Approach for Analyzing Arrhythmias. Cardiotext Publishing;
2018.
3. Klein GJ. Strategiesfor ECG Arrhythmia Diagnosis: Breaking down Complexity. Cardiotext Publishing; 2016.
4. Klein GJ, Sharma AD, Yee R, Guiraudon GM. Classification of supraventricular tachycardias. Am l Cardiol.
1987;60(6):27-31. doi:l0.1016/0002-9149(87)90705-3
5. Wellens HJ, Wesdorp JC, Duren DR, Lie Kl. Second degree block during reciprocal atrioventricular nodal
tachycardia. Circulation. 1976;53(4):595-599.
6. Wu D, Denes P, Amat-Y-Leon F, et al. Clinical, electrocardiographic and electrophysiologic observations in
patients with paroxysmal supraventricular tachycardia. Am J Cardiol. 1978;41 ( 6): 1045-1051.
CHAPTER 12 • Narrow QRS Tachycardia 299
7. Gillette PC. The mechanisms of supraventricular tachycardia in children. Circulation. 1976;54(1):133-139.

8. Gallagher JJ, Smith WM, Kasell J, Grant AO, Benson JR DW. Use of the esophageal lead in the diagnosis of mech-
anisms of reciprocating supraventricular tachycardia. Pacing Clin Electrophysiol. 1980;3{4):440-450.
9. Benditt DG, Pritchett EL, Smith WM, Gallagher JJ. Ventriculoatrial intervals: diagnostic use in paroxymial
supraventricular tachycardia. Ann Intern Med. 1979;91(2):161-166.
10. Prystowsky EN, Pritchett EL, Gallagher JJ. Origin of the atrial electrogram recorded from the esophagus. Circulation.
1980;61(5):1017-1023.
11. Kuchar DL, Kelly RP, Thorburn CW. High-frequency analysis of the surface electrocardiograms of patients with
supraventricular tachycardia: accurate identification of atrial activation and determination of the mechanism of
12. Ruckel A, Kasper W, Treese N, Henkel B, Pop T, Meinertz T. Atrioventricular dissociation detected by suprasternal
M-mode echocardiography: a clue to the diagnosis of ventricular tachycardia. Am l Cardiol. 1984;54(6):561-563.
13. Kuchar DL, Thorbum CW, Sammel NL, Garan H, Ruskin JN. Surface electrocardiographic manifestations of
tachyarrhythmias: clues to diagnosis and mechanism. Pacing Clin Electrophysiol. 1988;11{1):61-82.
14. Bir FW; Brugada P, Dassen WR, Wellens HJ. Differential diagnosis of tachycardia with narrow QRS complex
(shorter than 0.12 second). Am J Cardiol. 1984;54(6):555-560.
15. Green M, Heddle B, Dassen W, et al. Value of QRS alternation in determining the site of origin of narrow QRS
supraventricular tachycardia. In: Smeets JLRM, Doevendans PA, Josephson ME, Kirchhof Ch, Vos MA, eds. Profes-
sor Hein/./. Wellens: 33 Years of Cardiology and Arrhythmology. Dordrecht: Springer Netherlands; 2000:313-319.
doi:l0.1007 /978-94-011-4110-9_29
16. Morady F, DiCarlo LA, Baerman JM, Buitleir MD, Kou WH. Determinants of QRS altemans during narrow QRS
tachycardia. l Amer Coll Cardiol. 1987;9(3):489-499. doi:10.1016/S0735-1097{87)80040-2
17. Kay GN, Pressley JC, Packer DL, Pritchett EL, German LD, Gilbert MR. Value of the 12-lead electrocardiogram in
discriminating atrioventricular nodal reciprocating tachycardia from circus movement atrioventricular tachycar-
dia utilizing a retrograde accessory pathway. Am J CardioL 1987;59(4):296-300.
18. Waxman MB, Wald RW, Sharma AD, Huerta F, Cameron DA. Vagal techniques for termination of paroxymial
supraventricular tachycardia. Am J Cardiol. 1980;46(4):655-664. doi:l0.1016/0002-9149(80)90517-2
19. Waxman MB, Bonet JF, Finley JP, Wald RW. Effects of respiration and posture on paroxysmal supraventricular
20. WenZC, Chen SA, Tai CT, ChiangCE, Chiou CW, Chang MS. Electrophysiologicalmechanisms and determinants of
vagal maneuvers for termination of paroxymial supraventricular tachycardia. Circulation. 1998;98(24):2716-2723.
21. Chugh, A. Adenosine and atrial tachycardia. Circ Arrhythm ElectrophysioL 2016;9{8):e004449.
22. DiMarco JP, Sellers TD, Berne RM, West GA, Belardinelli L. Adenosine: electrophysiologic effects and therapeutic
use for terminating paroxysmal supraventricular tachycardia. Circulation. 1983;68(6):1254-1263.
23. Griffith MJ, Ward DE, Linker NJ, Camm AJ. Adenosine in the diagnosis of broad complex tachycardia. Lancet.
1988;331 (8587) :672-675.
24. McCabe JL, Adhar GC, Menegazzi JJ, Paris PM. Intravenous adenosine in the prehospital treatment of paroxysmal
supraventricular tachycardia. Ann Emerg Med. 1992;21(4):358-361.
25. Paul T, Pfammatter JP. Adenosine: an effective and safe antiarrhythmic drug in pediatrics. Pediatr Cardiol.
1997;18(2):118-126. doi:10.1007/s002469900129
26. Kowey PR. Marinchak RA, Rials SJ, Filart RA. Intravenous amiodarone. l Am Coll Cardiol. 1997;29(6):1190-1198.
27. Rinne C, Klein GJ, Sharma AD, Yee R, Milstein S, Rattes MF. Relation between clinical presentation
and induced arrhythmias in the Wolff-Parkinson-White syndrome. Am J Cardiol. 1987;60(7):576-579.
doi: 10.1016/0002-9149(87)90308-0
Wide QRS Tachycardia
George J. Klein, MD
Wide QRS tachycardia (WCT) is traditionally defined as tachycardia having QRS duration
greater than 120 ms, the upper limit of normal QRS duration.1 Tachycardia fitting this general
description may be broadly classified by mechanism into 3 groupsZ-1 as depicted in Figure 13-1
These include ventricular tachycardia (VT). supraventricular tachycardia (SVT) with aberra-
tion, and preexcited tachycardia. To these 3, it is useful to consider and rule out paced rhythm
(with rate response. trac.king of atrial rhythm, or pacemaker-mediated tachycardia) and arti-
factua1 tachycardia (Figure 13-2). which may at times look deceptively like VT. Finally, sinus
or supraventricular tachycardia with gross ST elevation may occasionally be mistaken for VT.
SVT may be defined for this discussion as any tachycardia utilizing the normal atrioventricu-
lar (AV) conduction system for ventricular excitation. with the tachycardia either originating
in the atria or AV node or requiring 1 of the latter structures for their perpetuation. These
tachycardias inc:lude AV node reentry. orthodromic atrioventricular reentry, atrial ilutter, atrial
fibrillation, sinoatrial node reentry, and atrial tachycardia.
Aberration of conduction or aberrancy has been variously defmedM but may be simply
defined as conduction delay or block in the His-Purkinje system during anterograde con-
duction of impulses over the normal AV conduction system. Conduction block may be fixed
or functional. A sudden acceleration of rate, as with the onset of SVT, is a frequent cause
of aberration of conduction that may be perpetuated by continuous concealed retrograde
conduction into the blocked pathway. Although any part of the His-Purkinje system may be
involved in this functional block, right bundle branch block and left bundle branch block
are by far the most frequent aberration pattems.s-t The term pruxcited tachycardia refers to
any tachycardia where the ventricles are activated anterogradely over an accessory pathway.
The accessory pathway may be a bystander to the tachycardia mechanism as in atrial fibril-
lation or a part of the circuit or mechanism as in antidromic tachycardia. The most common
preexc:ited tachycardia is atrial fibrillation with the ventricular response predominantly a
result of anterograde accessory pathway conduction. Other preex.dted tachycardias include
true antidromic tachycardia (anterograde conduction over an accessory AV pathway with
retrograde conduction over the normal AV conduction system) and tachycardias utiliz-
ing a second accessory pathway as the retrograde limb of a reentrant circuit. i.e., pathway-
to-pathway reentry.
Panel A PanelB
PanelC PanelD
FIGURE 13-1 • Depiction of wide QRS tachycardia by mechanism. The figure is self-explanatory although pseudo tachycardia
due to artefact Is not Included. Panel A represents VT, Panel B SVT with bundle branch block, Panel C preexclted tachycardia, and
Panel D paced rhythm.
Put more simply, the clinician confronted with a wide QRS tachycardia must decide whether
it is:
1. VT
2. SVT with aberrancy (usually functional right or left bundle branch block)
3. Preexcited tachycardia using an accessory AV pathway to activate the ventricles
4. Ventricular pacing
5. Artefact.
CLINICAL ASSESSMENT
The history may provide the most valuable clue to tachycardia diagnosis before the electro-
cardiogram (ECG) is even viewed. In general, individuals with preexcited tachycardias are
younger than those with VT, the latter usually being in the "'coronary prone" age group. Patients
with preexcited tachycardia or paroxysmal SVT with or without aberrancy will more frequently
provide a history of previous episodes, often dating back to childhood or early adulthood. A
history of heart disease and in particular previous myocardial infarction should initially lead to
a strong suspicion of VT, appreciating that such patients may also have the full gamut of wide
complex tachycardia (WCT).
It is often unappreciated that the hemodynamic status of the patient during tachycardia is not
helpful in clarifying the diagnosis. 8 Many are under the misconception that patients with VT
present in dire straits and patients with SVT are not hemodynamically compromised. In fact,
patients with VT may present with very little or no evidence of hemodynamic compromise
CHAPTER 13 • Wide QRS Tachycardia 303
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FIGURE 1!-2 • This wcr looks deceptlvely llke VT, whld'I was me reason for referral In this patient asymptOmattc at the time the
tracing was reco~ed. The clues to artefact Include the broad nonphyslologlcal signals ol:Mousty noise that usher the WCT In and
out and furthl!t' nonphyslologlcal behavfor such as seen In the second row, next to last amnvwflere a PVC llke complex precedes
the normal QRS at an apparent aiupllng Interval that defles reasonable ventricular refractoriness. It Is cllnched by the obseMltlon
that the nonnal QRS complexes (arrows) •march" through the WCT.
and, conversely, patients with SVT may present with severe hypotension. Determinants of the
patient's hemodynamic status are complicated and include the rate oftachycardia, left ventric-
ular function, peripheral vascular tone, and medication.
Physical examination may be valuable in elucidating the physical signs of AV dissociation. Atri-
oventricular dissociation, with infrequent exceptions, is diagnostic of VT. lt is present in many
if not most patients with VT and is even more prevalent with advancing age, heart disease, and
faster tachycardia rates. The findings are identical to those expected in complete AV block and
result from asynchronous activation of the atria and the ventricles. These include intermittent
cannon A waves in the jugular venous pulse, variable intensity of the first heart sound, and vari-
ability in the magnitude of the systolic blood pressure. These findings are ea.sily overloohd unless
the examiner specifically looks for them. Carotid sinus massage or more commonly used ade-
nosine accompanied by ECG monitoring will often be helpful With few exceptions (adenosine-
sensitive VT or AT). termination of a tachycardia after this maneuver suggests that the AV node
is a critical link in the tachycardia ~ntrant circuit Transient AV block may expose atrial flutter
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Panel A
PanelB
FIGURE 13-3 • Carotid massage in wide QRS tachycardia. Panel A demonstrates tachycardia with a notch in the ST segment, indicat-
ing atrial activity (arrow). The AV relationship is 1:1 and the mecnanism of tachycardia is not certain. Wrth carotid massage (Panel 8),
the Pwaves are transiently eliminated (asterisk) and the tachycardia Is not affected. The latter essentially seals the diagnosis of VT.
or atrial tachycardia. It may even be valuable in exposing ventricular tachycardia with VA con-
duction if transient retrograde VA block is observed with the maneuver (Figure 13-3).
ELECTROCARDIOGRAPH IC ASSESSMENT
A careful analysis of the 12-lead ECG and rhythm strips of reasonable quality (free of signifi-
cant noise) will provide a diagnosis to the experienced observer in the majority of instances.6.7•9
The following points are important in considering the ECG during tachycardia:
1. A previous 12-lead ECG, if available, should always be examined concurrently. If the tachy-
cardia has a bundle branch block pattern identical to that seen in sinus rhythm, the likely
diagnosis is SVT with bundle branch block. On the other hand, if a different QRS pattern
(either wider or narrower!) is present during tac.hycardia in a patient with ftud bundle
branch block, the diagnosis is invariably VT (Figure 13-4). In a patient with preexcitation,
a similar QRS pattern in sinus rhythm and tachycardia suggests a preexdted tachycardia.
2. AV dissociation is frequently present in patients with VT, and its incidence is greater in
older patients and those with faster VT. On the other hand. AV dissociation in AV nodal
I
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FIGURE 13-4 • Resting bundle branch block pattern with diffefent WCT. Panel Ashows atJlal fibrillation with RBBB. old lnf'erlor Ml.
Panel 8 now shows a regular tachycardia with a different QRS that suggests in itself VT. Jn addition, thl!fe is a l.888 type of QRS but
very atypical for LBBB, much more suggestive ofVT.
......... .. ..
" .... :- :::: ~·:: :::· :::: :: ::· ' ... :;:::
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FIGURE 13-:S • Wide QRS tachycardia. AV dissociation Is evident In multiple leads but clearly In the lead 2 rhythm strip (red arrows
lnd/aztePwavrs). In this example, a natable•fooler"ls the second small positive deflection In theQRS In lead 2.1.e. an R'llke deffec-
tion. This gives the appearance of a retrograde P. A useful exerdse ls what can be tenned defining the QRS bo<Jndorles. One draws a
line at the ORS onset as assessed by multiple leads and QRS termination. When one does this {blue dotted lines), it is apparent that
the second deflection is.within•thea.RS boundary and an unlikely P candidate.
reentry or other SVT is relatively rare. Thus, the presence of AV dissociation electrocar-
diographically in a WCT is generally diagnostic of VT (Figure 13-S). Atrioventrlcular dis-
sociation is often best seen in lead V1 but may be seen in any lead in a given individual.
The rhythm strip should be run using the lead in which P waves appear to be particularly
prominent. A Lewis lead may be helpful in amplifying P waves. This is a special ECG lead
oriented to optimize atrial depolarization. The right-arm electrode is positioned in the
right parasternal area near the base of the heart, using a suction electrode. The left-arm
electrode is generally in the fourth or fifth interspace, usually in the right or left parastemal
region but it can be moved until an identifiable P wave is observed. The ECG is recorded
in the lead I position. Although AV dissociation is a valuable finding. it is often difficult to
detect electrocardiographically.
3. Capture beats or fusion beats may be seen in the presence of AV dissociation when a dis-
sociated P wave totally (capture) or partially (fusion) activates the ventricle in advance of
the next VT cycle. This results in a "premature• beat during tachycardia that is of supraven-
tricular morphology and usually "narrow"' (Figure 13-6). Factors favoring the observation
of fusion beats and capture beats include slower VT rates with AV dissociation and good
anterograde conduction over the AV node. In addition, pseudo normalization may occur,
resulting in premature complexes of narrower QRS morphology than the dominant wide
FIGURE 1H • Wide QRS tachycardia. The ml a/TOWS Indicate 3 capture beats wld'I variable fusion depending on the relatlve tim-
ing of arrival of the capture beat to the tachycardia beat From left to right, ttiere Is relatlwfy less fusion as the capture beats arrive
progressively earlier and the QRS becomes more normal. Note the P wave In front of each capture beat. Ideally, It Is useful to see an
entirely normal beat and satisfy oneself that d'le fusion beat Is a n!asonable summation between the pure normal and pun! wide
QRSbeat
QRS morphology. For example, a ventricular ectopic from the opposite ventricle could
fuse with a VT complex resulting in a narrow QRS. Although frequently cited as "classic"
for VT, capture and fusion beats are seen relatively infrequently and may be difficult to
interpret.
4. A QRS width greater than 0.14 s has been observed to occur more frequently in VT than
SVT with aberration.6.1° This is not surprising, because the QRS duration in uncomplicated
right bundle branch block and left bundle branch block is usually less than or equal to
0.12 sand these are the most common aberration patterns. The QRS in VT secondary to
ischemic heart disease is usually wider than VT associated with no apparent heart disease.
Unfortunately; the QRS can obviously be prolonged greater than 0.14 s with aberrancy
during supraventricular rhythm in the presence of heart disease, preexcitation, and/or anti.-
arrhythmic drugs. For the above reasons, QRS duration in isolation is not terribly useful in
distinction between VT and SVT.
5. It has been observed that a mean QRS axis within the normal range favors a diagnosis of
SVT with aberration, while left axis deviation or right axis deviation favors a diagnosis of
VT. Certainly. extreme right axis or left axis deviation (northwest ws) is seldom seen in
instances other than VT.
RA _ _ _...,.__ _ _'lr-------'1...---~----'ll'----"~
v
HB
r.--fr
II I I I I I I I I I I I I I I I I I I
FIGURE 1S-7 • There Is an abrupt transition after a PVC from one WCT to another slightly faster one. The transition from one WCT
to another WCT with a different frontal axis Is suggestive of VT for both WCT all things being equal. In this Instance. the diagnosis Is
reinforced by A-V dissociation. In addition, the ventricular activation from the awllable lntracardlac tradngs shows preystollc ven-
tricular activation at the His channel, an impossibility for aberTaney at least for the initial WCT.
6. Slight irregularity in tachycardia cycle length may be seen with VT or SVT and is generally
not helpful in diagnosis. Of course. striking irregularity should suggest atrial fibrillation
with bundle branch block or conduction over an accessory pathway.
7. The rate of tachycardia in itself is of no value in distinguishing VT from SVT.
8. An abrupt change from 1 regular wide QRS morphology to another wide QRS morphology
is relatively infrequently seen in SVT and suggests VT with multiple morphologies as an
initial preswnptive diagnosis (Figure 13-7).
9. Identification ofisolated ectopic complexes during sinus rhythm identical to that observed
during the wide QRS tachycardia may be helpful in identifying the latter (Figure 13-8). If
an isolated ectopic complex is clearly a PVC, it is likdy that wide QRS tachycardia of the
same morphology is ventricular. This can be misleading with single-lead recordings.
10. Concordance of QRS complexes (Figure 13-9) in the precordial leads is rarely seen in
SVT with aberration and strongly supports a diagnosis of VT. Positive concordance (QRS
predominantly positive from V1 to V6) suggests a basal origin of VT while negative concor-
dance suggests an apical localization.'
11. Many ECG criteria have been proposed over the years to distinguish VT from SVT with
aberrancy.7,10-iz In distinguishing right bundle branch block aberration from VT resem-
bling right bundle branch block, a typical triphasic pattern in V1 favors aberrancy as does
a qRs complex in V6 (R greater than s). An rS or a QS complex in V6 favors a diagnosis of
VT. To distinguish left bundle branch block aberration from VT resembling left bundle
branch block, V1 may be helpful. With aberrancy, V1 generally has a small initial r wave
(less than 30 ms), with a steeply down-sloping S wave. When the initial r is greater than
30 ms in duration and the down slope of the S wave is broad and notched, a diagnosis
of VT is more likely. V6 is less helpful, but a qR or a QS complex favors VT. Many other
"sure fire" criteria have been published.
Panel A
Panel B
FIGURE 13-9 • Utility of Isolated ectopic beats In evaluation ofWCT. The tracing ls not continuous. It was recorded on telemetry
on a mediCill ward in an ambulatory patient and the quality is not excellent. Consequendy, a search for atrial activity during the
WCT is almost futile. On the other hand, the upper tracing shows an ectopic beat (Panel A) that is clearly a PVC which does not dis-
rupt atria! actMty. This PVC has ldentlc:al morphology to the WCT (Panel 8), making that hlghly llkelyto be VT.
ECG Criteria in Perspective

Are the above criteria an incomprehensible mass of empirical observations to be memo-
rized or can these criteria be logically understood? We have said that the most common
types of aberration are due to functional right bundle branch block or left bundle branch
block. Thus, it is apparent that right bundle branch block aberration should in general
have the characteristics of typical right bundle branch block1M 5 as described in standard
textbooks (Figure 13-lOA). The same obviously holds true for typical left bundle branch
block (Figure 13-lOB).
Ventricular tachycardia can be confused with bundle branch block only when the activation
pattern in VT results in a QRS complex that closely resembles right bundle branch block or left
bundle branch block. However, when VT mimics bundle branch block, the QRS pattern will
generally be atypical to varying degrees. This is rea11y the unifying concept that brings some ortkr
to the criteria listed above. That is, when a wide QRS tachycardia is absolutely typical ofa classic
T
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FIGURE 13-9 • WCT with •concon:tance"of preccrdlal leads. The QRS during this WCT Is relatlvely nal'l'O'N but wtth prominent posi-
tive concordance from V1 to VS. This pattern suggests origin of ventTlcular activation at the base of the LV, compatible only with VT
(as In this and most examples) or preexdtation. The VT terminates at end exposing sinus tachycardia, which has been"lsorhythmlc"
with the VT, l.e~ competing with It to become the manifest rhythm. This Is evident If one tracks the P waves back and sees a small
positive spike appearing variously throughout the tracing at the beginning of the WCT complexes.
right bundle (or left bundle) branch block pattern (Flgure 13-11) it is logic.al that it is more
likely to be a true right bundle (or left bundle) branch pattern. (See also Chapter 8.)
Conversely, the more atypical the bundle branch block pattern, the more likely the tachycardia
is to be ventricular. W1um we use the above QRS criteria, we are essentially saying that a very
typical bundk branch b'lock pattern is indeed more Ukely to be SVT with bundle branch block and
a very atypical one is more Ulcdy to be VT masquerading as bundk branch block (Figure 13-12).
An understanding of this principle immediately makes it possible to appreciate the limitations

of these generally very useful criteria. Anti.arrhythmic drugs and organic heart disease can dis-
tort the QRS complex and result in atypical bundle branch block patterns even in the presence
of svr with aberration. It is thus intuitively obvious that the criteria would be most helpful
when the underlying QRS in sinus rhythm is nonnal Second, VT originating near the bundle
branch system or incorporating the bundle branch system may more closely resemble typical
bundle branch block patterns and thus be mistaken for SVT with aberration. Finally, preexcited
tachycardias involve direct ventricular activation over an accessory AV pathway that bypasses
the normal AV conduction system. Ventricular depolarization would then be expected to be
identical to a focal vr originating at a site near the distal insertion of the accessory pathway. It
is thus obvious that preexclted tachycardia can never be distinguished from focal VT near the
base ofthe heart by morphological criteria unless one knows that the patient has Wolff-Parkinson-
White syndrome (Figure 13-13).
Panel A
PanelB
FIGURE 13·10 • Typical right bundle branch block CRBBB) (Panel A) and left bundle branch block (LBBB) (Panel B).In LBBB,
V, characterlstlcally has a small to tiny rand a deep S with a very rapid, aim cm vertical down slope. In RBBB, V, typically Is trfphaslc,
with the lnltlal Rof lesser amplitude than the subsequent R1• V6 has a terminals that Is widened and scooped with less amplltude
than the Initial R. Memorizing these•typ1ca1• patterns facilitates comparing them to the unknown WCT and asking tfle question,
•How closely does the unknown resemble a 'typical' 88 block patternr
~/YYYYYYY~F
FIGURE 13·11 • LBBB type WCT. The WCT has a very typlcal LBBB pattern making It most probable that It l.s SVT with LBBB aber-
rancy, which this was. A typical LBBB morphology .should also raise the pos.sibility of 88 reentry or preexcited tach)'Cilrdia over
an atriofascicular pathway, both of which can be associated with eartiest ventricular activation at the distal RBB region. Atermi-
nal deflection well seen In lead 2 suggests retrograde atrial activation although atrtal tachYC:ardla wtth a long PR lnteMI Is not
excluded without further evidence.
. -1+--·-- -
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FIGURE 13-12 • This WCT has LBBB type morphology but direct comparison (espedally of the anterior prec:ordlal leads) to true
LBBB In Agure 13-1 QB makes It clear that It would be very atypical for LBBB aberrancy. AV dissociation ls readily dear In V1 In this
indMdual (a"ows) although the diagnosis could be made with reasonable confidence from the ORS aiteria alone.
312
Panel A
'' I 11 I 'I
I l
Panela
FIGURE 13-13 • The WCT of Panel A has positive concordance across the precordlal leads, most compatible with an LV basal origin
of ventTlcular depolariZBtlon.This would be campatlble with a VT focus or a left accessory atrloventricular pathway. A spontaneous
termination is st!E!n in Panel B. The last tachycardia QRS is not f'ollowed by a Pwave now evident (atTOWS). VT is thus reasonably
ruled out. as tflis would involve the unlikely coincidence ofVT tennin;rting with concurrent VA block on the last VT cycle. On tfle
other hand, the termination is compatible with anticlromic AVFrr (which this was) or preexcited atrial tachycardia.
ANCILLARY INVESTIGATIONS
Although the history, physical examination, and 12-lead ECG should provide a diagnosis in the
majority ofinstances, it is worth remembering a few points that could be helpful in difficult cases.
The presence of AV dissociation results in a beat-by-beat variability of chamber size, ejection
times, and hemodynamics. Consequently; the presence or absence of AV dissociation is generally
readily evident on an echocardiogram {Figure 13-14). The variation in mitral valve opening time
in particular is usually striking in the presence of AV dissociation. The M mode shows these
clearly for illustration16-18 but there are many ways to appreciate AV dissociation by echocardiog-
raphy in general. The proliferation of point-of-care ultrasound makes this relatively available. It is
perhaps even easier to appreciate AV dissociation by echo than ECG in many instances.
Esophageal ECG can be done with routinely available equipment including an ECG cart, alli-
gator connectors, and a pacing lead. 19 A bipolar permanent pacing lead is especially suitable
for this purpose and can be advanced through the nares into the esophagus as far as it will
go. The bipolar leads are then connected to the right- and left-arm leads of the ECG, respec-
tively, and lead 1 is monitored. The pacing lead is then withdrawn slowly until an adequate
atrial deflection is visualized. It is helpful if the hi-pass and lo-pass of the recording system
can be manipulated to optimize the quality of the ECG signal. Electrophysiologic testing using
intracardiac recording and programmed stimulation should rarely be required for the initial
diagnosis, although ultimately it is the most accurate and predictable way of determining the
mechanism of tachycardia.
A pharmacologic test that would readily distinguish VT from SVT with aberration would be
very useful in the emergency setting. The ideal pharmacologic agent would have to be safe
regardless of the mechanism of tachycardia and specific for 1 mechanism. Verapamil is gener-
ally relatively specific for prolonging AV nodal conduction and refractoriness and terminating
paroxysmal SVT while generally being ineffective in the great majority of VT. Unfortunately,
verapamil is a peripheral vasodilator and has negative inotropic properties that create a
dangerous situation in many patients with VT or preexcited tachycardia.20 On the other
hand, adenosine is ultra-short-acting, making it a much better agent when SVT is still in the
differential.21.22 When administered intravenously by rapid bolus, adenosine results in a marked
transient increase in AV nodal conduction time and refractoriness. The effect of this agent is
too transient (seconds) to have any serious adverse consequences, but it generally serves to
terminate paroxysmal SVT, utilizing the AV node as a critical link, or at least to cause transient
AV block in cases of atrial tachycardia or flutter with aberrant QRS conduction (Figure 13-15).
Therefore, adenosine is arguably a useful diagnostic test for wide QRS tachycardia suspected to
be SVT, although it must be remembered that some AT and idiopathic VT can be adenosine-
sensitive. There is an increase in sympathetic tone after adenosine is given but this usually is
not hemodynamically important.
Most wide QRS tachycardia can be diagnosed by the experienced observer electrocardiograph-
ically provided that the tracing is of sufficient quality. A few examples of tips follow. It is often
productive to look at previous ECGs with the goal of finding ectopic beats identical to the WCT.
The goal of this becomes obvious when one examines Figure 13-16. Perhaps the most useful
is the notion that the beginning of a tachycardia is the most productive part of the tracing if
~ECG
..._ MVOT (msec)
?; .
Posterior
f wall of L.V.
Panel A
+-- ECG
~ Atrial
electrogram
~ Aortic root
(ant)
..____ Aortic valve
r Aortic root
.., (post.)
..-- LVET(msec)
PlnelB
FIGURE 13-14 • M-mode echocardlography with AV dissociation. In this example of AV dissociation with ventJIC1llar pacing.
there Is a striking varlablllty of mltral valve opening time (MVOT) (PaMI A) and ejection time {I.VET) {Panel B). MVOT Is the time
from mitral opening to miual closure while LVET is the time from aortic valve opening to dosure. The wriability in MVOT and LVET
reflects variability of stJoke volume with AV dissociation.
500 msec
Panel A
500 msec
PanelB
FIGURE 13·15 • Adenoslne In wide QRS tac:hycan::tla. This WCT has a 1:1 AV relatlonshlp (Panel A) and the diagnosis ls not readlly
forthcoming. An Intravenous bolus of adenoslne 6 mg In Panel 8 l'e$ults In continuation of atrtal tachycardia In the pYe$enC:e of AV
block. unequlwcally establlshlng the diagnosis.
available. If onset is captured, the diagnosis is usually forthcoming with a tracing of sufficient
quality. The termination of the tachycardia can also be very useful if spontaneous termination
is observed (Figures 13-17 and 13-18). Onset with a supraventricular beat would be a rare
occurrence with a VT. SVT would be most unlikely with a PVC that initiates tachycardia of the
same QRS morphology.
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·0T I "\) :\J \I -:!"( ; ~
I I
I I I j I I
FIGURE 13·16 • A relatlvely"narrow"WCT Is shown. The QRS morphology ls compatible with LBBB ahhough somewhat atypical.
The single ectopic beat on dte right is clearly ventricular and identical to dte WCT, essentially clinching the diagnosis of VT.
Previous tracings are especially useful and worth a careful look. The baseline tracing may show
an entirely normal QRS, bundle branch block pattern, preexcitation, infarction, hypertrophy,
etc., all of which obviously provide valuable clues as to the likelihood ofthe tachycardia mech-
anism in question (Figures 13-19and13-20).
INITIAL THERAPY ••• AFEW COMMENTS

It is evident that therapy for wide QRS tachycardia depends on the specific arrhythmia diagno-
sis ifthis is .known with some degree ofconfidence. When tachycardia is associated with cardio-
vascular collapse or significant hemodyna.mic compromise, cardioversion is always appropriate
and does not require knowledge of the mechanism of tachycardia. A 12-lead ECG should be
done, if possible. before cardioversion. Situations will arise. however, where the physician is
confronted with a relatively well-tolerated wide QRS tachycardia that allows time to make a
diagnosis as outlined above. Empirical intravenous drugs have been used in such instances
and continue to be appropriate in some circumstances. Verapamil is reasonable when there is
reasonable certainty that the tachycardia is supraventricular but is not to be used unless ventric-
ular tachycardia (with rare exceptions, such as the verapamil-sensitive idiopathic LV VT») has
been ruled out. Verapamil is negatively inotropic and causes vasodilatation, a bad combination
for any tachycardia that is not otherwise slowed by verapamil (VT, pree:rcited AF). The intro-
duction of adenosine made a huge difference to the acute treatment of an unknown tachycar-
dia. The great majority of SVTs will be terminated or at least unmaslred by temporary AV bloc.k.
II
+~
-+--+++-
I I
FIGURE 13-17 • Ashort run ofWCT Is observed In this tracing. Inspection of the t wave of the first wcr beat reveals a positive
deflection G.e~ in lead 2) sitting on the t wave not present on the previous beat This can only be a P wave realistically, essentially
dinching the diagnosis of SVT even though atrial activity is not clearly apparent during the remainder of the tachycardia.
Ch1 -~~~ ~ V
. :\ :
,__,'
! \,___..:
A.
- -"'
---+·
·· _......~ ,~ ~;V;tY ll.
P. . : ::;; : .J'i.· -.T J \ /,\ I \ I \ .
< r ~ .. - .~'
h
--v ~ 2
---+:
Y\: : .
Ch2 -( I :: ..... · ll ~ IAI I lI I I I If .
;
i ; ; ; i ;
FIGURE 13-11 • This brief run ofWCT begins with a wide QRS beat that has no bellevable P wave In front of It and therefore
dearlyventrlcular. The rest of the WCT has the $ame QRS morphology and miut be VT. If cne runs callpers over the P waYe$ prior to
the wcr, one finds that the tiny far field deftectlon at the onset of the first wide QRS beat times with the P wave upstroke. Anally,
one can also note that a negative P wave appears after the last wide QRS beat followed by a nonnal QRS. This Is most readlly
explained by retrograde conduction over a slow AV node pathway after the last wide QRS beat, which Initiates an AV nodal echo.
FIGURE 13-1' • wcr wfd'I atyplal RBBB type QRS. It Is fair to say that this wcr resembles RBBB but has slgnlflcant atypical fea-
tures suggesting VT. V1 Is monophaslc and wide and the transition to V2 and V3 Is also unusual. The frontal axis ls rightward and
probably more In the nordlwest corner. This would suggest VT as more probably from a QRS morphology point of view.
FIGURE 13-20 • The ECG from d'le patient In Agure 13-19 ls taken from a previous admission. The QRS although somewhat
bizarre Is identlcal to the WCT which Is then far more probably SVT. This reminds us that diagnosis by QRS morphology Is making a
statement of probablllty and, ald'lough exceedlngly usefu~ must always be Interpreted wld'I caution.
TABLE 13-1 Acute assessment of wide QRS tachycardia.

• History-age, previous myocardial infarct.
• Examination-evidence for AV dissociation, cannon A waves, variables,. variable pulse pressure.
• ECG-AV dissociation, •typical" or•atypical" bundle branch block pattern.
• Echocardlogram-varlable mltral or aortic valve opening time.
• Esophageal recording.
• When in doubt, the working diagnosis is ventricular tachycardia.
and the very short duration of action greatly limits any potential adverse effect. Most VT will
not be influenced at all by adenosine. In the setting of a relatively stable VT, a class 1 agent such
as procainamide is a reasonable choice, as it would have efficacy for both VT and most SVT. A
reasonable sequence of interventions in an unknown reasonably tolerated WCT might consist
of adenosine, followed by procainamide if still present and diagnosis is unclear, followed by
cardioversion if necessary. It might be noted that intravenous amiodarone is widely used as a
catchall tachycardia treatment. In fact, the acute pharmacology of amiodarone is that of alpha
and beta blockade (potentially useful for rate control in AF or in recurrent VF or unstable VT).
The membrane-active effects on myocardial refractoriness and conduction take many hours to
become evident related in part to the requirement of active metabolite. This limits its use for
acute treatment of stable WCT.
COMMENTARY
In the majority of instances, a diagnosis ofWCT can be made on the basis of history, physical
examination, and ECG analysis {Table 13-1). Adenosine can be useful diagnostically. If the
physician is uncertain of the diagnosis after this, it is reasonable to assign a working diagnosis
of VT until proved otherwise. Most adult patients with structural heart disease presenting with
wide QRS tachycardia are ultimately shown to have VT, and therapy directed at VT in most
cases is also reasonable for SVT. A still common pitfall in diagnosis is to make a mistaken diag-
nosis of SVT with aberration instead of VT when the arrhythmia is "too well tolerated for VT"
or the "QRS is not wide or bizarre enough for VT."
REFERENCES
1. Goldman MJ. Definitions of electrocardiographic configurations. In: Goldman, MJ. Principles of Clinical Electro-
cardiography. 11th ed. Lange Medical Publications; 1982:23-28.
2. Akhtar M. Electrophysiologic bases for wide QRS complextacltycardia. Pacing Clin Electrophysiol. 1983;6(1):81-97.
3. Miles WM, Prystowsky EN, Heger JJ, Zipes DP. Evaluation of the patient with wide QRS tachycardia. Meil Clin N
Am. 1984;68(5):1015-1038.
4. Watanabe Y. Terminology and electrophysiologic concepta in cardiac arrhythmias. II. Concealed conduction.
Pacing Clin Electrophysiol. 1978;1(3):345-356.
5. Akhtar M, Shenasa M, Tchoun PJ, Jazayeri M. Role of electrophysiologic studies in supraventricular tachycardia.
Cardiac arrhythmias: where to go from here. 1987:233-242.
6. Wellens HJ, Brugada P. Diagnosis of ventricular tacltycardia from the 12-lead electrocardiogram. Cardiol Clin.
1987;5(3) :511-525.
7. Wellens HJ, Bar FW, Lie Kl. The value of the electrocardiogram in the differential diagnosis of a tacltycardia with
a widened QRS complex. Am JMed. 1978;64(1):173-181.
8. Morady F, Baerman JM, DiCarlo LA, DeBuitleir M, Krol RB, Wahr DW. A prevalent misconception regarding
wide-complex tachycardias. /AMA. 1985;254( 19):2790-2792.
9. Baroid SS, Schamroth L, Agathangelou N. QRS normalization by ventricular fusion: a study in intraventricular
conduction. Pacing Clin Electrophysiol. 1981;4{4):448-450.
10. Brugada P, Brugada J, Mont L, Smeets J, Andries EW. A new approach to the differential diagnosis of a regular
tachycardia with a wide QRS '°mplex. Circulation. 1991;83(5):1649-1659.
11. Vereckei A, Duray G, Szenasi G, Altemose GT, Miller JM. New algorithm using only lead aVR for differential
diagnosis of wide QRS '°mplex tac.hy<:ardia. Heart Rhythm. 2008;5(1):89-98.
12. Pava LF, Perafan P, Badiel M, et al. R-wave peak time at DII: a new criterion for differentiating between wide
complex QRS tachy~dias. Heart Rhythm. 2010;7(7):922-926.
13. Sandler lA, Marriott HJ. The differential morphology of anomalous ventrkular '°mplexes of RBBB-type in lead
Vl: ventrkular ectopyversus aberration. Circu/ation.1965;31(4):551-556.
14. Cooksey JD, Dunn M, MaHie E. Clinical Vectorcardiography 1md Electrocardiography. Year Book Medkal
Publishers; 1977.
15. Massie E, Walsh TJ. Clinical vectorcardiography and electrocardiography. Acad Med. 1961;36(2): 197.
16. Manyari DB, Ko P, Gulamhusein S, Boughner DR, Kostuk. WJ, Klein GJ. A simple echocardiographic method to
detect atrioventricular dissociation: a useful aid in the differential diagnosis of regular tachycardia with wide QRS
complexes. Chest. 1982;81(1):67-73.
17. Drinkovic N. Subcostal M-mode echocardiography of the right atrial wall for differentiation of supraventricular
tac:hyarrhythmias with aberration from ventricular tachycardia. Am Heart/. 1984;107(2):326-331.
18. Drinkovic N, Ferek B, Jursic M. Subcostal M-mode echocardiography of the right atrial wall in evaluation of
cardiac arrhythmias and pacing. Pacing Clin Electrophysiol. 1985;8(1): 110-122.
19. Hammill SC, Pritchett EL. Simplified esophageal electrocardiography using bipolar recording leads. Ann Intern
Med. 1981;95(1):14-18.
20. Buxton AE, Marchlinski FE, Doherty JU, Flores B, Josephson MB. Hazards of intravenous verapamil for sustained
ventricular tachycardia. Am/ Cardiol. 1987;59(12): 1107-1110.
21. Chugh, A. Adenosine and atrial tachycardia. Circ Arrhythm ElectrophysioL 2016;9(8):e004449.
22. McCabe JL, Adhar GC, Menegazzi JJ, Paris PM. Intravenous adenosine in the prehospital treatment of paroxysmal
supraventricular tac:hy~dia. Ann Emerg Med. 1992;21 (4):358-361.
23. Klein GJ, Millman PJ, Yee R. Recurrent ventricular tachycardia responsive to verapamil. Pacing Clin Electrophysiol.
1984;7(6):938-948.
Undiagnosed Syncope, Dizzy
Spells, Palpitations
George J. Klein, MD
The entities in this section constitute relatively frequent referrals to cardiologists and electro-
physiologists for suspected arrhythmia. The most accurate way of making or excluding arrhyth-
mia is obviously recording the electrocardiogram (ECG) during a clinical episode. an exercise
complicated when symptoms are infrequent and sporadic, and clinical clues are nonspecific or
absent Since the original publication ofthis book in 1994, technology has moved on providing
us with a plethora of ECG monitoring products, including implantable types capable of Iong-
term monitoring in the range of months and years. Ambulatory monitoring of blood pressure
has become available and it is likely that ambulatory monitoring utilizing novel sensors will
be available in the foreseeable future. This has probably contributed the most to streamlining
the current management of most of these patients, leaving us to grapple only with those who
have specific unique issues complicating diagnosis or treatment.
I.~.~~.~1.~~I.~~.~~. ~.f.f~~~q~~.~.~~~~J~~f).~~~ .......................................................................

The differential diagnosis of transknt loss ofconsdousness is very extensive and covers a broad
spectrum of associated cardiac and noncardiac conditions. The more common categories of
disorder potentially causing loss of consciousness are listed in Table 14-1. The term syncope is
more specifu: and refers to a transient loss of consciousness due to temporary impairment of
cerebral perfusion related to drop of blood pressure for various reasons as per Table 14-1. That
said, the term syncope is frequently used as ifinterchangeable with "transient loss ofconscious-
ness.• Fortunately. the differential diagnosis can usually be narrowed considerably by a careful
history and physical examination and some simple laboratory assessment4-5
The broad goals of assessment in a patient presenting with LOC are threefold. The key goal,
but often the most elusive, is the recording of physiological parameters (especially the ECG)
during a spontaneous episode. Under ideal circumstances, the spe11 is witnessed by a physician,
who documents physical findings, blood pressure, ECG, and perhaps even an electroenceph-
alogram (EEG) during the episode! Failure to monitor or witness an actual clinical episode is
the fundamental problem and results in diagnosis by inference, with all its potential vagaries.
A secondary goal is the documentation ofassociated medical and. in particular, cardiac disease.
This can narrow the diagnostic possibilities and help predict prognosis.6 Finally, the third goal
is to identify by laboratory testing abnormalities that suggest a potential diagnosis. Reproduc-
tion of symptoms by provocative maneuvers improves the degree of confidence of the implied
TABLE 14-1 Major categories of loss of consciousness.

A. Neurological
i. Seizure
B. Cardiogenic/vascular (•syncope")
i. Arrhythmic (bradycardia or tachycardia)
II. Hemodynamlc, such as LV outflow obstruction, left atrial myxoma, pulmonary embolus, lschemla
(rare), exertion with fixed cardiac output, pulmonary hypertension
iii. Reflex peripheral vascular, such as vasovagal (most common), carotid hypersensitivity, micturition,
cough and swallow syncope, orthostasis, vasodilating medications
c. Miscellaneous
I. Includes hysteria, mallngerlng, hyperventllatlon, hypoglycemla
diagnosis. In the absence of actual data during LOC, the history and such indirect evidence
may be compelling enough to initiate a therapy.
Assessment
A careful history is arguably the single most productive part of the diagnostic workup. Obvi-
ously, the patient may not be the most helpful person in providing this history. A diligent effort
to obtain the version of events from one or more reliable witnesses if available can be very
enlightening. In the same vein, it is worth the effort to obtain the observations and notes of
ambulance attendants if these are reasonably available. A family history of unexpected sudden
death or seizures may provide clues. A long history of recurrent LOC especially without serious
injury is generally unlikely to be related to significant arrhythmia.
It is fair to say that the great majority of patients with syncope will prove to have vasovagal
or other "'reflex" or hypotensive syncope related to posture, medications, and the like. Such
patients may have a strong clue in the history7 such as a tell-tale prodrome, nausea, vomiting,
sweating, a specific circumstance such as bloodletting, or strong emotion or occurrence only
when going to the toilet at night. Although many, especially the elderly, may not experience
a prodrome, the recovery to full mentation and activity after a vasovagal or reflex syncope is
characteristically more gradual ("postdrome") and they may feel tired or light-headed for hours
or the rest of the day.
Syncope related to arrhythmia although statistically less frequent is the most critical to rec-
ognize as this is most likely to be lethal or causative of injury. A tachycardia or bradycardia
sufficient to cause LOC will either stop spontaneously in a reasonable time measured in min-
utes or result in sudden death. Thus, syncope due to an arrhythmia is typically associated with
a usually brief or momentary prodrome of light-headedness or no prodrome. The period of
LOC is relatively brief (a few minutes or less) and the patient generally awakes without any
significant impairment of mentation of symptoms. Sudden LOC and rapid recovery is the hall-
mark of arrhythmic syncope and is perhaps the most useful historical feature to select patients
for an aggressive diagnostic strategy and a heightened index of suspidon for potentially lethal
arrhythmia. Of course, a seizure related to cerebral ischemia may complicate a more prolonged
vasovagal syncope, occasionally complicating this picture.
A history of rapid heartbeat prior to syncope may suggest tachycardia as the cause but is prob-
ably not as specific as one might think. Consider that patients with a rapid tachycardia such as
CHAPTER 14 • Undiagnosed Syncope, Dizzy Spells, Palpitations 325
VT related to repolarization syndromes will characteristically present with seizure or syncope

without any awareness of a racing heart.
A thorough general physical examination with emphasis on the cardiovascular and neurologic
systems is aimed at diagnosing conditions potentially associated with LOC. This examination
obviously includes assessment of blood pressure, both supine and upright. Carotid sinus mas-
sage has probably become less frequent as a "go to" maneuver but can be useful in selected
patients especially when the history suggests we due to carotid hypersensitivity,8•9 for exam-
ple, during head movement or shaving. This should be performed with ECG monitoring and
should be done very gently or not at all when there is evidence for significant carotid disease
assessed at least by auscultation and more specifically by carotid ultrasound. 10 Initially, gentle
massage is performed 1 side at a time on the right and left carotid sinus areas in the neck. This
is followed by more aggressive pressure if no response is noted. Asystole longer than 3 s is
suggestive of cardioinhibitory carotid sinus syndrome, while a marked fall in blood pressure
even after the heart rate resumes suggests the vasodepressor variety. If initially negative, it is
useful to repeat this maneuver on other occasions. Unfortunately, pauses of 3 s and longer can
occur in the aged without a history of symptoms. Thus, a positive result without reproduction
of symptoms must be interpreted with caution.
Laboratory Assessment
Because LOC is sporadic and may be due to a wide range of disorders, it is difficult to rec-
ommend a list of laboratory investigations on a "cookbook" basis. Specific laboratory inves-
tigations must be guided by clues provided during the history and physical examination. It is
intuitively obvious that no single test will be terribly rewarding or cost-effective if the cause is
not evident by an informed history and physical examination. 11 - 1~
In the overtly normal patient with LOC, general assessment for potentially contributing condi-
tions (anemia, thyroid disease, etc.) is appropriate.
The most frequently considered investigations include the following:

• The 12-lead ECG.
• The graded treadmill exercise test.
•The ECG.
• The EEG, imaging of the brain with CT, MRI, or other.
• Ambulatory monitoring.
• Upright tilt testing.
• Cardiac electrophysiologic assessment.
Twelve-lead electrocardiogram
It is a given that the 12-lead ECG is the starting point for any diagnostic testing with LOC. All
ECGs available need to be reviewed looking for preexcitation, conduction defects, myocardial
infarction, or other abnormalities suggesting a possible cause of syncope. A high index of sus-
picion is appropriate for the repolarization syndromes such as long QT syndrome, Brugada
syndrome, Jwave syndromes, and the like. The arrhythmias associated with the latter, namely
torsade de pointes (TdP), ventricular tachycardia (VT), and other polymorphous VT or VF,
I 111 lI aVF va
'
V6
FIGURE 1•1 • This ECG was recorded In a 32-year-old woman with 2 episodes of LOC wtthout wamlng and a relattvefy rapid
recovery. Several ECGs from this patient were reported as normal but the QT was clearly prolonged on the 1 avallable to us and
diagnosis of LQT1 was made and verified by genetic testing. It Is most probable thBt she was having syncope secondary to poly-
morphous VT and had no further spells after treatment with nadolol.
frequently present as syncope or "seizure," and often the only diagnostic clue short of recording
the ECG during an episode is the finding of a "signature.. abnormality on the standard ECG
(Figure 14-1).
Graded treadmill exercise test

A graded treadmill exercise test is especially useful when syncope is associated with exercise
(Figures 14-2 and 14-3). Subnodal AV block may become more evident or appear with exer-
cise whereas AV nodal conduction delay or block generally improves with exercise. Treadmill
testing is indicated when silent myocardial ischemia is a consideration, although ischemia per
se is not a usual cause of syncope. Its routine use with no clinical suggestion of the former is
otherwise not likely to be productive. That notwithstanding, this test is arguably sufficiently
inexpensive and noninvasive to justify its use if a cardiac cause of syncope is suspected. Of
course, a negative exercise test does not rule out an arrhythmia that occurs with competitive
sports or after prolonged periods ofexercise, for example, long-distance running.
Echocardlogram
The 2-dimensional ec.b.ocardiogram will again not be cost effective when applied to a large
population of patients with undiagnosed syncope. It will obviously virtually never provide a
direct diagnosis and therefore its diagnostic yield might be said to be zero. Nonetheless, it is an
excellent test for detecting associated cardiac disease such as left atrial myxoma, asymmetric
septal hypertrophy, or early cardiomyopathy that may elude physical examination and provide
an assessment of ventricular function, ofcourse a key prognosticator. The echocardiogram and
ECG provide key data relating to presence or absence of cardiac disease that affects prognosis
and subsequent evaluation.
EEG, Imaging ofthe brain with er, MRI, orother modality
Neurological testing such as EEG,15 imaging, or consultation is generally not rewarding unless
there are specific historical clues to suggest seizure. Otherwise, routine and extensive neuro-
Iogic tests will usually not be productive.
Ambulatory monitoring"
Ambulatory (Holter) monitoring is of most value in patients with very frequent symptoms
(several per week). because the probability iB high that aggressive ambulatory monitoring will
be successful in providing an ECG during a spell (Figure 14-4).
Ambulatory monitoring for periods of 24 to 48 h is considerably less helpful in patients with

infrequent episodes of syncope because it is unlikely that the recording will be obtained during
PanalA
FIGURE 14-l • These ECGs are recorded from an ctherwlse-wen 65-year-old man with a long history of brief palpltatlonund 2
recent syncopal spells, the second of which aused him to seek attention. His family history provided no suggestion of sudden
death. The resting ECG of Panttl A ls entirely nonnal. Pan1I B was recorded during treadmlll exercise and shows rapid VT that teJ-
mlnatl!d spontineously. Shortfy thereafter, the SVT In Pa net C was recorded. At EP study, AV node reentry was diagnosed and he
underwent slow pathway ablation. Extensive Investigation Including coronary angiography and cardiac MRI were normal. He was
discharged on bisoprolol and remained well. Repeat exercise testing did not reproduce arrhythmias. Exercise testing proved very
useful Indeed In thb lndlvldual.
PlnelB
PlnalC
FIGURE 14-2 • (Conttnued)

a spell Nonetheless, arrhythmias and conduction abnormalities may be detected even during
asymptomatic periods, and these can provide clues to the etiology of syncope.17•18 One must be
cautious in ascribing the cause of syncope to asymptomatic abnormalities, especially those that
are frequently observed in populations without syncope (Figure 14-S).
It is reasonable to assume that the more serious the abnormality, the more likcly it is to be
related to the cause ofsyncope, keeping in mind that any abnormality occurring in the absence
ofsymptoms must be interpreted with caution. The optimal recording 1ime has not been estab-
lished In general, recording longer than 24 h probably improves the yield only marginally for
patients with infrequent symptoms. Longer-term ambulatory monitoring, both looping and
nonlooping, will be far more useful in patients with infrequent episodes.
Nonlooping recording devices activated by the patient or bystander may work if the syncope
is preceded by a prodrome sufficiently long to allow activation of the device. Such devices may
be activated automatically with prespecified tr:lggers such as prolonged pause or critical heart
rate. The use of remote monitoring centers with continuous surveillance also facilitates the
capturing of an episode.
PanelA
FIGURE 14-3 • This lndMdual with no structural heart disease had syncope during exercise. The treadmlll test resulted In a grand
mal seizure. Exercise-Induced seizure Is a poorly unde1stood entity but at least consistent occurrence during exercise testing all0W1
for ability to assess efficacy of therapy.
FIGURE 14-l • (Continued)
23:20:59-2 Pau89 HR=41

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FIGURE 14-4 • This patient underwent Holter monitoring for recurrent LOC without slgnlflcant wamlng and sustJllned a con-
amlon during a spell. The Inset (smaller comp/fxes at bottom ofJfldf!) provides a more panoramic view of a prolonged pause and
shows a relatively gradual sinus slowing prior to asystole, f'ollowed by acceleratlon. This Is most consistent with vasovagal syncope.
Although vasovagal syncope Is not generally an lndlciltlon f'or pe1manent pacing, It Is reasonable to offer pacing to an lndlvldual
such as this with a prolonged documented clinical pause, especially with significant injury.
FIGURE 14-5 • This elderly woman with recurrent LOC had multlple episodes such as this on ambulatory monitoring. There
Is.tunb. sinus slowlng and PR prolongatlon prior to the nonccnducted P wave, a hallmark of a vagal cause. In addition, this was
recorded at 3:59 am during sleep, another clue to a vagal etiology. This type of event is relatively common during monitoring in a
general population and does nat reliably infonn on the events during an actual clinical syncope.
Ambulatory looping ECG recorders are capable of storing the previous several minutes or lon-
ger of ECG to facilitate capturing ofthe episode by the patient or providing a record of the ECG
immediately preceding the triggering event. A variety of these are available utilizing various
innovative electrode systems designed for muimizing patient compliance and comfurt such as
watches or smart phone attachments. Relatively small multilead patches applied to the torso facil-
itate longer-term Holter monitoring. These all permit patient surveillance for longer time frames,
including wedcs to months. Finally. several implantable loop recording systems are available to
optimize patient compliance and permit recording over a time span of months to years.1'·22 These
devices are quite small and can be implanted relatively simply as an office procedure permitting
automatic or patient activation or surveillance by a remote center. Figures lU through 14-8
provide specific examples highlighting the utility of these longer-term ambulatory monitoring
systems to provide a diagnosis.ll,23
It is fair to say that advances in longer-term ambulatory monitoring strategies have revolu-
tionized the assessment of the more infrequent or sporadic spells of any kind suspected to be
potentially related to arrhythmia. The importance of history notwithstanding, the history is
frequently unclear or misleading for many reasons and many experienced clinicians (including
the authors!) have undoubtedly bun surprised by unexpected diagnostic observations.
UprighttilttestingH-2'
Clinically, the classic vasovagal episode has been diagnosed by a history suggesting a typical
precipitating event. prodrome, and sequelae, although it is obvious that presentations not fit-
ting a typical presentation are frequent The tendency to vasovagal syncope can be exposed by
a relatively simple test-namely, upright tilt testing.mo Although the mechanism for an abnor-
mal response is not definitively established. it is thought to be a reflex related to venous pooling,
which leads to more aggressive left ventricular contractility in a chamber with decreased vol-
Uine. The use of tilt testing has been deemphasised after great enthusiasm after its introduction,
i~ l ?Jir l l~ l tl:!11 l~ l l l l:¥ll l l*- l?ItlIIirlr tl

1 1
...............................
FIGURE 14-6 • LOC In an elderly lndlvlduel with LBBB and remote Inferior myocardlel Infarction. A wide QRS tachycardle different
from the basellne LBBB Is almost Invariably VT as It was In this patient with an Implanted loop recorder.
but it is still potentially useful diagnostically to screen for a tendency to vasovagal syncope. It
is not used currently as an end point to assess therapy as done previously with drugs such as
beta blockers and disopyramide,31 in part due to the failure to convincingly verify efficacy for
any of the many agents initially proposed as effective and issues with reproducibility of the test.
The decreased use of tilt testing currently relates to unresolved issues such as standardization
of protocols, reproducibility. sensitivity, and speciftdty. Long-term ambulatory monitoring can
be diagnostic and records an actual clinical episode. removing the vagaries ofthe former issues.
Tilt testing still has a place and can be useful to expose a propensity to or to reproduce vasovagal
syncope. While a positive test doesiit prove that the patient's clinical syncope is related to the
result. reproduction of a patient's unique prodrome during an induc.ed syncope or presy.ncope
116:23:02
:16:23:07
FIGURE 14-7 • Episode of complete AV blodc recorded by a loop recorder In another lndMdual with baseline l.BBB.
is rather convincing that the test is indeed a true positive. It is most useful when there is an
intermediate clinical probability of vasovagal syncope. It is dearly not useful when the patient
provides a relatively typical history af vasovagal syncope; this can only verify what is known
if positive or, conversely. be negative when it is probably a false negative. Alternatively, a typ-
ical arrhythmic syncope with sudden onset and relatively quick recovery in a patient with a
~
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06:0tl!2 1--V'-'--------_,_~-t-.,_,_--I
FIGURE 14-1 • Recorded In a patient with recent onset syncope with an Implantable loop recorder, the episode Is suggestive of
vasovagal syncope with a more gradual slowlng and recovery. A pacemeket' although not generally shown to be effective In wso-
vagal syncope may have some efficacy In patients with longer asystollc pauses recorded during clln!cal (not necessarily Induced
during tilt testing). This is intuitively reasonable because pacing should be superior to total a systole even in tfte face of hypotension
associated with the vasodepressor component.
previous myocardial infarction will not benefit substantially from a tilt test, since the pretest
probability of arrhythmia is very high in such a patient solely on the basis of history.
Electrophysiologic testing
The techniques of intracardiac recording and programmed stimulation have proven very useful
in the management of patients with paroxysmal tachycardia and these techniques have been
utilized in the assessment of patients with LOC of unknown etiology.3•11 •12.32.33 Electrophysio-
logic (EP) assessment, described in more detail in Chapter 16, has the potential to provide a
clear diagnosis or more realistically provide important clues to a potential etiology or other
prognostic information. EP testing entails:
1. The recording of basic intervals, ie., the PA, atrio-His (AH), and His-ventricle (HV) intervals.
2. Assessment of sinus node function, including determining the sinus node recovery time and
the sinoatrial conduction time.
3. Incremental atrial pacing (to induce arrhythmias and assess potential block below the His
bundle) and incremental ventricular pacing.
4. Atrial and ventricular extrastimulus testing at multiple sites and multiple cycle lengths to
induce arrhythmias. The sensitivity of induced ventricular arrhythmias increases with the
aggressiveness of the stimulation protocol, but specificity deteriorates concomitantly
(Figure 14-9). A ventricular arrhythmia induced with 3 or more extrastimuli is less likely to
be related to reality than one induced with more conservative techniques unless the arrhyth-
mia induced is sustained monomorphic VT, an arrhythmia that is considered specific, typi-
cally but not invariably associated with a substrate abnormality.
5. Tests directed at assessing the integrity of the autonomic nervous system at EP study. For
example, reversal of severe bradycardia or conduction abnormality with atropine suggests
hypervagotonia, because atrioventricular node conduction and refractoriness are highly
dependent on autonomic tone.
EP testing is a reasonable means of detecting abnormalities of AV conduction and sinus node

dysfunction. Both supraventricular tachycardias and ventricular tachycardias may be induced.
Some tachycardias may be considered highly specific, especially when they are rarely induced
in an overtly normal population (such as AV node reentry). EP abnormalities are often detected
when short-term ambulatory monitoring has not been productive. Generally, the yield of
abnormalities is lowest in patients without any evidence of heart disease and highest in patients
with organic heart disease. For example, predictors of a positive EP study include an ejection
fraction less than 40, left bundle branch block on the ECG, the presence of coronary artery
disease, previous myocardial infarction, male gender, presence of late potentials, and injury
sustained during syncope.
Although data exist supporting the efficacy of EP testing, especially in uncovering abnormali-
ties, it is apparent that the technique inherently entails issues of sensitivity and specificity, the
former poor in patients with no significant heart disease and specificity, the latter worsening in
patients with significant heart disease.
Currently, EP testing is reasonable to consider in any patient with recurrent syncope when the
diagnosis is not evident after noninvasive assessment and attempts to document the causes
during syncope electrocardiographically. It has a higher priority in patients with organic heart
II
v,
RV
RA j t
l ~ .
HBE
Panel A
FIGURE , . , • Induction cf sustained polymorphous VT during electrophyslologlc testing for syncope In a 54-year-old woman
without heart disease. The slgnlflcance of this arrhythmia Is not clear, but It Is generally thought to be nonspeclflc. The patient had
no further syncope over 2 years of follow-up without treatment Arrows lndlCBte ventrlailar extrastlmull after a standard drive of
8c:ycles.
disease suspected to have VT, especially those with previous myocardial infarction. EP testing
may be justified in the patient who has sustained a significant injury during the episode or if
severe organic heart disease with a potential for a life-threatening arrhythmia is present. Syn-
cope associated with advanced congestive heart failure carries an ominous prognosis regardless
of etiology or results of EP testing.
Intuitively, the results ofEP testing would be expected to be most reliable when an abnormal-
ity is reproduced that exactly reproduces the patient's spontaneous symptoms. Otherwise, the
results of EP testing are merely inferential and, in effect, a therapeutic trial is embarked upon
based on this inference. In theory, the more severe and specific the abnormality, the more likely
it is to be related to the cause of syncope. It has been suggested that these severe abnormalities
include sinus node recovery time greater than 3 s, HV interval greater than 100 ms, block below
the His bundle during spontaneous or atrial paced rhythm when this cannot be explained by
an Ashman phenomenon, unimorphic sustained VT, and supraventricular tachycardia when it
is secondary to AV nodal reentry or AV reentry. Atrial flutter or fibrillation may be considered
as potentially causative of syncope if sustained and reproduces the patient's spontaneous symp-
toms. Syncope in the former may be related to the AF itself or conversion pauses.
Patients with severe organic heart disease may exhibit several abnormalities possibly suggesting
both tachycardia and bradycardia. Patients with ECG left bundle branch block may have both
severe infra-His conduction abnormalities and inducible VT. The availability of the modern
implantable defibrillator has provided us with a powerful tool, both diagnostic and therapeutic.
When syncope occurs in a high-risk patient with poor ventricular function or other concern-
ing cardiac issue such as cardiac sarcoidosis or hypertrophic cardiomyopathy, EP testing is
reasonably bypassed completely unless a treatable condition such as bundle branch reentrant
VT is suspected. Regardless of the risk category, the significance of a negative study is not clear.
Many potentially high-risk patients such as those with hypertrophic cardiomyopathy may not
have inducible VT. A negative study certainly does not rule out a paroxysmal bradycardia either
related to sinus node dysfunction or AV conduction disease (Figure 14-10). For these reasons,
the use of EP testing has declined in importance in the modern management of syncope or
intermittent unexplained spells, largely supplanted by modem monitoring techniques or direct
implantation of an implantable cardioverter-defibrillator (ICD) in a patient thought to be at
significant risk of sudden death.
COMMENTARY
In spite of many scholarly publications on syncope, many clinicians still feel uneasy with our cur-
rent management of these patients. Many facts conspire to make recurrent syncope a frustrating
problem. The patient may relate a poor history or no witness may be available to describe the
spell Infrequent occurrences of syncope frustrate attempts to document the disorder electro-
cardiographically. The patient is frequently elderly, with chronic medical diseases and multiple
potential etiologies for syncope.6.:M-40 The diagnostic work.up may suggest no abnormalities or
multiple abnormalities of unclear specificity. In the absence of ECG documentation during a
spell, our therapy is essentially inferential, with variable degrees of confidence in the inference.
Several points can be kept in mind even if a diagnosis has not been reached after extensive
evaluation:
1. The prognosis in patients with syncope is highly variable and depends on the prognosis ofthe
pathologic process causing syncope. A great deal of anxiety can be relieved by telling healthy
patients without demonstrated medical disease that their prognosis is most likely good.
2. Recurrence of syncope is highly variable and spontaneous remission is frequent, especially
after single episodes or clusters of episodes.
3. Close companions or relatives can often be trained to take the pulse, listen to the chest for
the heartbeat, or apply a recording device. Some patients do not find it difficult to adopt
2----------' ------------.-J '-----------.../ '----
3---------------------.------------.
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AH-80
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PanalB
FIGURE 14-10 • Panel Ashows normal conduction Intervals In a 55-year-<ild man with recurrent syncope. The anterograde
Wendcebach cycle length was 380 ms. The EP study was negative. Panel Bshows transient complete heart blodc. as subsequently
recorded during spontaneous syncope.
a "cautious" lifestyle until the prognosis is clear or until a diagnosis is made. This would
include refraining from driving and other situations where LOC might cause serious injury
to the patient or others.
Can an empirical trial of therapy without any corroborating data ever be considered? Empirical
cardiac pacing in patients with a typical history of Stohs-Adams disease is intuitively argu-
able. although the high spontaneous remission rate complicat.es any scientific assessment of
the principle. Nonetheless, great pressure can be exerted in cases where syncope is recurrent,
injury has occurred, and the workup is negative. An argument can be made for a therapeutic
trial of pacing in selected instances especially in the elderly where there is strong suggestion of
a causative bradycardia by monitoring, especially if serious injury has resulted from syncope.
In the final analysis, the diagnosis of syncope is most unequivocally achieved with ECG mon-
itoring to capture a clinical episode. The many advances in long-term ambulatory monitoring
and diagnostic capabilities of implanted pacemakers and defibrillators have contributed greatly
in reducing the burden of recurrent undiagnosed LOC.
UNDIAGNOSED DIZZY SPELLS AND PALPITATIONS

Symptoms oflight-headedness, dizzy spells, and palpitations occur very commonly and frequently
do not have an arrhythmic basis when assessed with ambulatory monitoring. Routine Holter
monitoring is reasonable if the spells are sufficiently frequent or with longer-term ambulatory
monitors if they are less frequent. At times, it may suffice to teach patients to take their own
pulse during symptoms and report the result to the physician. Technologies linked to smart
phones are available for concerned individuals to record their own ECG. More detailed investi-
gation and, in particular, EP testing are infrequently indicated in the majority of these patients,
as the essential diagnostic information should be obtainable by monitoring techniques. A
recorded clinical arrhythmia is also highly useful even if the patient goes on to EP testing with
a view to ablation, linking the reality of a clinical arrhythmia to any observed EP findings.
It may even be argued that episodes that are too brief or too infrequent to be captured after a
reasonable monitoring effort in a low-risk individual are not worth investigating further.
REFERENCES
1. Shen W-K, Sheldon RS, Benditt DG, et al. 2017 ACC/AIWHRS guideline for the evaluation and management of
patients with syncope. J Am Coll Cardiol. 2017;70(5):620-663.
2. Brignole M, Moya A, de Lange FJ, et al. Practical instructions for the 2018 ESC guidelines for the diagnosis and
management of syncope. Eur Heart]. 2018;39(21):e43-e80.
3. 2018 ESC Guidelines for Diagnosis and Management of Syncope. Am Coll CardioL http%3a%21%2fwww.acc
.org%2flatest-in-cardiology%2ften-points-to-remember%2f2018%2fil4%2fi>4%2tl4%2f28%2f2018-esc-guidelines-
for-syncope. Accessed June 23, 2019.
4. Kapoor WN, Karpf M, Wieand S, Peterson JR, Levey GS. A prospective evaluation and follow-up of patients with
syncope. N Engl JMed. 1983;309(4):197-204.
5. Brignole M, Hamdan MH. New concepts in the assessment of syncope. J Am Coll Cardiol. 2012;59( 18): 1583-1591.
6. Khera S, Palaniswamy C, Aronow WS, et al. Predictors of mortality, rehospitalization for syncope, and cardiac
syncope in 352 consecutive elderly patients with syncope. JAm Med Dir Assoc. 2013;14(5):326-330. doi:l0.1016/j.
jamda.2012.12.001
7. Sheldon R, Rose S, Connolly S, Ritchie D, Koshman M-L, Frenneau:x M. Diagnostic criteria for vasovagal syncope
based on a quantitative history. Bur Heart]. 2006;27(3):344-350. doi:10.1093/eurheartj/ehi584
8. Parry SW, Richardson DA, O'Shea D, Sen B, Kenny RA. Diagnosis of carotid sinus hypersensitivity in older adults:
carotid sinus massage in the upright position is essential. Heart. 2000;83(1):22-23. doi:l0.1136/heart.83.l.22
9. Sachpekidis V. Vogiatzis I, Dadous G, Kanonidis I, Papadopoulos C, Sakadamis G. Carotid sinus hypersensi-
tivity is co=on in patients presenting with hip fracture and unexplained falls. Pacing Clin Electrophysiol.
2009;32(9): 1184-1190. doi:l0.1111/j.1540-8159.2009.02463.i::
10. Richardson DA, Shaw FE, Bei::ton R, Steen N, Kenny RA. Presence of a carotid bruit in adults with unex-
plained or recurrent falls: implications for carotid sinus massage. Age Ageing. 2002;31(5):379-384. doi:l0.1093/
ageing/31.5.379
11. Linzer M, Yang EH, Estes NM, Wang P, Vorperian VR, Kapoor WN. Clinical guideline: diagnosing syncope: part 1:
value of history, physical examination, and electrocardiography. Ann Intern Med. 1997;126(12):989-996.
12. Linzer M, Yang EH, Estes NM, Wang P, Vorperian VR, Kapoor WN. Clinical guideline: diagnosing syncope: part 2:
unexplained syncope. Ann Intern Med. 1997;127(1):76-86.
13. Krahn AD, Klein GJ, Yee R, Skanes AC. Randomized assessment of syncope trial: conventional diagnostic testing
versus a prolonged monitoring strategy. Circulation. 2001;104(1):46-51.
14. Kapoor WN. Syncope. N Engl JMed. 2000;343(25):1856-1862.
15. Abubakr A, Wambacq I. The diagnostic value ofEEGs in patients with syncope. Epilepsy Behav. 2005;6(3):433-434.
16. Steinberg JS, Vanna N, Cygankiewicz I, et al. 2017 ISHNE-HRS expert consensus statement on ambulatory ECG
and external c:ardi« monitoring/telemetry. Heart Rhythm. 2017; 14{7):e55-e96.
17. Drake T. Diagnostic efficacy of24-hour electroc:ardiographic monitoring for syncope: Gibson TC, Heitzman MR.
Am J Cardiol 1984;53:1013-1017. Journal ofEmergency Medicine.1984;2(1):65.
18. Gibson TC, Heitzman MR. Diagnostic efficacy of 24-hour electrocardiographic monitoring for syncope. Am l
Cardiol. 1984;53(8):1013-1017.
19. Krahn AD, Klein GJ, Yee R, Norris C. Final results from a pilot study with an implantable loop recorder to
determine the etiology of syncope in patients with negative noninvasive and invasive testing. Am J Cardiol.
1998;82(1):A8-A9.
20. Furukawa T, Maggi R, Bertolone C, Fontana D, Brignole M. Additional diagnostic value of very prolonged
observation by implantable loop recorder in patients with unexplained syncope. J Cardiovasc E/ectrophysiol.
2012;23(1):67-71.
21. Boersma I., Mont I., Sionis A, Garcia B, Brugada J. Value of the implantable loop recorder for the management of
patients with unexplained syncope. EP Europace. 2004;6(1):70-76.
22. Edvardsson N, Frykman V. Van Mechelen R, et al. Use of an implantable loop recorder to increase the diagnostic
yield in unexplained syncope: results from the PICTURE registry. Europace. 2010;13(2):262-269.
23. Krahn AD, Klein GJ, Yee R, Hoch JS, Skanes AC. Cost implications oftesting strategy in patients with syncope: ran-
domized use55ment of syncope trial JAm Coll Ctirdiol. 2003;42(3):495-501. doi:10.1016/S0735-1097(03)00659-4
24. Sutton R, Petersen MEY. The clinical spectrum of neurocardiogenic syncope. J Cardiovasc Electrophysiol.
1995;6(7):569-576. doi: 10.1111/j.1540-8167.1995.tb00429.x
25. Benditt DG, Ferguson DW, Grubb BP, et al Tilt table testing for assessing syncope. l Am Coll Cardiol.
1996;28(1):263-275.
26. Benditt DG, Remole S, Bailin S, Dunnigan A, Asso A, Milstein S. Tilt table testing for evaluation of neurally-
mediated (cardioneurogenic) syncope: rationale and proposed protocols. Pacing Clin Electrophysiol. 1991;
14(10):1528-1537.
27. Kapoor WN, Smith MA, Miller NL. Upright tilt testing in evaluating syncope: a comprehensive literature review.
Am JMed. 1994;97(1):78-88.
28. Sheldon R. Tilt testing for syncope: a reappraisal. Cu" Opin Cardiol. 2005;20(1 ):38-41.
29. Waxman MB, Yao L, Cameron DA, Wald RW, Roseman J. Isoproterenol induction of vasodepressor-type reaction
in vasodepressor-prone persons. Am l Cardiol. 1989;63(1):58-65.
30. Almquist A, Goldenberg IF, Milstein S, et al Provocation of bradycardia and hypotension by isoproterenol and
upright posture in patients with unexplained syncope. N Engl l Med. 1989;320(6):346-351.
31. Morillo CA, Leitch Jw. Yee R, Klein GJ. A pi«ebo-controlled trial of intravenous and oral disopyramide for pre-
vention of neurally mediated syncope induced by head-up tilt./ Am Coll Cardiol. 1993;22(7):1843-1848.
32. Fujimura 0, Yee R, Klein GJ, Sharma AD, Boahene KA. The diagnostic sensitivity of electrophysiologic testing in
patients with syncope caused by transient bradycardia. N Engl JMed. 1989;321(25):1703-1707.
33. Gulamhusein S, Naccarelli GV. Ko PT, et al Value and limitations of clinical electrophysiologic study in assessment
of patients with unexplained syncope. Am JMed. 1982;73(5):700-705.
34. Kapoor W, Snustad D, Peterson J, Wieand HS, Cha R, Karpf M. Syncope in the elderly. Am l Med. 1986;80{3):
419-428. doi:l0.1016/0002-9343(86)90716-3
35. Lipsitz LA, Wei JY, Rowe JW, Syncope in an elderly, institutionalised population: prevalence, incidence, and asso-
ciated risk. QJM. 1985;55(1):45-54. doi:l0.1093/oxfordjournals.qjmed.a067852
36. Lipsitz LA. Syncope in the elderly. Ann Intern Med. 1983;99( 1):92. doi:l 0.7326/0003-4819-99-1-92
37. Mcintosh S, Costa DD, Kenny RA. Outcome of an integrated approach to the investigation of dizziness, falls and
syncope, in elderly patients referred to a 'syncope' clinic. Age Ageing. 1993;22(1):53-58. doi: 10.1093/ageing/22. l.53
38. Kenny RA. Syncope in the elderly. J Cardiovasc Electrophysiol. 2003;14{s9):S74-S77. doi:l0.1046/j.1540-8167.14.
s9.8.x
39. Jansen RWMM, Connelly CM, Kelley-Gagnon MM, Parker JA, Lipsitz LA. Postprandial hypotension in
elderly patients with unexplained syncope. Arch Intern Med. 1995;155(9):945-952. doi:l0.1001/archinte.1995.
00430090087010
40. Lipsitz LA, Pluchino FC, Wei JY, Rowe JW, Syncope in institutionalized elderly: the impact of multiple pathologi-
cal conditions and situational stress./ Chronic Dis. 1986;39(8):619-630. doi:l0.1016/0021-9681(86)90187-6
Sudden Cardiac Arrest/Sudden
Cardiac Death
HISTORICAL CONSIDERATIONS, DEFINITIONS, AND

EPIDEMIOLOGY OF SUDDEN CARDIAC ARREST
In 1956, Claude Beck.and colleagues described a case with resuscitation from out-of-hospital sud-
den cardiac arrest (SCA).H The patient. a practic:ing physician, had long suffered from what he
had self-diagnosed as indigestion. He experienced a persistent episode, went to the hospital and
was diagnosed with posterolateral. myocardial infarctJon (MI). Given the absence of treatment
at that time, he was discharged, but he collapsed just outside the hospital and was retrieved. He
underwent thoracotomy, open cardiac massage, then internal defibrillation and recovered.
External defibrillation (both AC and DC) was described in the middle of the twentieth century
by Zoll and colleagues' and independently by Gurvich in the Soviet Union.5 Accidents related
to the electrification ofsociety in part spurred this research.6 The success ofexternal defibrilla-
tion, applied promptly upon SCA due to ventricular fibrillation (VF), fostered the development
of dedicated coronary care units and ambulances equipped with defibrillators.6
Cardiac arrest is defined as a cessation of cardiac mechanical activity and an absence of

circulation.2.3 Focusing in on cardiovascular causes of cardiac arrest, it is helpful to subdivide
cardiac arrest into medical (cardiac arrest due to cardiac or other medical cause or unknown),
traumatic, drug overdose, drowning, electrocution, or asphyxia.2-7 See Table 15-1. A subset of
cardiac arrest is denoted as SCA, a term often used interchangeably with sudden cardiac death
(SCD), but with the latter denoting an absence ofsuccessful resuscitation. SCD has been denned
as "unexpected death without an obvious noncardiac cause occurring within 1 hour of symp-
tom onset" if witnessed or within 24 hours oflast being observed in normal or baseline health
if unwitnessed.M The definition, although logical, is difficult to implement on a broad scale,
and even in clinical trials, events committees struggle with classifkation.9 •11 A 1990 consensus
conference held at the Utstein .Abbey on a Norwegian island. spawned terminology bearing the
abbefs name.12 SCA classiflcation according to these conventions has included a number of
parameters, including the following: site of cardiac arrest (home, public, or other), preceding
clinical status, whether witnessed or not, precipitating event, bystander CPR, arrest before or
after emergency personnel arrival, initially recorded rhythm, treatment, return of spontane-
ous circulation (ROSC). hospital admission and discharge outcomes, neurologic status, and
others. Most studies have focused on out-of-hospital SCA, as in-hospital cardiac arrest has
Coronary artery disease

Acute lschemla +/-prior myocardial Infarction Long-duration post Ml benefits from ICD. CABG reduces SCA risk In chronle
ischemic cardiomyopathy.
Acute coronary occlusion {no prior CAD Size of ischemic zone; genetic determinants. Molecular mechanisms relatively
events) wel I-understood.
Coronary artery spasm Diagnosis may be occult. Vasodilator therapy. ICD need unclear. Prognosis
worse If atherosclerotlc CAD too.
Coronary artery dissection,,, Female predominance. Arterltls and connective tissue disease such as flbro-
muscular dysplasla. Diagnosis challenging; IVUS, OCT may help.•
Prior myocardial infarction, no acute ischemia The prior infarct may be clinically evident or silent.
HFrEF (ischemic cardiomyopathyl Beta blockers, ACE-I, statins, and other drugs. For EF s35, an ICD is indicated
after 40 days; further risk stratification has been suggested but no consensus.
HFmEF {ischemic) Beta blockers, ACE-I, statins, and other drugs. Number of SCA may outnumber
HFrEF though per-patient risk lower; largely unstudied.
HFpEF {lschemlc) Statlns; most pharmacologlc trials have been neutral.
Diiated, Idiopathic cardlomyopathy
HFrEF (nonischemic) For EF s3S, an ICD is indicated after 90 days; further risk stratification may be
warranted, however. Beta blockers, ACE-I, statins, and other drugs. Presence/
amount of OH E/scar by MRI may be predictive.
HFmEF (nonischemic) ICD not indicated for primary prevention but SCA risk may be high. Presence/
amount of DH E/scar by MRI may be predictive.
HFpEF (nonlschemlc) Statins; most pharmacologic trials have been neutral:
Other cardiac
Inherited/acquired Ion channel dysfunction Sudden arrhythmic death syndrome. Drug-Induced aT prolongation.
Hypertrophlc cardlomyopathy Risk factors for SCA Include severe hypertrophy (3.0 cm), NSVT, abnormal blood
pressure response to exercise, LVOT obstruction, LV aneurysm, syncope, sus-
pected VT, FH of SCD, extent of LGE.
Inherited cardiomyopathy Desmosomal proteins (ARVC/ALVC/AC); lamin A/C; other proteins.
Congenital heart disease Related to VT, VF, or also AT with rapid ventricular response; bradyarrhythmias.
Cyanotlc lesions, tetralogy, transposition of great vessels, unlventrlcular hearts,
and Ebsteln's are common causes.
Sarcoidosis17 May cause AV block, monomorphic or polymorphic VT, atrial arrhythmias, right
and/or left ventricular dysfunction. MRI or PET for diagnosis.
Mitral valve prolapse Bileaflet prolapse; need not be severe; outflow and fascicular or papillary mus-
cle ectopics; localized fibrosis near mitral annulus.
Aortic disease Aortic dissection.
Subsets at risk for non-VF arrests
At-risk for PEA PEA may be due to hypoxia, hypovolemla, hyperkalemla, hypothermia, pulmo-
nary thromboembolism, toxins, tension pneumothorax, cardiac tamponade.
PEA more common in women, African Americans, older patients, pulmonary
disease, anti psychotic drug use, prior syncope; OHT recipients. Seizure patients
with SUDEP may present with PEA and without antecedent seizure. Survlval
higher than asystole but lower than VF. Women survive PEA> men.
(Continued)
CHAPTER 15 • Sudden Cardiac Arrest/Sudden Cardiac Death 343
TABLE 15-1 Subsets of sudden cardiac arrest. (Continued)

rt111.1r.r.11~.1-111• .·u · ......... .~
At-risk for primary asystole Nonischemic causes of SCA; dialysis patients; OHT recipients; laryngospasm in
SUDEP; pulmonary disease; Asians.
Other
Obstructive sleep apnea Nocturnal SCA predominance; role of stretch, lschemla, autonomic
changes, hypoxia.
Neuromuscular disorders Myotonic dystrophy; Emery-Dreifuss; limb-girdle; facio-scapulo-humeral;

mitochondrial; dystrophinopathies (Duchenne, Becker, other).
Schizophrenia'" Anti psychotic drugs, coronary risk factors, DVT/PE, other.
Hypercoagulable states Pulmonary embolism.
(Adapted with permission from Narayan SM, Wang P, Daubert JP. New concepts in sudden cardiac arrest ro address an introctable epidrmic: JACC State-of-the
Alt Review. J Am Coll cardiol.20 I 9;73(1):70-S&J
different epidemiology and outcomes. 2 Important studies have included the Resuscitation Out-
comes Consortium (ROC),13 and the Cardiac Arrest Registry to Enhance Survival (CARES). 14
The ROC investigators estimated the incidence of out-of-hospital SCA to be 110.8 per 100,000
population, or 356,500 in the US in 2015.2 The Oregon Sudden Unexpected Death Study put
forward a slightly lower rate of 76 per 100,000 per year, after excluding noncardiac causes.15
ETIOLOGV OF SUDDEN CARDIAC ARREST

Arrhythmia Triggering Sudden Cardiac Arrest
The presenting arrhythmia includes ventricular tachycardia {VT}, VF as well as asystole/
bradycardia or nonpulsatile arrhythmias (pulseless electrical activity [PEA], formerly electrome-
chanical dissociation). The relative frequency ofVTNF or asystole/PEA differs for in-hospital
versus out-of-hospital cardiac arrest. PEA has been distinguished from pseudo-PEA where,
despite a nondetectable peripheral pulse, cardiac contractility is present producing a small aor-
tic pressure evident. True PEA, on the other hand, lacks aortic pressure, and usually cardiac
motion is absent. The prognosis is better for pseudo-PEA if the underlying cause can be treated
quickly. Table 15-1 lists the common causes. The electrocardiogram (ECG) during PEA has
been examined regarding QRS width, rate, and A-V relationship. The QRS is most often wide,
and often slow. Somewhat surprisingly; a more normal QRS may not predict survival.16
As compared with recording the rhythm minutes after the onset of SCA, special insight into
the mode of SCA has been gained with episodes of SCD occurring in subjects undergoing
Holter monitoring. Bayes de Luna et al assembled a case series of 127 patients suffering SCD
while wearing a Holter monitor. He excluded patients admitted with acute coronary events
or suffering end-stage heart disease. In this dataset, 83% suffered a fatal VTNF, whereas 17%
experienced a bradycardic arrest. 17 Initial VT with degeneration to VF was most common, but
about 12% of arrests were ascribed to torsade de pointes (TdP) and 8% to primary VF.
The incidence of in-hospital cardiac arrest has been estimated to be 1.6 per 1000 hospital
admissions. Survival to hospital discharge was approximately 24% but substantially higher at
49% when the initial rhythm was shockable versus 10.5% for asystole or PEA. Unfortunately,
over two-thirds of in-hospital arrests presented with a rhythm not amenable to defibrillation
(ie., not VT or VF).18
Of patients treated by EMS in 2015, 21.3% had an initial shockable rhythm (i.e., VT or VF). Sim-
ilar to in-hospital cardiac arrest, those presenting with VTNF survived to hospital discharge
more often than those presenting with a PEA or asystole, 29 .1 % versus 6.0%. 2 Out-of-hospital
SCA survival increased slightly between 2006 and 2015 from 10.2% to 12.4%.2 Approximately
one-half of out-of-hospital SCAs are unwitnessed, about 40% bystander witnessed, and 10%
EMS witnessed. Survival is better when SCA occurs in a public setting, or when witnessed, but
unfortunately, 70% ofSCAs occur in the home.2
Several demographic features of SCA are notable. First, SCA is highest in blacks at I 0.1 per
100,000 adults versus about 6.5 for Hispanic and 5.8 for non-Hispanic whites.2 Second, low
socioeconomic status doubles the incidence of SCA, and portends a much worse outcome, too.
Third, although the absolute incidence of total mortality and of SCA is higher in more symp-
tomatic heart failure (NYHA III-IV), the proportion of total deaths due to SCA is higher in less
symptomatic heart failure (NYHA 11).19 Fourth, a family history of SCA in a first-degree relative
doubles an individual's risk of SCD.2°Fifth, the proportion of SCA caused by VF seems to have
declined, resulting in PEA comprising a greater proportion of SCA events.21.22
Coronary Artery Disease-Related Sudden Cardiac Death

Acute ischemia and/or MI due to coronary artery disease (CAD) represent the most common
mechanism identified in victims of SCD. However, the proportion of SCD attributed to CAD
appears to be declining over time. Moreover, in women, non-CAD events are relatively more
common. SCA related to CAD is multimodal and exhibits important temporal behavior
(Figure 15-1 and Table 15-1).2' The first phase of acute ischemia (0-30 minutes) may result
in polymorphic VT and VF. Such events are often the first symptom of CAD. Ischemia sets
off a complex pathophysiologic process including acidosis, extracellular accumulation of
potassium, cellular depolarization followed by conduction block, and an initial shortening
then prolongation of refractory periods. A second phase, between 30 and 90 minutes after the
onset of ischemia, exhibits a lower burden of VT/VF than the first phase. However, the
third phase, beginning 90 minutes after vessel closure, results in arrhythmias stemming
from regional inhomogeneity in terms of conduction and refractoriness, as well as trig-
gered activity from calcium overload and catecholamine excess.u.27 The superimposition of
acute ischemia on top of prior infarction appears to be especially risky. 28 On the other hand,
reperfusion occurring after about 5 to 30 minutes of acute ischemia is also a potent stimulus
for polymorphic VT and VF." The risk of VT/VF remains heightened for the first 48 hours
of an acute Ml. Given the unique physiology at play during this complex period, survivors
of VT /VF events tend not to have an increased risk oflate recurrence (when adjusted for
size of infarction)." Although SCA risk declines somewhat after 48 hours, it remains ele-
vated to about 30 days, especially for those with ejection fraction below 30%.29
An occlusive or nonocclusive coronary thrombus was identified in 74% of 100 CAD patients
with SCD in London.:ro.J1 Subsequent studies, however, report a lower incidence of acute cor-
onary occlusion.' 1.32 Occlusion was most frequently identified in individuals without prior
infarction whereas those with healed infarction and/or multivessel disease often did not have
an acute thrombus.' 1.J2 A Swedish study cataloged the findings at coronary angiography in 638
consecutive patients undergoing catheterization due to SCA." Most patients who underwent
CHAPTER 1 S • Sudden Cardiac Arrest/Sudden Cardiac Death 345
PanelA Pan•IB Pantle Panel D

lschemic
cardiomyopathy
Stable Acute
plaque- occlusloo
Unstable
plaque
MODIFIERS:
lschemlc burden
Hemodynamic fluctuations
Autonomic variations
Drugs/electtotytes
Genetic profile
FIGURE 15-1 • Mechanllmsfor SCD In th• salting of CAD. The Interplay and etiologyoflschemla and Infarction as causing SCD
is illustrated. (Reproduced with permission from Myerburg RJ, Junttila MJ. Sudden cardiac death caused by coronary heart disease.
Circulation. 2012;125:1043-1052.)
catheterization were found to have an acute occlusion, including 37% of patients lacking ST
elevation. Importantly, these patients with SCA in the fust 48 hours ofan acute infarct would
not qualify for an implantable cardioverter-defibrillator (ICD) as will be highlighted below.
Dilated, Nonischemic Cardiomyopathy (NICM)-Related Sudden Cardiac Arrest

VT/VF likely accounts for most SCA in NICM. However, in a small series of patients with very
advanced, non-ischemic heart failure, awaiting transplantation, 7/7 SCAs were due to bradyar-
rhythmia or PEA.34 Anderson et al examined the myocardial substrate of NICM patients in vivo
immediately prior to cardiac transplantation.'5 Propagation was impaired in some but not all
patients particularly transverse to fiber orientation, and even longitudinally in some. Conduc-
tion disturbance was related to the degree offibrosis found.
RESUSCITATION FROM SUDDEN CARDIAC ARREST

Survival rates from SCA average about 7.6%, but vary substantially in different communities.36
Unfortunately, survival has not improved substantially over the past 30 years.j7 Factors pre-
dicting survival from SCA include presence of 1 or more of the following: arrest witnessed by
either a bystander or by EMS, provision of bystander CPR, a shockable rhythm (as opposed to
asystole or PEA). and return ofspontaneous circulation (ROSC) at the scene. ROSC is by far the
strongest predictor and shockable rhythm is second.l 7 Pooled analysis of the effect of bystander
CPR showed that it is most beneficial in communities having a relatively low baseline survival
rate, likely reflecting long EMS arrival times. In part this may be because CPR can forestall the
deterioration of VF to asystole (Figure 15-2).37 Compression-only CPR has been found to gen-
erate equivalent outcomes to chest compression plus ventilation.3""
Confirm cardiac arrest
High-quality (PR
Attach monitoring
Assess rhythm
Shock.able Consider and treat High-quality CPR: Non-shock.able

reversible causes: Chest compressions
'
~-
Hypoxia
Hypovolaemia
Hyperlc.alaemia
Hypothermia or
hyperthermia
of5-6cm
Rate of chest
compressions
100-120 min·•
Avoid leaning
- ill
Thromboembolism Minimal
Deliver shock x1 Toxins interruptions
Tension Ventilations 10 min·•
pneomothorax Manage airway
Continue CPR 2 min Tamponade Consider drug Continue CPR 2 min
NoROSC
Reassess rhythm and restart loop
Consider prognostic factors
Continue, terminate, or transport
ROSC
Start post·resosc.itation care
Transport to hospit.-il
FIGURE 15-1 • Flow chlrt for l'ffUSdtatlon of SCA. The sequence for CPR, deflbrtllatlon, and dlagnosUc considerations are shown.
(Reproduced with pHmlsslon from Ong MEH, Perkins GD, Carlou A. Out-of-hospltal cardiac arrest: prehospltal management.
The Lancet. 2018;391 :98C>-988. Copyright C Elsevler.)11$
Evidence for early defibrillation comes from many observational studies and from a random-
ized community-based trial where some neighborhoods (community units) received CPR
training and others CPR training plus automated external defibrillator (AED) training and pro-
vision. Survival from SCA in the AED arm was about double that in the CPR-only group.40 An
Italian community study supports early defibrillation using AED deployment by community
volunteers with achievement of earlier response, more shockable rhythms, and substantially
higher survivals of-3096!1 Some controversy exists on the relative benefits, primacy. and tim-
ing concerns for CPR and defi.brillation.36.•1-43 Defibrillation should not be delayed to perform
CPR for a monitored arrest caused by VTNF. CPR is advocated for a short period with an
unmonitored arrest until the AED is available,36 although there is no clear advantage ofdelaying
defibrillation to provide additional CPR.'"
Antiarrhythrnic drugs have long been used to treat refractory or recurrent ventricular arrhyth-
mias during the course of defibrillation attempts.45 Kudenchuk et al conducted a randomized,
blinded trial of amiodarone vs lidocaine vs placebo, enrolling about 1500 patients in each arm.46
The primary endpoint, survival to discharge, was not different in the 3 arms (about 21 %-24%).
Nor was neurologic outcome affected by either drug. Lidocaine and amiodarone increased sur-
vival to admission modestly. When subjected to meta-analysis, only lidocaine and amiodarone
have performed better than placebo in increasing ROSC and survival to hospital admission.
Unfortunately, no antiarrhythrnic drug has shown an improvement in survival to hospital dis-
charge or survival free from neurologic impairment.45
After ROSC has been accomplished, treatment goals include a temperature of 32°C-36°C (for
unresponsive patients), initial use of 100% oxygen to avoid hypoxia followed by titration to
avoid hyperoxia, and deferring a decision on neurologic outcome for 72 hours. Emergent cor-
onary angiography should be performed in the presence of STEMI or if occlusion is strongly
suspected.47 A recent trial indicated that in the absence of obvious STEMI, emergent catheteri-
zation was not superior to clinically guided, delayed catheterization.48
Extracorporeal CPR (ECPR) has been used for refractory SCA as well as hypothermic and other
arrests in adults and especially in pediatric patients. This involves establishing large venous and
femoral arterial access and implementing venoarterial extracorporeal membrane oxygenation
from extracorporeal circulation and oxygenation (ECMO). Current guidelines are sparse, but
mention consideration ofECPR for SCA ongoing for 10 minutes without ROSC in individuals
under 75 years of age.49·so
EVALUATION OF SURVIVORS OF SUDDEN CARDIAC ARREST

Coronary Artery Disease-Related Sudden Cardiac Arrest Survivors
Although fewer than 10% of SCA victims survive, these survivors remain at high risk of recur-
rent VF. CAD is the most common cardiac finding in SCA survivors, but can take several forms,
including STEMI, NSTEMI, and prior infarct. Patients with prior infarction who present with
SCA in the absence of a new acute MI are a very high-risk group for recurrent VT/VF. The sit-
uation is more complex when an acute MI (or acute ischemia) is apparent VF may occur at any
time after an Ml, but (assuming the patient is resuscitated) its prognosis varies according to its
timing from the MI onset (~48 hours, early or primary vs >48 hours, late or secondary). The
incidence of early VF in acute MI has averaged about 3%-5%,51 but has declined slightly with
reperfusion.52 The risk factors for early VF include large infarct (by enzyme level), new BBB, male
gender, absence of prior angina, low potassium, smoking, and AV block. Early VF patients, due to
the association with larger infarct, face a higher in-hospital mortality, but, interestingly, their risk
of late VF is not increased. Studies in the reperfusion era have shown that patients with late VF
fared worse in follow-up compared to those with early VF.53-55
The incidence of sustained VTNF is 1.5% in non-ST elevation MI (NSTEMI). Unlike STEMI,
VF occurs more often after 48 hours. However, as for STEMI, late VF has a worse prognosis por-
tending a 20-fold increased mortality risk.~ Nonsustained VT during NSTEMI predicts late VF. 57
The Antiarrhythmics Versus Implantable Defibrillators (AVID) trial randomized about

1OOO patients who were either survivors of SCA (due to VT or VF) or had sustained VT
(Table 15-2) to an ICD or to antiarrhythmic medication (-95% amiodarone, initially).58
CASH120 2000 VT NF Arrest. Excluded If revers- 288 ICD vs antl-arrhyth- 23% nonslgnlflcant reduction
Ible cause of arrhythmia. mlcdrug In ACM (~.08) and 58%
reduction in SCD (p=0.005).
MADIT"' 1996 Prior Ml, EF s35%, NSVT, NYHA 196 ICD vs medical 54% reduction in ACM
1-111 and positive EP study. therapy (~.009) with ICD.
AVID58 1997 VF; VT & syncope; or symptom- 1013 ICD vs amiodarone 31 % reduction in ACM
atlcVTwlth EF :!>40. orsotalol (p<0.02) with ICD at 3 years.
AVID Reglstry65 2001 VTNF due to a transient, cor- 287 N/A Survival slmllar or worse for
rectable cause (e.g., acute Ml or patients with seemingly tran-
ischemia or electrolytes). sient cause of VTNF compared
to AVID-eligible patients.
CABG Patch 122 1997 <80 yo, EF <36%, abnormal 1055 ICDvsnolCD 7% nonslgnlflcant Increase In
SAECG undergoing elective ACM with ICD.
CABG.
MUSTT"" 1999 CAD, EF s40% and NSVT, plus 704 EPS vs no EPS: (If 27% reduction in SCD (pri-
inducible VT-S. +EPS, antiarrhyth- mary endpoint) (~.04). 20%
mlc drug or ICDJ reduction In ACM (~.06).
SCD reduction driven entirely
by ICD implantation.
CIDS' 24 2000 SCA or VT with syncope or syn- 659 ICD vs amiodarone 20% nonsignificant reduction
cope & NSVT. Exclude reversible in ACM (~.142). 33% non-
or genetic causes. significant reduction In SCD
(P=0.094).
MADITll':u 2002 Ml at least 30 days prior; EF 1232 ICD vs medical 31 % reduction in ACM
s30%. Excluded 2" prevention, therapy (P=0.016). First large trial to
serious comorbidities with show benefit of ICDs as pri-
<1 year prognosis. mary prevention modality.
CAT73 2002 New-onset dllated cardlomyop- 104 ICDvsnolCD Trlal stopped due to less than
athy, EF s30%. 30% mortality In control arm
in 1 year. No reduction in ACM.
DEFINITE" 2004 NICM, EF <36%, PVCs or NSVT. 458 ICD vs medical 35% reduction in ACM
therapy (~.06). 80% reduction in
SCD (p=0.006).
DINAMIT126 2004 EF s35%, 6-40 days after acute 674 ICD vs medical No reduction in ACM. 58%
Ml, HR <80. Exclusions: indi- therapy reduction in SCD (P=0.009).
cation for ICD for sustained ICDs not helpful early after
VT NF; anticipated survival acute Ml (40 days).
<1 year; 3-vessel CAD and
revascularization.
SCD-HeFT72 2005 EF s35%, NYHA II, Ill. ICM or 2521 Amiodarone vs 23% reduction in ACM
NICM. placebo vs ICD (~.oon. No difference in
placebo vs amiodarone.
IR1s121 2009 HR >90 on first ECG after Ml; 898 ICD vs medical No reduction In ACM. Con-
post Ml-2-30 days, EF s40%; therapy firmed DINAMIT. SCD reduced
NSVT > 150 bpm on days 5-31. but offset by increased rate of
non-sudden death.
(Continued)
DANISH74 2016 NICM, EF :!":35%, NYHA II, Ill, (IV 1116 ICD vs standard 13% nonslgnlflcant reduction
If CRT}. Excluded: permanent care (Included CRT In ACM (p=0.28). 50% reduc-
AF with HR >100; comorbidities in58%) tion in SCD (p=0.005). lnter-
with anticipated survival <S pretation confounded by high
years. use of CRT in control arm.
Notrs: The endpoint was all-cause mortalityIn all trials excrpt MUSrTIn which It was SCD.
Abbreviations: ACM, all-cause mortality; SCD, sudden cardiac death; EF. ejection fraction; Ml, myocardial infarction; HR, heart rate; NICM, nonischemic car-
diomyopathy; ICM, ischemic cardiomyopathy; NSVT, nonsustained VT.
Adjusted total mortality was reduced by 33% in the ICD arm (Figure 15-3). An individual
patient data meta-analysis of AVID and 2 similar trials supported this observation, with a
50% reduction in arrhythmic mortality. On subgroup analysis, the benefit was not apparent
when the EF was above 35%.59 Given these observations, guidelines warrant implantation of
an ICD in survivors of SCA. VT/VF occurring in the first 48 hours of an MI represents an
1.0
0.8
~
l:
~ 0.6
i
IS
~D. 0.4
E!
a..
0.2
o.o~~~~~~~~~~~~~~~~~~~~~~~~~~~~-
o 2 3
Years llftar randomization
Patients at risk 1016 644 333 104

Percent surviving
Defibrillator group 89.3 81.6 75.4
Antiarrhyth mic-drug group 82.3 74.7 64.1
FIGURE 15-3 • Survival free from all-cau5e-mortillity in AVID. SCA survivors were randomized to ICD or amiodarone in the Anti-
arrhythmics versus Implantable Defibrillators (AVID} trial. (Reproduced with permission from Antiarrhythmics versus implantable
deflbril lators I. A comparison of antlarrhythmlc-drug therapy with Implantable deflbrlllators In patients resuscitated from near-fatal
ventricular arrhythmias. N Engl J Med. 1997;337:1576-1583. Copyright C 1997 Massachusetts Medical Society.)
ICD exclusion.60 Importantly, beta blockers, ACE inhibitors (or ARBs), and mineralocorti-
coid receptor antagonists are also indicated for HFrEF with EF <40%.60 AVID also reported
on a registry of patients ineligible for randomization due to an apparently reversible cause
with results similar to the main cohort (Table 15-2). 61 •62
In the rarer situation of coronaryvasospasm-induced VF, an ICD is recommended when medi-

cal therapy (calcium blockers, smoking cessation) is ineffective or not tolerated (Class IIA indi-
cation) and receives a cautious endorsement (Class IIB indication) even for those not failing
medical therapy. 60
Dilated, Nonischemic Cardiomyopathy-Related Sudden Cardiac Arrest Survivors

AVID58 and similar trials59 also studied NICM patients. Based on these studies, an ICD is advis-
able for NICM patients who are survivors of SCA, and those with stable or unstable VT. In the
setting of syncope and NICM, an EP study is appropriate to assess for inducible VT (unless a
primary prevention ICD is already indicated, see below). 60
Sudden Cardiac Arrest Survivors without CAD or Left Ventricular Dysfunction

Up to 20% of patients resuscitated from SCA do not demonstrate significant CAD, or signifi-
cant LV dysfunction. Moreover, one should keep in mind that LV dysfunction immediately
after resuscitation from SCA may represent transient stunning.63 One then considers inherited
causes (ARVC, HCM, LQT, Brugada, CPVT, and others), infiltrative disease (e.g., sarcoido-
sis, amyloidosis), and primary arrhythmic causes such as WPW and 1:1 AFL (Table 15-3).
The resting ECG and any tracings prior to, during, or after the arrest warrant scrutiny for the
above causes. However, early post SCA the ECG may falsely exhibit a Brugadalike pattern,64
and the QT may be transiently long (especially during therapeutic hypothermia). The Car-
diac Arrest Survivors with Preserved Ejection Fraction Registry (CASPER) enrolled 63 SCA
patients who presented with an apparently normal ECG, no CAD, and preserved LV func-
tion. CASPER adopted a standardized battery of testing, including MRI, exercise, epinephrine
and/or procainamide drug challenge, signal-averaged ECG, and electrophysiologic (EP) study.
The etiology for the SCA (LQTS, CPVT, ARVC, early repolarization, coronary spasm, Brugada,
and myocarditis) was ascertained in over half of patients, whereas 44% were labeled idiopathic
VF (Figure 15-4). An ICD is recommended for essentially any of these conditions when pre-
senting with SCA, with possible exceptions noted in Table 15-4.
RISK STRATIFICATION AND PRIMARY PREVENTION IN ISCHEMICAND

NONISCHEMIC CARDIOMYOPATHY
Because only a small minority (-8%-10%) of SCA victims are successfully resuscitated, intense
interest has been directed toward risk stratification in an effort to identify high risk of SCA
and intervene accordingly. In particular, the intervention most studied has been the ICD. The
Myerburg "paradox" notes that high risk groups can be identified, and aggressive interventions
such as an ICD can be deployed, but the preponderance of SCA events in the overall population
occurs in individuals either not recognized to have cardiac disease or those cardiac patients
with an ostensibly low SCA risk (Figure 15-5).23 Organized follow-up of MI survivors in the
1970s and early 1980s identified low ejection fraction and/or complex ventricular ectopy as
SCA risk factors (Figure 15-6).65-01 It was subsequently hypothesized that the suppression of
Inherited
Hypertrophic cardiomyopathy Usually abnormal; LVH, T-wave Localized or diffuse LV wall VF,AF,MMVT
(HCM) inversion, Q waves thickness >13-15 mm; often
septa I; resting LVOT g rad lent
(30%), only exertlonal LVOT
gradient (30%); LGE may be
present.
Arrhythmogenic RV cardiomy- T-wave inversion in V1-V3; MRI showing focal RV akinesis, PVCs; MMVT, VF; AF
opathy/dysplasla (ARVC/D) delayed termlnal component RV enlargement; flbrofatty
of QRS In V1-V3; epsilon replacement; frequently
waves (rare) involves LV too.
Long QT syndrome (LQTS) QRS normal, QTc >460 Normal Torsade de pointes, VF
(male)/470 (female); QTc may
be normal; abnormal T-wave
morphology
Brugada syndrome V1-V3 exhibits R'and 2-mm Echo normal; reports of PMVT, VF; AF; MMVT
J-point elevation, coved ST abnormal MRI in RVOT.
elevation, T-wave inversion
Catecholaminergic polymor- Normal at rest. PVCs and Normal PVCs; bidirectional VT,
phlc VT (CPVTJ bldlrectfonal VT with exercise PMVT,VF;AF
or stress
Short QT syndrome (SQTS) QTc <350, especially <330; Normal rapid PMVT, VF; AF
(possibly <370)
Early repolarization (ER) Inferior or lateral precordial Normal VF
syndrome notch (J wave) or slur on the
downslope
Idiopathic VF Normal Normal VF
Nonlnherlted (usually}
Sarcoidosis Many possible abnormalities RV or LV dysfunction and VT, VF,AF
including AV block scarbyLGE.
Myocarditis Sinus tach, ST-T changes, Inflammation, scar by LGE, LV VT,VF
BBB,etc. dysfunction.
Mftral valve prolapse PVCs, posslble T-wave Blleaflet prolapse; MR need PVCs (OT, fasclcular or papll-
changes not be severe; localized fibre- lary muscle), VF, VT
sis near mitral annulus.
Note: I.GE, late gadolinium enhancement on MRI.
PVCs in post-MI patients would reduce SCA risk. Seeking to test the PVC hypothesis, the
Cardiac Arrhythmia Suppression Trial (CAST) randomized MI survivors with a mean LVEF
of 0.40 and with >6 PVC/hour to either flecainide, encainide, or moricizine versus placebo.68
Although PVCs were indeed suppressed, and only such responders during a run-in phase were
randomized, mortality was actually increased with the active drugs. Recurrent ischemia likely
triggered a fatal arrhythmia in the antiarrhythmic group vs those on placebo.68M Amiodarone
also failed to reduce total mortality in post-MI and low EF patients, although it did reduce SCA
to some degree, especially when combined with beta blockers.70 Meanwhile beta blockers were
Idiopathic Diagnosed
Myocarditis
FIGURE 15-4 • Diagnostic yield in SCA survivors with preserved EF. A prospective, systematic study evaluating 63 SCA survivors
with preserved ejection fraction uncovered a diagnosis in 56%. (Reproduced with permission from Krahn AD, Healey JS, Chauhan V.
et al. Systematic assessment of patients with unexplained cardiac arrest: Cardiac Arrest Survivors With Preserved Ejection Fraction
Registry (CASPER). Circulation. 2009;120:278-285.)
found to benefit MI survivors and even HFrEF patients for whom they had previously been
contraindicated. Presently, only beta blockers are indicated for primary prevention of mortality
or SCA in post-MI or low EF patients, and not Class I or III agents.60
With the failure of antiarrhythmic drugs to reduce SCA, the ICD was evaluated. Initially, ische-
mic cardiomyopathy patients with low EF were targeted and a reduction in total mortality was
evident with the use of the ICD (see Figure 15-7 and Table 15-2). Thereafter, patients with non-
ischemic cardiomyopathy were studied and also found to benefit upon meta-analysis, although
the individual trials were borderline in significance. 71-73 A recent trial did not identify a sig-
nificant mortality reduction, but it may have been underpowered given the large percentage of
patients receiving cardiac resynchronization therapy, also a lifesaving intervention.7• Even with
the latest trial, meta-analyses show a reduction in mortality with ICD treatment in this popu-
lation, yet controversy persists (see Figure 15-7 and Table 15-2).75 Several neutral studies have
identified scenarios where an ICD seems not to be beneficial: (1) in low EF post-Ml patients
undergoing coronary artery bypass grafting (CABG) where the benefit of revascularization
curtails much of the sudden death risk in the short term and (2) early after MI where a reduc-
tion in sudden death appears offset by competing risks (Table 15-2).
Over half of SCA events occur in patients not presently indicated for an ICD, and, conversely,
most primary prevention ICD recipients do not suffer what would have been a fatal arrhythmic
event in the first several years after implantation. Consequently, improved risk stratification
remains a holy grail. Innumerable tests have been considered, and while many are predictive,
only LVEF, despite its limited sensitivity and specificity, is clinically used. The presence of scar
on MRI offers some promise. Table 15-5 summarizes some of the most common tests. Several
recent reviews address risk stratification for SCA.76-82
While many SCAs occur in patients with preserved EF and other apparent low-risk features,
numerous patients seemingly meet ICD implant criteria on paper but may in reality be poor
candidates. Age alone is a poor discriminator, but in DANISH, younger patients tended to
TABLE 15-4 Implantable cardioverter-defibrillator (ICD) indications.60.64·96•128

Secondary Prevention ln lschemlc or Nonlschemlc Cardlomyopathy
Class I Survivors of cardiac arrest due to VF or hemodynamically unstable sustained VT after evaluation to define
the cause of the event and to exclude any completely reversible causes;VTNF in the first 48 hours of an Ml is
excluded.
Class I Patients with structural heart disease and spontaneous sustained VT, whether hemodynamlcally stable or unstable.
Primary Prevention In lschemlc or Nonfschemfc Cardiomyopathy

Class I Patlents with clinically relevant, hemodynamlcally significant sustained VT or VF Induced at electrophysfologlc
study.
Class I Patients with LVEF <35% due to prior Ml who are at least 40 days post-Ml and are NYHA functional Class II or Ill;
patients should be receiving GDMT.
Class I Patients with nonischemic DCM who have an LVEF s35% and who are NYHA Class II or Ill; patients should be
receiving GDMT.
Class I Patients with LV dysfunction due to prior Ml who are at least 40 days post-Ml, have an LVEF <30%, and are NYHA
functional Class I; patients should be receiving GDMT.
Class I Patients with nonsustained VT due to prior Ml, LVEF <40%, and inducible sustained VT at electrophysiologic study;
patients should be receiving GDMT.
ClassllA Patients with unexplained syncope, significant LV dysfunction, and nonischemic DCM.
ClassllA Patients with sustained VT and normal or near-normal ventrlcular function.
ClassllA Ambulatory NYHA class IV symptoms who are candidates for cardiac transplantation or an LVAD.
ClassllB Patients with nonlschemlc heart disease who have an LVEF of s35% and who are In NYHA functional Class I.
ClassllB Patients with syncope and advanced structural heart disease in whom thorough invasive and noninvasive investiga-
tions have failed to define a cause.
Class Ill ICD therapy is not indicated: A) for patients who do not have a reasonable expectation of survival with an acceptable
functional status for at least 1 year, even if they meet ICD implantation criteria specified in the Class I, Ila, and llb rec-
ommendatlons above; 8) for patients with Incessant VT or VF; CJ In patients with significant psychlatrlc Illnesses that
may be aggravated by device implantation or that may preclude systematic follow-up; D) for NYHA Class IV patients
with drug-refractory congestive heart failure who are not candidates for cardiac transplantation or CRT-D; El for syn-
cope of undetermined cause in a patient without inducible ventricular tachyarrhythmias and without structural heart
disease; F) when VF or VT Is amenable to surglcal or catheter ablation.
Cardiac Sarcoldosls
Class I Patients with cardiac sarcoldosls who have spontaneous sustained ventricular arrhythmias, Including prior cardiac arrest.
Class I Patients with cardiac sarcoidosis who have LVEF s35% despite optimal medical therapy and a period of immunosup-
pression (if there is active inflammation).
ClassllA Patients with cardiac sarcoidosis who have LVEF >35% but an indication for permanent pacemaker implantation;
OR unexplained syncope or near-syncope, felt to be arrhythmic in etiology; OR inducible sustained ventricular
arrhythmlas.
ClassllB Patients with cardiac sarcoldosls who have LVEF 36% to 49% and/or an RV ejection fraction <40%, despite optimal
medical therapy for heart failure and a period of immunosuppression (if there is active inflammation).
Hypertrophlc Cardlomyopathy
Class I HCM patients with SCA due to VT or VF; or hemodynamically not tolerated or syncopal sustained VT.
ClassllA HCM patients who have 1 or more major risk factors for SCD (maximum LV wall thickness 01:30 mm, or SCD in 1 or
more first-degree relatives presumably caused by HCM, or 1 or more episodes of unexplained syncope within the
preceding 6 months).
(Continued)
•r~1=1•::1 Li:!'· IJF.li1F.li'l~ '" 11'.f:.JU:.JC! ;~iJ iJ1llf:h •]•11••llUI[' n..-'U

......... . 11• ... 111[;(1
ClassllA HCM patients who have NSVT or abnormal BP response to exen::ise and an additional non-major criterion (age <30 years,
DHE on MRI, LVOT obstruction, distant syncope).
Class llB HCM patients who have NSVT or abnormal BP response to exen::ise but no additional nonmajor criterion.
Lamin A/C Mutation
Class I Survivors of sudden cardiac arrest (due to VTNFJ.
ClassllA Patients with NICM due to a Lamln A/C mutation who have 2 or more risk factors (NSVT, LVEF <45%, nonmlssense
mutation, or male sex).
Arrhythmogenlc RV Cardlornyopathy
Class I ARVC patients with prior SCA or hemodynamically not tolerated sustained VT.
ClassllA ARVC patients with prior hemodynamically tolerated sustained VT or syncope presumably due to VT.
ClassllA ARVC patients with 3 major or 2 major and 2 minor or 1 major and 4 minor criteria.
Class 118 ARVC patients with 2 major, or 1 major and 2 minor or 4 minor criteria.
BNgada Syndrome
Class I Brugada syndrome patients who are survivors of SCA (due to polymorphlcVTNF).
ClassllA Brugada syndrome patients who have syncope or documented VT that has not resulted In cardiac arrest.
Class llB Patients with type I Brugada pattern ECG without syncope or prior SCA but with lnduclble sustained polymorphic VT/
VF during EP study (limited to 2 VES).
Long QT Syndrome
Class I LQTS patients who are survivors of SCA (due to polymorphic VTNF).
Class I LQTS patients who have had syncope while taking a beta blocker; an alternative treatment is left cardiac sympathetic
denervatlon.
Class llB LQTS patients who have not had syncope or SCA but have a QTc >500 (on beta blocker); an alternative treatment Is
left cardiac sympathetic denervation.
Catecholaminergic Polymorphic VT
Class I CPVT patients who are survivors of SCA (due to polymorphic VTNF). Maximal medica I therapy recommended before
and/or during ICD therapy.
Class I CPVT patients who have syncope while taking maximally tolerated beta blocker; alternative is left cardiac sympa-
thetlc denervatlon or flecalnlde. Maximal medical therapy recommended before and/or during ICD therapy.
Short QT Syndrome
Class I SQTS patients who are survivors of SCA (due to polymorphic VTNF).
Class I SQTS patients with documented sustained VTNF.
Early Repolarization Syndrome
Class I Survivors of sudden cardiac arrest (due to polymorphicVTNF).
Class 118 ERS patients with syncope and FH of SCA at young age.
Class llB ERS patients with asymptomatic status but definite, high-risk ER pattern and FH of SCA at young age.
Myotonic Dystrophy
Class I Survivors of sudden cardiac arrest (due to VTNFJ.
Class llB Patients with myotonlc dystrophy type 1 who have an Indication for a permanent pacemaker; use of an ICD with
pacing capability is a valid alternative.
'ICD candidates should have antidpated survival with acceptable quality of/ffe for 1ymr or longer.
Incidence Populatlon subgroup Events
EF<30"1o; heart failure
Cardiac arrest survivor
Arrhythmia risk markers,

post-myocardial infarction
0 10 20 30 o 150,000 300,000
Percent Absolute number
FIGURE 15-5 • Schematic of problem with primary prevention of SCA. See text for details regarding the Myerburg "paradox."
(Reproduced with permission from Myerburg RJ, Junttila MJ. Sudden cardiac death caused by coronary heart disease. Circulation.
2012;125:1043-1052.)
50
15 (<20%)
Sudden cardiac
14
~ 40
death N=799
13
12
(55)
P value
•
'C
0
MEAN EF=46"1o
11 Cvs N <0.01 E
Cvs S < 0.03 ~ 30
~ 10
Svs N < 0.09 1!
' n
9
0
E 8 .. 20
'E
~
7
6 f
c
l. 5 .,.
0 10
4
(~O"lo)
3
2 00 15 30 45 60 75
1 Radionuclide ejection fraction {%)
00 10 20 30 40 50 N- 21 244 382 152
Panel A PanelB
FIGURE 15-6 • Prognostic significance of PVCs and low ejection fraction In post-Infarction patients. Data from The Multl-
center Postlnfarctfon Research Group, which enrolled 866 patients from 4 geographic areas and followed them for outcomes.
(Reproduced with permission from Moss AJ, Davis HT, Decamilla J, Bayer LW. Ventricular ectopic beats and their relation to sudden
and nonsudden cardiac death after myocardial-Infarction. Circulation. 1979;60:998-1003 and Multicenter Postinfarction Research
Group. Risk stratification and survival after myocardial infarction. N Engl J Med. 1983;309:331-336. Copyright e 1983 Massachusetts
Medical Soclety.) 116
ICD (N) I No ICD (N) Weight HR(95%CI)
MAOITI 1996 95 I 101 i 12.85% 0.46 ! 0.26 • 0.82 J
I
MADITlf 2002 742 490
~1 27.83% o.69 ! o.51 • o.93 J
COMPANION 2004 325 I 331

I t I
26.28% 1.01!o.74,1.40 J
SCO-HeFT 2005 431 I 452

I • ! 33.04% o.79 I o.62. 1.00 J
Summary, random effects (p=0.02) 100.ooo;. o.76 ! o.so. o.96 I
0.25 0.50 1.00 2.00

ICD better Hazard ratio ICD worse
Panel A
ICD (N) I No ICD (N) Weight HR(95%CI)
CAT2002 50 I 54 5.59% o.80 ! o.39 , 1.64 J
AMIOVIRT 2003 52 I 51 2.78% o.87 ! o.32 • 2.42 J
I 2.29 o.65 ! 0.40 • 1.06 J

~
DEFINITE 2004 229 11.95%
COMPANION 2004 270 I 2as ~1 12.28% o.55 ! o.34 , o.89 J
SCO-HeFT 2005
DANISH2016
398
556
I 394
I 560
--i
~
24.91%
42.49%
o.73 ! o.52, 1.02 J
o.87 ! o.sa, 1.12 J

i
'
Summary, random effects (p=0.001) 1oo.ooo;. o.76 ! o.64 , o.90 J
0.25 0.50 1.00 2.00 4.00

ICD better Hazard ratio ICD worse
PanelB
FIGURE 15-7 • Primary prevention ICD trials. This shows a meta-analysis of ICO and alkause mortality in ischemic: c:ardi~
myopathy (Panel A) and In nonlschemlc: c:ardlomyopa'Chy patients (Panel 8). (Reproduced with permission from Shun-Shin MJ,
Zheng SL, Cole GD, Howard JP, Whlnnett ZI, Francis OP. Implantable can:lloverter deflbrtllators fer primary preventfon of death In
left ventricular dysfunction with and without lschaemlc heart disease: a meta-analysls of 8567 patients In the 11 trials. Eur Heart J.
2017;38(22):1738-1746.)117
benefit more from ICD therapy. Relatively few very elderly patients were enrolled in pivotal trials,
including only 25% of SCD-HePT being over age 68, and only 16% over 75 years in MADIT-11.
While some short-term studies have found benefit in these moderately old individuals,c data are
limited. Clearly, the number ofcomorbidities such as renal dysfunction increases with age. Even
moderately severe degrees of renal d-y5function (GFR <35) may eliminate benefit of an !CD due
to competing risk.s.84 Guidelines stress that patients should be anticipated to survive for 1 year
with a good quality of life. Scoring systems have been developed in patients with systolic heart
failure to estimate survival and the likelihood for a SCA versus the myriad competing mortality
risks to occur.85 Implementing these considerations requires a comprehensive understanding
ECG-based
QRS width or LBBB Delayed depolarization due to scar; abnormal ventricular activation.
SAECG Detection of late activating tissue due to surviving tracts in and around
scar tissue.
MlcrovoltT-wave alternans Rate-dependent tendency for spatially discordant action potential alter-
nans which may result In reentry.
QRS-Tangle Abnormal relation between depolarization and repolarization; probably

mostly due to abnormal repolarization.
Fragmented QRS Inhomogeneous activation due to scar, ischemia, or conduction
disturbance.
T-peak to T-end Dispersion of repolarlzatlon.
Delayed QRS transltlon In the precordlal leads Chamber enlargement, loss of anterlor forces, hypertrophy
Autonomic
Baroreflex sensitivity (BRS) Phenylephrine bolus elevates BP and baroreceptor reflexes slow heart
rate. Vagal tone may be protective and sympathetic activity pathogenic
for ventricular arrhythmias; heart failure and infarction lead to loss of BRS.
May predict HF death equally or more than sudden death.
Heart rate varlablllty Measure of vagal tone. (See BRS.)
Heart rate turbulence Acute heart rate effect of PVC-Induced transient hypotenslon; similar
toBRS.
A"hythmla
PVCsorNSVT Ambient arrhythmias may predict future ventricular arrhythmias.
Atrial fibrillation RR interval irregularity may be arrhythmogenic; may cause heart failure.
Inducible VT at EPS Identifies presence of a reentrant VT circuit.
Imaging
Echo, other LV mass, relatlve wall thickness (ratio of posterior wa II thickness to cham-
ber dimension); concentric and eccentric hypertrophy. Hypertrophy Is
associated with dispersion of depolarization and especially repolarization
and arrhythmic risk.
MRI LGE-detected fibrosis may represent substrate for VTNF.
MIBG Sympathetic nerve regional variability due to Infarction.
of the patient's medical comorbidities, goals of therapy, and a meaningful exchange among the
doctor, patient, and family. The use of a patient-centered decision-aid tool86 is now required in
the United States for ICD implantation in patients aged over 65 years.
RELATIVELY RARE INHERITED AND NON INHERITED CONDITIONS WITH SCA RISK
Sarcoidosis
Sarcoidosis is generally an idiopathic acquired process but it does display familial clustering. 87
As many as 20% of pulmonary or systemic sarcoidosis patients may harbor occult cardiac
sarcoid, whereas about 5% exhibit manifest disease. Furthermore, isolated cardiac sarcoid is
30 LGE
30 FDG
(fused)
FIGURE 15-1 • lm1glng In cardiac sarmldosls. Late gadollnlum enhancement (LGE) (arrows In UfJPf!I'paneh) represents replace-
ment fibrosis and tends to favor the septum and other walls In a mid or subeplcardlal pattem. Lowerpanels show fluorodeoX)'glu-
cose positron emission tomography scan Identifying areas of active lnffammatlon. (Reproduced with pennlsslon from Blmle DH,
Nery PB, Ha AC, Beanlands RS. Cardiac sarcoidosis.JAm Coif Cardiof. 2016;68:411-421. Copyright c Amefican College of Cardiology
Foundation.)
increasingly recognized. Cardiac manifestations include AV block. VT/VF, and RV or LV dys-

function, due to noncaseating granulomatous inflammation that may result in replacement
fibrosis (Figure 15-8). Its cause is unknown but an immunologic response to an uncertain anti-
gen has been hypothesiled. The ECG may show atrial or ventricular arrhythmias, RBBB, LBBB,
or AV block. Cardiac MR facilitates diagnosis of cardiac sarcoid, usually manifested as patchy
mid or epicardial fibrosis (Figure 15-8). Fluorodeoxyglucose PET imaging may show evidence
of inflammation (Figure 15-8). High-resolution CT can help provide evidence of pulmonary
involvement. Biopsy of noncardiac disease is preferable, but cardiac biopsy can be targeted by
mapping when necessary. Medical management includes standard drug therapy for heart fail-
ure, when appropriate. Immunosuppression is indicated for new-onset AV block or ventricular
dysfunction, and possibly for VT activity. Class I indications for ICD therapy include sustained
VT, cardiac arrest. and drug refractory, severe LV dysfunction (LVEF S35%). These and inter-
mediate indications are summarized. in Table 15-4. Risk stratification in sarcoidosis patients
with mildly reduced (EF of 36%-49%) or preserved EF is imperfect and detection of LGE in
the LV and inflammation in the LV and/or RV may be additive to other recognized factors like
VT inducibility.88 Firmly establishing the correct diagnosis may be difficult in some instances.
A diagnosis of cardiac sarcoidosis generally elicits considerable anxiety. Risk stratification and
better waderstanding of the natural history are evolving, but clinical judgment and individ-
ualization are required for ICD decisions in the meantime. As it is often progressive, careful
follow-up is important too.
Hypertrophic Cardiomyopathy (HCM)

Although randomized trials are difficult in rare conditions like inherited causes of SCA, reg-
istries have been conducted and guidance exists for the prophylactic use of an ICD. Hypertro-
phic cardiomyopathy (HCM) is the most common of these. affecting about 1:500 individuals.
It usually stems from a sarcomeric gene mutation, leading to distortion of various contractile
processes, and ultimately pathologic hypertrophy, myocyte disarray, and interstitial fibrosis. 89•90
The most frequently identified mutations occur in ~-myosin heavy chain (MYH7) or myo-
sin binding protein C (MYBPC3). Manifestations include unexplained, left ventricular end
diastolic wall thickness exceeding 15 mm. The hypertrophy often exhibits a septal predilec-
tion, which contributes to variable left ventricular outflow tract obstruction present in two-
thirds of patients. Risk factors for SCA with HCM emanate from single and multiple center
studies and include: marked hypertrophy (especially wall thickness :2:30 mm), unexplained
(presumably arrhythmic) syncope, nonsustained VT, a family history of SCA presumably due
to HCM, and abnormal systolic blood pressure response to exercise. ACC/AHA guidelines
place a Class IIA indication for a primary prevention ICD for 1 or more of the following:
marked hypertrophy (~30 mm); unexplained, presumably arrhythmic, syncope within the
preceding 6 months; or a family history of SCA (Figure 15-9).90 A Class IIB indication was
put forth for HCM patients exhibiting only nonsustained VT or abnormal systolic blood
pressure response to exercise, but in the presence of either of those plus an additional mod-
ifier risk, delayed enhancement (especially >15% of LV mass), LVOT obstruction, apical
aneurysm, or genetic factors, the recommendation was enhanced (IIA). The risk attributed
to nonsustained VT intensifies when the runs are more prolonged (>7 beats), more rapid
(>200 bpm), and/or recurrent, as well as in younger patients (age <30 years).91 Although
L
,, -
:
'\
.,
I: I:
II -~
...
..
-";;
;;
..
3
~ l.H A .!i...
'
,.. } "' .. ~
•~ •~ •~ I " •~ •~
I
'~ '
;:
~ ~ ~ ~ ·~
mH ' i'. "' :i'. I'.""""
... ,.
.-- --
~ ~~ ~~~~~~·~
"' "' "' "'
,.. "i .:::
.. :a , . :
"""
·~ :a , ':
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'
II ft ft ft ll II•++ II II ft---
~ F+
Panel A
FIGURE 15·9 • Hypertrophlc cardlomyopathy (HCMJ. Panel A shows a 12-lead from a patlent with nonobstructlve HCM demon-
strating a q-wave in lead I and LVH. He had a history of syncope that was abrupt on 2 occasions, 3 episodes of NSVT on event moni-
toring at 200 bpm, family history of HCM, and an uncle O.e~ not first-degree relative) who died suddenly. His echocardiogram showed
a 25 mm septal wall and 16 mm posterior wall thickness and no LVOT gradient Hiss-year risk of SCA wascalailated at 12% (http-JI
www.doc2do.com/hcm/WebHCM.html). A subcutaneous ICD (SICD) was planned. In order to evaluate and conflnn appropriate SICD
sensing an exercise test was performed. This elicited sustained VT (Panel B) with near syncope. See Figure 19-6 for image ofSICD.
:;; :; ; :;:
·" II
j ·- t t
·'·
:;; :;; 'l!
·"
I1 I l
' ~
I L
·1 \ " LI .\ IJ n r
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-·
-
m
- ;;-
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·- ·- ... I
\ I
' ' - , \. I
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TI
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I •~
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_j I :U I II f
: GE ~ TI # 11:11 '" lHJ'f! I '~
! fi 1~~·~a'fil.:ia1im11ri11mHtl1,_tf£11:lffiltH.l li:,•',':iim<tltll1t<~ n'!';~;; 1
~!1:fnzu ~J z 9·~ fi E!ffi;+o H =A·
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.I 1 l:lr
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PanalB
somewhat controversial, the apical variety of HCM may convey a lower SCA risk.90.92 How-
ever, the risk of VT or VF is appreciable when apical HCM exhibits an aneurysm and/or
significant delayed enhancement.
Delayed hyperenhancement (scar) involving 10% or more of the myocardium increased the
risk of SCA by over threefold.93 The ESC guidelines and online calculator attempt a quantitative
approach, advising a primary prevention ICD with a level of IIA for an estimated SCA risk
exceeding 6% within 5 years or IIB if the SCA risk is 4%-6% over the ensuing 5 years.94 The ESC
approach includes multiple more intermediate risk factors (e.g., LVOT gradient, LA size) and in
certain situations would not recommend an ICD when the ACC/AHA guidelines would (e.g.,
LVH >30 mm; or even FH of SCA plus NSVT with age >4S),9D.94•95
Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)

ARVC stems from a desmosomal or other mutation resulting in fibrofatty replacement of
right ventricular myocytes. Not infrequently the LV becomes involved too, or disease is
isolated to it (ALVC). Indeed, the most up-to-date term is arrhythmogenic cardiomyopathy,
which encompasses these conditions and similar ones. The most frequent genes implicated
include plakophilin-2, desmoglein-2, desmocollin-2, desmoplakin, and others. ARVC with
SCA, sustained VT, or syncope presumed due to VT qualifies for an ICD. Its ECG findings
and diagnosis are detailed in Chapter 11. Primary prevention ICD indications result from
an accumulation of major {NSVT, LVEF ::!>49%, inducible sustained VT) and/or minor risk
factors {male sex, RVEF ~40% with akinetic segment, proband status, ~1000 PVC/24hours,
2 or more desmosomal mutations).96 See Table 15-4. 60 Guidelines recommend a beta blocker,
especially if VT has occurred. An online calculator has become available. 97 Conversely, the
genotype positive-phenotype negative gene carrier is not indicated for an ICD, nor is the
diagnosed patient lacking sufficient of the above risk factors. 98 (See Figures 11-22 through
11-27 in Chapter 11.)
Brugada Syndrome
Brugada syndrome is an exception to many arrhythmia management rules because events
increase during elevated vagal tone and beta blockers are contraindicated. The hallmark is a
right bundle branch block-like ECG with down sloping ST segment elevation in the right pre-
cordial leads. The ECG pattern is often intermittent, but displacing the VI and V2 leads to the
third or second intercostal space may facilitate detection, as may sodium channel blocker chal-
lenge.99 Chapter 11 covers diagnosis and ECG findings (see Figures 11-22 through 11-27). The
signature arrhythmia is polymorphic VT/VF leading to syncope or SCA; monomorphic VT is
relatively rare. ICD treatment is warranted for prior SCA, and for syncope as well. A borderline
ICD indication (Class IIB) is present for asymptomatic patients with spontaneous type I pattern
who have inducible polymorphic VT/VF using single or double ventricular extrastimuli.60•100
Quinidine may prevent arrhythmias, and isoproterenol {not beta blockade) is recommended
for VT/VF storm. The observation that fever may trigger for both the ECG pattern and VT
episodes stems from demonstrated thermal variability in ion currents with some mutations.
Consequently, diagnosed patients should take antipyretics promptly during a febrile illness.
There is growing interest in ablating RV outflow tract epicardial tissue exhibiting low ampli-
tude, fractionated signals in symptomatic patients. This may eliminate the ECG pattern and
prevent VT/VF. 101-103
Long QT Syndrome
Long QT syndrome (LQTS) is usually diagnosed primarily with a resting ECG. Notwithstanding,
incorrect diagnoses are common because physicians are not skilled at measuring the QT interval
(see Chapter 11 ), which, to be fair, can be challenging and controversiaJ. 1Df.105 Chapter 11 presents
the nuances of this critical skill {see Figures 11-6 through 11-11). ECG recordings at different
heart rates (during a treadmill test) are often helpful. An epinephrine challenge test may be valu-
able in diagnosing borderline cases as well. Both tests may be especially useful in diagnosing
LQTl patients who have reduced ability to augment the repolarizing potassium current IKs with
adrenergic stimulation as normally occurs. 106
LQTS is an inherited disorder related to ion channel dysfunction, most commonly a loss of
function of a repolarizing potassium channel or a gain of function of the alpha unit of the
sodium channel (SCNSA). Symptoms include syncope or SCA due to torsades de pointes (TdP),
a polymorphic VT that may deteriorate to VF. With regard to therapy, and contrary to Brugada
syndrome, beta blockers have proven highly effective in LQTS, and thus are the mainstay for
the majority of patients.107 LQTS patients with prior events (syncope or SCA), or asymptom-
atic LQTS patients with 1 or more ECGs showing a QTc ~470, have a Class I indication for
beta blockers. Long-acting beta blockers, especially nadolol or propranolol, are advised and
compliance is critical to avoid rebound sympathetic surges. 107•101 Theoretical concern for harm
existed with respect to beta blockers for LQT3, but larger datasets show a benefit in female
LQT3 patients and no evidence of harm in males.109 In LQTS, avoiding drugs or electrolyte
disturbances that may further prolong the QT interval cannot be stressed enough. Restrictions
from intense or competitive sports have traditionally been advised, but such activity restric-
tions are becoming more lenient and tailored. 107 ICDs are indicated for LQTS patients who have
survived SCA, for syncope on BBL, but not for asymptomatic patients, or those who have not
been treated with beta blockers.
Catecholaminergic Polymorphic VT
Catecholaminergic polymorphic VT (CPVT) often presents in childhood with syncope or car-
diac arrest due to polymorphic VT sometimes degenerating to VF. The autosomal-dorninant
form stems from a ryanodine receptor mutation with calcium overload underlying the arrhyth-
mia. The resting ECG is generally normal but PVCs become more frequent with progressive levels
of exercise (or emotional stress), with development of couplets, and bidirectional VT, as shown
in Figures 11-16 and 11-17 of Chapter 11. Atrial tachycardia and atrial fibrillation also occur in
CPVT. All CPVT patients should be given beta blockers unless contraindicated. Flecainide and
cervicothoracic sympathetic denervation should be offered for recurrent syncope or for recurrent
VT on stress testing despite beta blockers. ICDs are clearly not a fail-safe treatment in CPVT.
Painful shocks may elicit a cycle of refractory arrhythmias and more shocks. When implanted,
adjunctive medical or sympathetic intervention is mandatory. ICDs are indicated for patients who
have survived SCA and possibly in the setting of syncope or VT despite medications.107
Short QT Syndrome
Short QT syndrome (SQTS), a very rare condition, can be due to a gain of function of certain
potassium channels or less often a loss of function of calcium channels (Figure 15-10). Most of
the less than 200 reported cases have defied genotyping. It results in an abnormal resting ECG
with abbreviated ST segment, and a QT often <330 msec. While only 0.5% of adults from a
population-based sample exhibit a QTc <340 msec, it is not believed that most of them actually
have SQTS. 110 SQTS patients exhibit a propensity for rapid polymorphic VTNF, especially at
rest. As with Brugada and CPVT, atrial fibrillation has been observed in young patients. A point-
based, diagnostic scoring system has been developed with diagnosis theoretically possible up to
370 msec for QTc. 110·m Quinidine may prolong the QT interval especially in SQTl (KCNH2 gain
of function mutation), and possibly other subtypes, whereas sotalol seems ineffective in the least
rare form (SQTl). ICD therapy is warranted if SCA or sustained VTNF has been observed.60
Early Repolarization Syndrome

Early repolarization syndrome (ERS), like Brugada syndrome, a J-wave syndrome, apparently
stems from inhomogeneous early repolarization, particularly in the epicardium, resulting in
J-point elevation (i.e., a J wave) and ST segment elevation (Figure 15-11). Also see Figures 11-18
through 11-21 in Chapter 11. J-point elevation in the inferior and lateral leads has been associated
with VF, albeit rarely. The benign pattern in the anterior precordial leads features a sharp QRS
termination, J-point elevation, and an ascending ST segment. The potentially more concerning
inferior and lateral pattern has a slurred QRS termination or a notch in the final 50% of the
R-wave downslope; Vl-V3 are excluded.MA horizontal or descending QRS is of some SCA
risk.Mona Nevertheless, it is vital to bear in mind that even the inferior (or lateral) "modern" ER
ECG pattern is common (-5%-10%) in the general population, especially young and/or ath-
letic patients, and very few of these will experience VF. Diagnosis of the ER pattern hinges on
Gene/genetic variant Mutation ECG (precordial lead) Pedigree QTc
~
~
ff E'P I
=1= I 1 = 291 milliseconds
N588K .... - 3
2 = 299 milliseconds
- 3 = 283 mllllseconds
+
=
KGNH2 "' 1
SQT1
T6181
l:l
rt
;
~·I
m: r;:
·-
I
l
J
-
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,,
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2 = 320 milliseconds
"' 1
.,,
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SQT2
R259H
:1
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=i=
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=+1 ,,
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I 'l±i
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+
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1 = 332 mllllseconds
:! ~
+
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-T-
lf:d±lf "'
=+ :1 \ .: I' :;
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t I' +··· , 1
.... "' ~.j' ~ "' !#I 'l
-
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;
l ·: '"
-t
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t
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tt ttc I' "' 1
FIGURE 15·1 O • Genetics and electrocardiography of short QT syndrome. See text for details. (Reproduced with permission
from Mazzanti A, Underwood K, Nevelev D, Kofman S, Priori SG. The new kids on the block of arrhythmogenic disorders: short QT
syndrome and early repolarization. J Cardiovasc Electrophysiol. 2017;28(10):1226-1236.)
finding ~l mm ST elevation on ~2 contiguous inferior or lateral ECG leads (Le., not Vl-V3).
Multiple genes have been implicated and there is overlap with Brugada syndrome.11-0 ERS
implies presence of the ER pattern and aborted SCA or documented polymorphic VT. Thera-
peutically, quinidine may be helpful; in addition, isoproterenol is advised for VF storm. ICDs
are definitely not indicated for asymptomatic ER pattern patients as they exhibit only a statisti-
cally increased SCA risk (-1:10000).11-0 Conversely, ICD implantation is indicated for survivors
of SCA and possibly for ER patients with arrhythmic syncope and a FH of ERS.60,64 Genetic
testing remains in a research mode for ER/ERS.
Idiopathic VF
Idiopathic VF (IVF) represents a diagnosis of exclusion.112 Even lacking an obvious cause for
SCA, a systematic approach, as used in CASPER, may characterize up to half of cases rendering
them nonidiopathic. m As conditions are identified, for example, ERS or SQTS, such cases are
CURRENT DEFINITION OF EARLY REPOLARIZATION
Isolated J-polnt elevallon Notched J wave Slurred J wave
0.1 mV
Baseline Baseline
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FIGURE 15-11 • Definition of early repolarization {ER) syndrome. A schematic and actual ECG illustrating the definition of ER
syndrome In Inferior or lateral precordlal leads. (Reproduced with permission from Mazzanti A, Underwood K, Nevelev D, Kofman S,
Priori SG. The new kids on the block of arrhythmogenlc disorders: short QT syndrome and early repolarlzatlon.J Cardiovasc Eiectro-
physiol. 2017;28(10):1226-1236.)
no longer deemed IVF. Some rare monogenic causes may still be lumped in as IVF, including
calmodulin mutations, or other causes of short-coupled PVCs resulting in TdP or VF. 112 Gen-
erally, an ICD is indicated for idiopathic VF survivors, as the recurrence rate is high. Nota-
bly, some otherwise-unexplained VF arises in the setting of (often unifocal) ventricular ectopy
largdy from Purkinj e fibers and may be amenable to ablation. 114
CONCLUSIONS
SCA remains common although the patterns and profile have evolved. Survival remains deplor-
able, emphasizing identification of at-risk individuals and new approaches to intervene more
quickly and effectively. The genetic arrhythmia syndromes (see also Chapter 11) are especially
difficult to manage with rapidly evolving data and best managed by specialized centers or at
least by those with a strong commitment to the area.
REFERENCES
1. Bed CS, Wedtesser EC, Barry FM. Fatal heart attadc and successful defibrillation: new concepts in coronary
artery disease. JAMA. 1956; 161:434-436.
2. Benjamin EJ, Blaha MJ, Chiuve SE, et al. Heart disease and stroke statistics-2017 update: a report from the
American Heart Association. Circuliition. 2017;135:e146-e603.
3. Jacobs I, Nadlcami v; Bahr J, et al. Cardiac arrest and cardiopulmonary resuscitation outcome reports: update and
simplification of the Utstein templates for resuscitation registries: a statement for healthcare professionals from
a task force of the International Liaison Committee on Resuscitation (American Heart Association, European
Resuscitation Council. Australian Resuscitation Council New Zealand Resuscitation Council. Heart and Stroke
Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Councils of Southern Africa). Circuliition.
2004;110:3385-3397.
4. Zoll PM, Linenthal AJ, Norman LR, Paul MH, Gibson W Treatment of unexpected cardiac arrest by external
electric stimulation of the heart. N Engl] Med. 1956;254:541-546.
5. Gurvich NL, Yuniev GS. Restoration of regular rhythm in the mammalian fibrillating heart Americiin Review of
Soviet Medicine. 1946;3:236-239.
6. Cakulev I, Efimov IR, Waldo AL. Cardioversion: past, present, and future. Circulation. 2009;120:1623-1632.
7. Perkins GD, Jacobs IG, Nadkarni VM, et al. Cardiac arrest and cardiopulmonary resuscitation outcome reports:
update of the Uutein Resuscitation Registry Template• for Out-of-Hoapital Cardiac Arrest: a atatement for
healthcare professionah from a task force of the International Liaison Committee on Resuscitation (American
Heart Association, European Resuscitation Council, Australian and New Zealand Council on Resuscitation,
Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Council of Southern
Africa, Resuscitation Council of Asia); and the American Heart Association Emergency Cardiovascular Care
Committee and the Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation. Circuliition.
2015; 132: 1286-1300.
8. Hinkle LE Jr, Thaler HT. Clinical classification of cardiac deaths. Circulation. 1982;65:457-464.
9. Epstein AE, Carlson MD, Fogoros RN, Higgins SL, Venditti FJ Jr. Classification ofdeath in antiarrhythrnia trials.
JAm Coll CardioL 1996;27:433-442.
10. Steinberg JS, Sadaniantz A, Kron J, et al. Analysis of cause-specific mortality in the Atrial Fibrillation Follow-up
Investigation of Rhythm Management {AFFIRM) study. Circuliition. 2004;109:1973-1980.
11. Farb A, Zuckerman BD. Clinical event adjudication in cardiovascular device trials: a Food and Drug Administration
perspective. Am Heart]. 2017;191:62-64.
12. Cummins RO, Chamberlain DA, Abramson NS, et al . Recommended guidelines for uniform reporting of data
from out-of-hospital cardiac arrest: the Utstein Style. A statement for health professionah from a task force of the
American Heart Association, the European Resuscitation Council the Heart and Stroke Foundation of Canada,
and the Australian Resuscitation Council. Circulation. 1991;84:960-975.
13. Morrison LJ, Nichol G, Rea TD, et al. Rationale, development and implementation of the Resuscitation Outcomes
Consortium Epistry-Cardiac Arrest RtsU$Citation. 2008;78:161-169.
14. Chan PS, McNally B, Tang F, Kellermann A, Group CS. Recent trends in survival from out-of-hospital cardiac
arrest in the United States. Circulation. 2014;130:1876-1882.
15. Stecker EC, Reinier K, Marijon E, et al. Public health burden of sudden cardiac death in the United States.
Circ Arrhythm Electrophysiol 2014;7:212-217.
16. Bergum D, Skjeflo GW. Nordseth T, et al. ECG patterns in early pulseless electrical activity-associations with
aetiology and survival of in-hospital cardiac arrest. Resuscitation. 2016; 104:34-39.
17. Bayes de Luna A, Coumel P, Leclercq JF. Ambulatory sudden cardiac death: mechanisms of production of fatal
arrhythmia on the basis of data from 157 cases. Am Heart]. 1989; 117:151-159.
18. Nolan JP, Soar J, Smith GB, et al. Incidence and outcome of in-hospital cardiac arrest in the United Kingdom
National Cardiac Arrest Audit. Resuscitation. 2014;85:987-992.
19. Effect ofmetoprolol CR/XL in chronic heart failure: Metoprolol CR/XL Randomised Intervmtion Trial in Congestive
Heart Failure (MERIT-HF). Lancet. 1999;353:2001-2007.
20. Jouven X, Desnos M, Guerot C, Ducimetiere P. Predicting audden death in the population: the Paris Prospective
Study I. Circulation. 1999;99:1978-1983.
21. Cobb LA, Fahrenbruch CE, Olsufka M, Copass MK. Changing incidence of out-of-hospital ventricular fibrilla-
tion, 1980-2000. JAMA. 2002;288:3008-3013.
22. Teodorescu C, Reinier K, Dervan C, et al. Factors associated with pulseless electric activity versus ventricular
fibrillation: the Oregon sudden unexpected death study. Circulation. 2010;122:2116-2122.
23. Myerburg RJ, Junttila MJ. Sudden cardiac death cawed by coronary heart disease. Circu/iition. 2012;125:
1043-1052.
24. Mehta D, Curwin J, Gomes JA, FU$ter V. Sudden death in coronary artery disease: acute ischemia versus myocar-
dial substrate. Circulation. 1997;96:3215-3223.
25. Myerburg RJ, Kessler KM, Mallon SM, et al Life-threatening ventricular arrhythmias in patients with silent myo-
cardial ischemia due to coronary-artery spasm. N Engl JMed. 1992;326:1451-1455.
26. Cascio WE, Yang H, Muller-Borer BJ, Johnson TA. bchemia-induced arrhythmia: the role of connexins, gap
junctions, and attendant changes in impulse propagation. / ElectTocardioL 2005;38:55-59.
27. Wit AL. Basic electrophysiologic mechanisms of sudden cardiac death caused by acute myocardial ischemia and
infarction. Card Electrophysiol Clin. 2017;9:525-536.
28. Garan H, McComb JM, Ruskin JN. Spontaneous and electrically induced ventricular arrhythmias during
acute ischemia superimposed on 2 week old canine myocardial infarction. J Am Coll Cardiol. 1988;1 l:
603-611.
29. Solomon SD, Zelenkofske S, McMurray JJ, et al. Sudden death in patients with myocardial infarction and left
ventricular dysfunction, heart failure, or both. N Engl JMed. 2005;352:2581-2588.
30. Davies MJ, Thomas A. Thrombosis and acute coronary-artery lesions in sudden cardiac ischemic death. N Engl
1 Med. 1984;310:1137-1140.
31. Farb A, Tang AL, Burke AP, Sessums L, Liang Y, Vll'mani R. Sudden coronary death. Frequency of active coronary
lesions, inactive coronary lesions, and myocardial infarction. Circulation. 1995;92:1701-1709.
32. Davies MJ. Anatomic features in victims of sudden coronary death: coronary artery pathology. Circulation.
1992;85:119-124.
33. Redfors B, Ramunddal T, Angeras 0, et al Angiographk: findings and survival in patients undergoing coronary
angiography due to sudden cardiac arrest in western Sweden. Resuscitation. 2015;90:13-20.
34. Luu M, Stevenson WG, Stevenson LW, Baron K, Walden J. Diverse mechanisms of unexpected cardiac arrest in
advanced heart failure. Circulation. 1989;80:1675-1680.
35. Anderson KP, Walker R, Urie P, Ershler PR, Lux RL, Karwandee SV. Myocardial electrical propagation in patients
with idiopathic dilated cardiomyopathy. J Clin Invest. 1993;92:122-140.
36. Travers AH, Perkins GD, Berg RA, et al. Part 3: Adult Basic Life Support and Automated External Defibrillation:
2015 International ConsenSU$ on Cardiopulmonary ReSU$citation and Emergency Cardiovascular Care Science
With Treatment Recommendations. Circulation. 2015;132:S51-S83.
37. Sasson C, Rogers MA, Dahl J, Kellermann AL. Predictors of survival from out-of-hospital cardiac arrest: a sys-
tematic review and meta-analysis. Circ Cardiovasc Qual Outcome5. 2010;3:63-81.
38. Olasveengen TM, de Caen AR, Mancini ME, et aL 2017 International Consensus on Cardiopulmonary Resusci-
tation and Emergency CardiOVllllcular Care Science With Treatment Recommendations Summary. Circulation.
2017;136:e424-e440.
39. Rea TD, Fahrenbruch C, Culley L, et al. CPR with chest compression alone or with rescue breathing. N Engl JMed.
2010;363:423-433.
40. Hallstrom AP, Ornato JP, Weisfeldt M, et al. Public-access defibrillation and survival after out-of-hospital cardiac
arrest. N Engl/ Med. 2004;351:637-646.
41. Capucci A, Aschieri D, Guerra F, et al Co=unity-based automated external defibrillator only re5U$cltation for
out-of-hospital cardiac arrest patients. Am Heart J. 2016;172:192-200.
42. Bardy GH. A critic's assessment of our approach to cardiac arrest. N Engl J Med. 2011;364:374-375.
43. Weisfeldt ML, Everson-Stewart S, Sitlani C, et aL Ventricular tachyarrhythmias after cardiac arrest in public ver-
sus at home. N Engl! Med. 2011;364:313-321.
44. Huang Y, He Q, Yang LJ, Liu GJ, Jones A. Cardiopulmonary resuscitation (CPR) plus delayed defibrillation versus
immediate defibrillation for out-of-hospital cardiac arrest. Cochmne Database of Systematic Reviews. 2014.
45. McLeod SL, Brignardello-Petersen R, Worster A, et al. Comparative effectiveness of antiarrhythmics for
out-of-hospital cardiac arrest: A systematic review and network meta-analysis. Resuscitation. 2017;121:90-97.
46. Kudenchuk PJ, Brown SP, Daya M, et al. Amiodarone, lidocaine, or placebo in out-of-hospital cardiac arrest.
N Engl/ Med. 2016;374:1711-1722.
47. Hazinski MF, Nolan JP, Aickin R, et al. Part 1: Executive Summary: 2015 International ConsenSU$ on Cardiopul-
monary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Cin:ula-
tion. 2015;132:S2-S39.
48. Lemkes JS, Janssens GN, van der Hoeven NW, et al. Coronary angiography after cardiac arrest without ST-segment
elevation. N Engl! Med. 2019;380:1397-1407.
49. Yam N, McMullan DM. E:rtracorporeal cardiopuhnonary resuscitation. Ann Trans/ Med. 2017;5:72.
50. Brooks SC, Anderson ML, Bruder E, et al. Part 6: Alternative Techniques and Ancillary Devices for Cardiopul-
monary Resuscitation: 2015 American Heart Association Guidelines Update for Cardiopulmonary ResU$cltation
and Emergency Cardiovascular Care. Cin:ulation. 2015;132:S436-S443.
51. Gheeraert PJ, De Buyzere ML, Taeymans YM, et al Risk factors for primary ventricular fibrillation during acute
myocardial infarction: a systematic review and meta-analysis. Eur Heart J. 2006;27:2499-2510.
52. Goldberg RJ, Yarzebski J, Spencer FA, Zevallos JC, Lessard D, Gore JM. Thirty-year trends (1975-2005) in the
magnitude, patient characteristics, and hospital outcomes of patients with acute myocardial infarction compli-
cated by ventricular fibrillation. Am l CardioL 2008;102: 1595-1601.
53. Mehta RH, Starr AZ, Lopes RD, et al. Incidence ofand outcomes associated with ventricular tachycardia or fibril-
lation in patients undergoing primary percutaneous coronary intervention. JAMA. 2009;301:1779-1789.
54. Bougouin W, Marijon B, Puymirat B, et al. Incidence of sudden cardiac death after ventricular fibrillation com-
plicating acute myocardial infarction: a 5-year cause-of-death analysis of the FAST-MI 2005 registry. Bur Heart J.
2014;35:116-122.
55. Al-Khatib SM, Stebbins AL, Califf RM, et al Sustained ventricular arrhythmias and mortality among patients
with acute myocardial infarction: results from the GUSTO-III trial Am Heart]. 2003;145:515-521.
56. Piccini JP, White JA, Mehta RH, et al. Sustained ventricular tachycardia and ventricular fibrillation complicating
non-ST-segment-elevation acute coronary syndromes. Circulation. 2012;126:41-49.
57. Scirica BM, Braunwald E, Belardinclli L, et al Relationship Between Nonsustained Ventricular Tachycardia After
Non-ST-Elevation Acute Coronary Syndrome and Sudden Cardiac Death: Observations From the Metabolic
Efficiency With Ranolazine for Less Ischemia in Non-ST-ffievation Acute Coronary Syndrome-Thrombolysis in
Myocardial Infarction 36 (MERLIN-TIMI 36) Randomized Controlled 'Iiial. Circulation. 2010;122:455-462.
58. Antiarrhythmia versus implantable defibrillators I. A comparison of antiarrhythmic-drug therapy with implantable
defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. N Engl JMed. 1997;337: 1576-1583.
59. Connolly SJ, Hallstrom AP, Cappato R, et al. Meta-analysis of the implantable cardioverter defibrillator secondary
prevention trials. AVID, CASH and CIDS studies. Antiarrhythmics vs Implantable Defibrillator study. Cardiac
Arrest Study Hamburg. Canadian Implantable Defibrillator Study. Bur Heart]. 2000;21:2071-2078.
60. Al-Khatib SM, Stevenson WG, Ackt:rman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients
With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: Executive Summary: A Report of
the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and
the Heart Rhythm Society. JAm Coll Cardiol. 2017.
61. Wyse DG, Friedman PL, Brodsky MA, et al. Life-threatening ventricular arrhythmias due to transient or correct-
able causes: high risk for death in follow-up. J Am Coll Cardiol. 2001;38:1718-1724.
62. Russo AM, Stainback RF, Bailey SR, et al ACCF/HRS/AHA/ASB/HFSA/SCAl/SCCT/SCMR 2013 Appropriate
Use Criteria for Implantable Cardioverter-Defibrillators and Cardiac Resynchronization TherapyA Report of the
American College ofCardiology Foundation Appropriate Use Criteria Task Force, Heart Rhythm Society, American
Heart Association, American Society of Echocardiography, Heart Failure Society of America, Society for
Cardiovascular Angiography and Interventions, Society of Cardiovascular Computed Tomography, and Society
for Cardiovascular Magnetic Resonance. J Am Coll CardioL 2013.
63. Zaugg CB, Ziegler A, Lee RJ, Barboaa V, Buser PT. Postresuscitation stunning: postfibrillatory myocardial dys-
function caused by reduced myofilament Ca2+ responsiveness after ventricular fibrillation-induced myocyte
Ca2+ overload. J Cardiovasc Electrophysiol. 2002;13: 1O17-1024.
64. Antzelevitch C, Yan GX, Ackerman MJ, et al. J-wave syndromes expert consensus conference report emerging
concepts and gaps in knowledge. Heart Rhythm. 2016;13:e295-e324.
65. Moss AJ, Davis HT, Decamilla J, Bayer LW. Ventricular ectopic beats and their relation to sudden and nonsudden
cardiac death after myocardial-Infarction. Circulation. 1979;60:998-1003.
66. Mukharji J, Rude RE, Poole WK, et al Risk factors for sudden death after acute myocardial infarction: two-year
follow-up. Am J Cardiol. 1984;54:31-36.
67. Bigger JT, Fleiss JL, Kleiger R, Miller JP, Rolnitzky LM. The relationships among ventricular arrhythmias,
left-ventricular dysfunction, and mortality in the 2 years after myocardial-infarction. Circulation. 1984;69:250-258.
68. Echt DS, Llebson PR, Mitchell LB, et al Mortality and morbidity in patients receiving encainide, flecainide, or
placebo. The Cardiac Arrhythmia Suppression Trial. N Engl l Med. 1991 ;324:781-788.
69. Peters RW, Mitchell LB, Brooks MM, et al Circadian pattern of arrhythmic death in patients receiving encainide,
flecainide or moricizine in the Cardiac Arrhythmia Suppression Trial (CAST)./Am Coll Cardiol.1994;23:283-289.
70. Boutitie F, Boisse! JP, Connolly SJ, et al Amiodarone interaction with beta-blockt:rs: analysis of the merged
EMIAT (European Myocardial Infarct Amiodarone Trial) and CAMIAT (Canadian Amiodarone Myocardial
Infarction Trial) databases. The BMIAT and CAMIAT Investigators. Circulation. 1999;99:2268-2275.
71. Kadish A, Dyer A, Daubert JP, et al. Prophylactic defibrillator implantation in patients with nonischemic dilated
cardiomyopathy. N Engl J Med. 2004;350:2151-2158.
72. Bardy GH, Lee KL, Mark DB, et al Amiodarone or an implantable cardioverter-defibrillator for congestive heart
failure. N Engl J Med. 2005;352:225-237.
73. Bansch D, Antz M, Boczor S, et al. Primary prevention of sudden cardiac death in idiopathic dilated cardiomyo-
pathy: the Cardiomyopathy Trial (CAT). Circulation. 2002;105:1453-1458.
74. Kober L, Thune JJ, Nielsen JC, et al. Defibrillator implantation in patients with nonischemic systolic heart failure.
N Engl] Med. 2016;375:1221-1230.
75. Al-Khatib SM, Fonarow GC, Joglar JA, et al. Primary prevention implantable cardioverter defibrillators in
patients with nonischemic cardiomyopathy: a meta-analysis. JAMA CardioL 2017;2:685-688.
76. Chugh SS. Sudden cardiac death in 2017: spotlight on prediction and prevention. Int J Cardiol. 2017;237:2-5.
77. Wu KC. Sudden cardiac death substrate imaged by magnetic resonance imaging: from investigational tool to clinical
applications. Cm Cardiovasclmaging. 2017;10.
78. Narayan SM, Wang P, Daubert JP. Sudden cardiac arrest: new concepts to address an intractable epidemic. J Am
Coll CardioL 2019;73(1):70-88.
79. Pathak RK, Sanders P, Deo R. Primary prevention implantable cardioverter-defibrillator and opportunities for
sudden cardiac death risk assessment in non-ischaemic cardiomyopathy. Bur Heart J. 2018;39:2859-2866.
80. Deyell MW, Krahn AD, Goldberger JJ. Sudden cardiac death risk stratification. Circ Res. 2015;116: 1907-1918.
81. Goldberger JJ, Subacius H, Patel T, Cunnane R, Kadish AH. Sudden cardiac death risk stratification in patients
with nonischemic dilated cardiomyopathy. J Am Coll Cardiol. 2014;63:1879-1889.
82. Halliday BP, Cleland JGF, Goldberger JJ, Prasad SK. Personalizing risk stratification for sudden death in dilated
cardiomyopathy: the past, present, and future. Circulation. 2017;136:215-231.
83. Huang DT, Sesselberg HW, McNitt S, et al. Improved survival associated with prophylactic implantable defi-
brillators in elderly patients with prior myocardial infarction and depressed ventricular function: a MADIT-11
substudy. J Cardio11asc ElectTOphysiol. 2007; 18:833-838.
84. Goldenberg I, Moss AJ, McNitt S, et al. Relations among renal function, risk of sudden cardiac death, and ben-
efit of the implanted cardiac defibrillator in patients with ischemic left ventricular dysfunction. Am J Cardiol.
2006;98:485-490.
85. Levy WC, Hellkamp AS, Mark DB, et al. Improving the use of primary prevention implantable cardioverter-
defibrillators therapy with validated patient-centric risk estimates. JACC Clin Electrophysiol. 2018;4:1089-1102.
86. Hazelton AG, Sears SF, Ford J, et al. Decisional balance among potential implantable cardioverter defibril-
lator recipients: development of the !CD-decision analysis scale {!CD-DAS). Pacing Clin Electrophysiol.
2014;37:63-72.
87. Birnie DH, Nery PB, Ha AC, Beanlands RS. Cardiac sarcoidosis. JAm Coll Cardiol. 2016;68:411-421.
88. Okada DR, Smith J, Derakhshan A, et aL Ventricular arrhythmias in cardiac sarcoidosis. Circulation.
2018;138:1253-1264.
89. Marian AJ, Braunwald E. Hypertrophic cardiomyopathy: genetics, pathogenesis, clinical manifestations, diagnosis,
and therapy. Circ Res. 2017;121:749-770.
90. Gersh BJ, Maron BJ, Bonow RO, et al. 2011 ACCF/ AHA Guideline for the Diagnosis and Treatment of Hyper-
trophic Cardiomyopathy: a report of the American College of Cardiology Foundation/American Heart Associa-
tion Task Force on Practice Guidelines. Developed in collaboration with the American Association for Thoracic
Surgery, American Society of Ecliocardiography, American Society of Nuclear Cardiology, Heart Failure Society
of America, Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions, and Society of
Thoracic Surgeons. J Am Coll CardioL 2011;58:e212-e260.
91. Wang W, Lian Z, Rowin EJ, Maron BJ, Maron MS, Llnk MS. Prognostic implications ofnonsustained ventricular
tachycardia in high-risk patients with hypertrophic cardiomyopathy. Circ Arrhythm Electrophysiol. 2017;10.
92. Eriksson MJ, Sonnenberg B, Woo A, et al. Long-term outcome in patients with apical hypertrophic cardiomyop-
athy. J Am Coll Cardiol. 2002;39:638-645.
93. Weng Z, Yao J, Chan RH, et al. Prognostic value ofLGE-CMR in HCM: a meta-analysis. JACC Cardio11asc Imag-
ing. 2016;9:1392-1402.
94. Authors/Task Force Members, Elliott PM, Anastasakis A, et aL 2014 ESC Guidelines on diagnosis and man-
agement of hypertrophic cardiomyopathy: the Task Force for the Diagnosis and Management of Hypertrophic
Cardiomyopathy of the European Society of Cardiology (ESC). Bur Heart J. 2014;35:2733-2779.
95. Maron BJ, Casey SA, Chan RH, Garberich RF, Rowin EJ, Maron MS. Independent assessment of the European Society
of Cardiology Sudden Death Risk Model forHypertrophic Cardiomyopathy. AmJCardiol. 2015;116:757-764.
96. Towbin JA, McKenna WJ, Abrams DJ, et al. 2019 HRS expert consensus statement on evaluation, risk stratifica-
tion, and management of arrhythmogenic cardiomyopathy. Heart Rhythm. 2019;16{1l):e301-e372.
97. Cadrin-Tourigny J, Bosman LP, Nou.a A, et al. A new prediction model for ventricular arrhythmias in arrhyth-
mogenic right ventricular cardiomyopathy. Eur HeMt J. 2019;40:1850-1858.
98. Corrado D, Wichter T, Link MS, et aL Treatment of arrhythmogenic right ventricular cardiomyopathy/dysplasia:
an international task force consensus statement. Circulation. 2015;132:441-453.
99. Brugada J, Campuzano 0, Arbelo E, Sarquella-Brugada G, Brugada R. Present status ofBrugada syndrome: JACC
State-of-the-Art Review./ Am Coll Cardiol. 2018;72:1046-1059.
100. Sroubek J, Probst V, Mazzanti A, et al. Programmed ventricular stimulation for risk stratification in the Brugada
syndrome: a pooled analysis. Circulation. 2016;133:622-630.
101. Nademanee K, Veerakul G, Chandana.mattha P, et al. Prevention of ventricular fibrillation episodes in Brugada
syndrome by catheter ablation over the anterior right ventricular outflow tract epicardium. Circulation. 2011; 123:
1270-1279.
102. Brugada J, Pappone C, Berruezo A, et al. Brugada syndrome phenotype elimination by epicardial substrate abla-
tion. Gire Arrhythm BlectrophysioL 2015;8:1373-1381.
103. Fernandes GC, Fernandes A, Cardoso R, et al. Ablation strategies for the management of symptomatic Brugada
syndrome: asystematic review. Heart Rhythm. 2018;15:1140-1147.
104. Vlllkin S, Rosovski U, Sands AJ, et al. Inaccurate electrocardiographic interpretation oflong QT: the majority of
physicians cannot recognize a long QT when they see one. Heart Rhythm. 2005;2:569-574.
105. Taggart NW, Haglund CM, Tester DJ, Ackerman MJ. Diagnostic miscues in congenital long-QT syndrome.
Circulation. 2007;115:2613-2620.
106. Vyas H, Hejlik J, Ackerman MJ. Epinephrine QT stress testing in the evaluation of congenital long-QT syndrome:
diagnostic accuracy of the paradoxical QT response. Circulation. 2006;113:1385-1392.
107. Priori SG, Wilde AA, Horie M, et al. HRS/EHRA/APHRS Expert Consensus Statement on the Diagnosis and
Management of Patients with Inherited Primary Arrhythmia Syndromes: Document endorsed by HRS, EHRA,
andAPHRSinMay2013 andby ACCF, AHA, PACES, andAEPCin June2013. Hearl Rhythm. 2013;10:1932-1963.
108. Chockalingam P, Crotti L, Girardengo G, et al Not all beta-blockers are equal in the management oflong QT syn-
drome types 1 and 2: higher recurrence of lM:llts under metoproloL l Am Coll CardioL 2012;60(20):2092-2099.
109. Wilde AA, Moss AJ, Kaufman ES, et al Clinical aspects of type 3 long-QT syndrome: an international multicenter
study. Circulation. 2016;134:872-882.
110. Mazzanti A, Underwood K, Nevelev D, Kofman S, Priori SG. The new kids on the block of a:rrhythmogenic dis-
orders: short QT syndrome and early repolarization. / Cardiovasc BlectrophysioL 2017;28(10):1226-1236.
111. Gollob MH, Redpath CJ, Roberts JD, The short QT ayndrome propoaed diagnostic criteria./ Am Coll CardioL
2011;57:802-812.
112. Vlllser M, van der Heijden JF, Doevendans PA, Loh P, Wilde AA, Hassink RJ. Idiopathic ventricular fibrillation:
the struggle for definition, diagnosis, and follow-up. Gire Arrhythm Electrophysiol. 2016;9(5):e003817.
113. Krahn AD, Healey JS, Chauhan V, et al. Systematic assessment of patients with unexplained cardiac arrest: Car-
diac Arrest Survivors With Preserved Ejection Fraction Registry (CASPER). Circulation. 2009;120:278-285.
114. Haissaguerre M, Shah DC, Jais P, et al. Role of Purkinje conducting system in triggering of idiopathic ventricular
fibrillation. Lancet. 2002;359:677-678.
115. Ong MEH, Perkins GD, Ca:riou A. Out-of-hospital cardiac arrest: prehospital management. Lancet. 2018;391:
980-988.
116. Multicenter Postinfarction Research Group. Risk stratification and survival after myocardial infarction. N Engl J
Med. 1983;309:331-336.
117. Shun-Shin MJ, Zheng SL, Cole GD, Howard JP, Whinnett ZI, Francis DP. Implantable cardioverter defibrilla-
tors for primary prevention of death in left ventricular dysfunction with and without ischaemic heart disease: a
meta-analysis of 8567 patients in the 11 trials. Bur Heart f. 2017;38(22):1738-1746.
118. Sharma S, Rozen G, Duran J, Mela T, Wood MJ. Sudden cardiac death in patients with spontaneous coronary
artery dissection. J Am Coll Cardiol. 2017;70:114-115.
119. Ll KJ, Greenstein AP, Delisi LE. Sudden death in schizophrenia. Gurr Opin Psychiatry. 2018;31(3):169-175.
120. Kuck KH, Cappato R, Siebels J, Ruppel R. Randomized compamon of antiarrhythmic drug therapy with
implantable defibrillators in patients resuscitated from cardiac arrest: the Cardiac Arrest Study Hamburg (CASH).
Circulation. 2000;102:748-754.
121. Moss AJ, Hall WJ, Cannom OS, et al. Improved survival with an implanted defibrillator in patients with coronary
disease at high risk for ventricular arrhythmia. N Engl I Med. 1996;335: 1933-1940.
122. Bigger JT Jr. Prophylactic use of implanted cardiac defibrillators in patients at high riak for ventricular arrhyth-
mias after coronary-artery bypass graft surgery. Coronary Artery Bypass Graft (CABG) Patch Trial Investigators.
N Engl JMed. 1997;337:1569-1575.
123. Buxton AE, Lee KL, Fisher JD, Josephson ME, Prystowsky EN, Hafley G. A randomized study of the prevention of
sudden death in patients with coronary artery disell$e. Multicenter Unsustained Tachycardia Trial Investigators.
N Engl JMed. 1999;341:1882-1890.
124. Connolly SJ, Gent M, Roberts RS, et al. Canadian implantable defibrillator study (CIDS) : a randomized trial of
the implantable cardioverter defibrillator against amioda:rone. Circulation. 2000;101:1297-1302.
125. Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarc-
tion and reduced ejection fraction. N Engl JMed. 2002;346:877-883.
126. Hohnloser SH, Kuck KH, Dorian P, et al. Prophylactic use of an implantable cardioverter-defibrillator after acute
myocardial infarction. N Engl JMed. 2004;351:2481-2488.
127. Steinbeck G, Andresen D, Seidl K, et al. Defibrillator implantation early after myocardial infarction. N Engl l Med.
2009;361:1427-1436.
128. Epstein AE, DiMarco JP, Ellenbogen KA, et al. 2012 ACCF/AHA/HRS focused update incorporated into the
ACCF/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the
American College of Cardiology Foundation/American Heart .Association Task Force on Practice Guidelines and
the Heart Rhythm Society./ Am Coll Cardiol. 2013;6l:e6-e75.
PART
Methods and Therapy

Chapter 16 Electrophysiologic Testing and Diagnostic Maneuvers
Chapter 17 Catheter Ablation of Supraventricular Tachycardias
Chapter 18 Catheter Ablation of Ventricular Tachyarrhythmias
Chapter 19 Cardiac Implantable Electronic Devices
Electrophysiologic Testing and
Diagnostic Maneuvers
Program.med electrical stimulation of the heart was introduced by Durrer and colleagues1 as
a technique to study the mechanisms of cardiac arrhythmias in humans. A critical adjunct to
this earlier work was the development of a catheter method to record His bundle potentials in
humans.2 Through the use of these techniques, it is possible to diagnose with certaintyvarious
forms of supraventricular and ventricular tachycardia as well as to identify the site ofatrioven-
tricular (AV) block. Clinical electrophysiology has undergone transformation from an esoteric
subspe<:ialty of cardiology, concerned primarily with diagnosing various cardiac arrhythmias
and investigating electrophysiologic (BP) properties of the heart, to an area vital to the manage-
ment of patients with arrhythmias, including the ability to cure patients by endocardial catheter
ablation. This chapter describes the techniques and applications ofEP testing.
CATHETER INSERTION AND RECORDING

EP procedures are specialized cardiac catheterizations that involve the recording of intracar-
diac electrograms and programmed electrical stimulation of the heart.' Insertion of catheters
is almost always performed using the percutaneous technique. The route chosen for cathe-
ter insertion depends primarily on the accessibility of the venous or arterial system and the
intracardiac catheter position required for study. Recordings of the His bundle electrogram
are obtained most easily with a catheter advanced from the femoral vein, which allows the
catheter position to be kept stable throughout the study. Placement of the catheter in the right
atrium or right ventricle can generally be accomplished easily from any venous route while
access to the left atrium and ventricle requires a transseptal approach or retrograde aortic
approach.
Recordings of intracardiac electrograms can be either unipolar or bipolar as demonstrated in

Figure 16-1. In this example, a quadripolar catheter was situated with its tip at the right ventric-
ular apex. Proximal and distal bipolar electrograms were recorded as well as unipolar electro-
grams from each pole of the catheter. An electrical 6.eld is present during activation of cardiac
muscle. In a unipolar lead. the rapid or intrinsic detlection represents activation of the myo-
cardium directly underneath the electrode:' Thus, only 1 rapid component will be present. The
electrogram configuration in a bipolar lead may contain several relatively .rapid deflections.
The bipolar electrogram is the algebraic sum of the 2 unipolar leads:' The closer the bipolar
11 - - - - - . . . /
HRA --i
HBE
RVp
~ -- +--
RVo
RV4
~ -+------··-
RV3
v v -
--v-
RV2
RV,
v ....
f- 200ms-1
v -
FIGURE 16-1 • BIpolar and unipolar electrograms. Simultaneous recordings from electro cardiogram (ECG) leads I and II and bipo-
lar lnb'acardlac electrograms from tfle high right atrium (HRA), His bundle area (HBE), and right ventricular proximal {RV,) and dlstal
(RVJ electrode pair. Unipolar RV electrograms are recorded using each of the 4 poles from the most proximal (RV) to tfle most
distal (RV,). {See text f'or details.)
spacing, the sharper the electrogram. Unipolar and bipolar electrogra:ms require different filter
settings, which vary depending on the equipment used. Typically. unipolar electrograms are
more unfiltered-for example, 0.05-400 Hz. Common bipolar settings range from 30-40 Hz to
400-SOOHz.
Local activation in healthy tissue is easier to determine with a unipolar tracing that demon-
strates a single rapid deflection when the electrical wavefront arrives at the electrode and is
useful for precise mapping purposes. Under routine circumstances. bipolar recordings are used
because of their stability and greater resistance to motion artefact and changes in amplitude
under various conditions throughout the study. Further, close-spaced bipolar electrodes-for
example, 1 to 2 mm interelectrode distance-enable excellent identification oftocal activation
and are preferred in many instances over unipolar electrograms.
The His bundle area is surprisingly easy to locate in the vast majority of patients. Using the
femoral approach, the catheter is initially manipulated to a site where the recording bipolar pair
overlies the middle of the spine during fluoroscopy in the posterior-anterior view. The goal is
to record a large His deflection with a relatively large atrial deflection at the same time. One
should fine-tune the catheter position to obtain such a recording.
CHAPTER 16 • Electrophysiologic Testing and Diagnostic Maneuvers 375
PROGRAMMED ELECTRICAL STIMULATION

Programmed electrical stimulation encompasses 2 basic modes of pacing. To assess conduc-
tion over the AV conduction system or an accessory pathway, incremental atrial or ventricular
pacing is used. The heart is paced starting at a relatively slow rate, and progressively faster
rates are used until block occurs over the tissue being evaluated. To evaluate refractoriness, a
drive train at a constant paced cycle length or during sinus rhythm is selected and extrastimuli
are introduced late in diastole and then at progressively more premature intervals until either
block occurs in the tissue evaluated or local refractoriness at the site of stimulation is encoun-
tered. Both incremental pacing and introduction of I or more extrastimuli are used to initiate
supraventricular and ventricular tachycardia; at times bursts of a rapid constant cycle length
are necessary to achieve this aim. In most situations, we recommend pacing stimuli of twice
diastolic threshold current strength and 2 ms pulse width.
Electrophysiologic Evaluation of the Sinus Node

Sinus node testing is infrequently done. Two atrial stimulation techniques are typically used to
test sinus nodal function.s-7 The most useful test to uncover sinus nodal dysfunction is atrial
overdrive pacing to determine the sinus node recovery time.6 This test is based on a normal EP
property of pacemaker cells known as overdrive suppression of spontaneous depolarization.8
After atrial overdrive pacing is terminated, the pacemaker cells in the sinus node remain qui-
escent for a period of time and then resume spontaneous activity. If a marked depression of
automaticity occurs at the end of pacing, a prolonged pause will be noted, and this presum-
ably identifies sinus node dysfunction. In our experience, this test is specific but insensitive to
diagnose sinus node dysfunction in patients in whom the diagnosis has not been confirmed by
routine electrocardiography (ECG).
Sinus node testing is performed by pacing the high right atrium after the patient is in a quiet,
restful state. Before pacing, the mean spontaneous sinus rate is calculated using approximately
10 intervals. It is important to use multiple pacing cycle lengths to obtain the maximal sinus
node recovery time.9 We use cycle lengths of 800 to 350 ms in 50 ms decrements as the paced
cycle lengths for testing, and we pace for 30 s with a 30 s rest between pacing runs. In patients
with slower spontaneous rates, we prefer to test the slowest atrial paced rate that can capture the
sinus node without interference. Measurement of the sinus node recovery time is taken as the
interval from the high right atrial depolarization of the last paced beat to the high right atrial
depolarization of the first return sinus beat, and this is considered the primary pause.6 In some
patients there may be an excessively long pause after the first sinus return beat; this is classified
as a secondary pause.1°Figure16-2 is an example from a patient with both a primary and sec-
ondary pause, the latter of which was excessively long. Because the sinus node recovery time
is influenced by the underlying basic sinus rate, a variety of methods have been proposed to
obtain the corrected sinus node recovery time (CSNRT). s We prefer the method of subtraction
of the mean sinus cycle length from the primary pause to obtain the CSNRT. The maximal
CSNRT is taken after evaluation of all paced cycle lengths. We prospectively evaluated 131
patients in a drug-free state and noted a 95% confidence interval for the upper value for maxi-
mal CSNRT of 500 ms, which was independent of age or gender.9 It should be remembered that
an abnormal maximal CSNRT suggests sinus node dysfunction but is not in itself an indication
for implantation of a permanent pacemaker.
II
Ill
2.52sec 14.40sec
HRA .-.--~~~--+~~~~~~~~~~~~~~~~~~~~~~~~~---~
S1 S
HBE il--illt-w-----M~--------··(~- ~
f
11 I H~I I
FIGURE 16-2 • Abnormal sinus node recovery time. There is a 252 s primary pause, which yielded a markedly abnormal CSNRT.
More lmpn!$sfve Is the 14.40 s secondary pause before n!$Umptton of sinus node activity. Ajunctional escape rhythm prevented
total asyrtole (note the His deflection before each ventrlcular electrogram on the HBE lead) In this patient The patient had a history
of recurrent syncope that did not recur after a pennenent pacemeket' was Implanted. The presumption was that a stable junctlonal
rhythm did not always occur with prolonged sinus pauses. (Reproduced with pennlss!on from Prystowsky EN, Noble RJ. Electro-
physiologic studies: who to refer. Heart Dis Strolre. 1992;1 :188.}
Determination of the sinoatrial conduction time (SACT) is another test ofsinus node function.7
The SACT is based on the principles of reset of an automatic focus. described in Chapter 2.
During sinus rhythm. the cardiac cycle is scanned by a premature atrial stimulus every eighth
cycle. .Attia! stimuli are introduced at the sinus node region beginning with an A 1A.,, interval
approximately 10 ms less than sinus cycle length and decrementing by 10 to 20 ms until the
stimulus fails to capture the atrium. A stylized sequence is illustrated in Figure 16-3. Initially,
the atrial extra.stimulus (A1A.,,) at late coupling intervals fails to alter the return cycle CAA)
(Figure 16-3A), indicating that the extrastimulus did not reset the sinus node (zone ofcompen-
sation or collision). At earlier coupling intervals, the return cycle is advanced (noncompe.nsatory
pause). indicating that the sinus node has been depolarized and reset (Figure 16-3B). The A,_A,
interval is then plotted as a function of A 1A.,, (Figure 16-4). At the reset zone, the SACT is cal-
culated as SACT =A.,,A, - SCU2, where A,.A3 is the interval from A,, to the return sinus cycle A,
and SCL is the sinus cycle length. It is assumed that the atrial impulse enters the sinus node retro-
gradely and resets the node. and the sinus impulse exits anterogradely to initiate the return cycle.
The SACT is then represented by the total interval A.,,A, minus the sinus cycle length-divided
by 2 because the interval includes both. conduction time into and out of the sinus node. At still
earlier coupling intervals (Figure 16-3C). the ext.rastimulus may be more or less interpolated,
indicating that the premature atrial stimulus failed to alter sinus node automatidty. presumably
because it encountered refractoriness in the sinus node region (sinus node refractory period).
Still earlier atrial e:r:trastimuli can initiate sinus node reentrant responses (Figure 16-30).
The technique for SACT is subject to substantial experimental error and is very difficult to use in
patients with sinus arrhytlunia. Normal values for SACT range from <100 to <170 ms. Overall. we
think that overdrive atrial pacing yields the most useful clinical assessment ofsinus node function.
CHAPTER 16 • Electrophyslologlc Testing and Diagnostic Maneuvers 377
REF
FIGURE 16-3 • Schematic lllustratlon of the result$ of the atrial extrastlmulus technique. A.,A:, Is the coupling Interval between the
last sensed high right atria! electrogram and the atria Ielectro gram following the extrastimulus. AA Is the retumed at:Tfal cycle.
A represents the zone of compensation, Bzone of reset, C zone of lnte1pol21tlon, and D zone of reentry. In this "Ideal' representa-
tion, there Is no sinus arrhythmia. REF, reference ECG lead.
Electrophysiologic Evaluation of Atrioventricular and Ventriculoatrial Conduction System

Incremental atrial and ventricular pacing iB used to ascertain anterograde block in the AV
node and His-Purltinje system and retrograde block in the ventriculoatrial system, respectively.
(See also Chapter 1.) Incremental atrial pacing is started at the longest pacing cycle length
that can consistently capture the atriwn without interference from the underlying sinus rate.
The cycle length is progressively shortened in 10 ms decrements until AV nodal block occurs
B
•
~
g
• . ~"-~ •
•
A
.f SCL •
.t --------------------------------------
·.•c
.:o
FIGURE 1H • SchemBtlc curve lllustratlng atrial extrastlmulus testing for calC\llation ofslnoatrlal conduction time. Four classic
zones are depicted, lndudlng the zone of compensation (A), the zone of reset (8), the mne of Interpolation (C), and the zone of
reentry (D), as discussed in the text SO.. sinus cycle length.
II I ~ : ; I IIIIIIIIIIIIIII IIIIIIIIIIIIIIIIIIII!: I I I : IiII I I II' I
11- - - - . A . . .
Ill~---------..... _______..., - - - - - - - - - - .... ..,,,-
v,------.
HRAJ~~k,. 500 S S \,..,, 5 1'.,,y
HBE r.~.'GS'ss ~ J ;
.: 1 H
1ss Jl
l~~~.~151· ,tJ;jI w75~ I~w
v140
~h
~ Jl I ao1J
1140
1L
155 _140
1
RFA~ .. --· · /c",'\~-----7~~---·-·

,..rT.,-, • · 1 1 ,-,-T • ~ ,_.....,-.-,-,--,--,-r-i 1 1 1 1 , -, r rt 1 . 1 "f-i-r-rTl 11 1' ----:::-
T.,--.-.-
'°" -
FIGURE 16-5 • Mobltz type II second-degree AV block. Atrial pacing at SOO ms results In block below the recorded His deflection
(arrow), and variable His-Purkinje conduction times from 75 to 85 ms are noted. There i5 also some slight variability in the AH inter-
val, possibly due to changes In autonomic tone depending on the Umlng of the arterlal pulse pressure before AV node ac:tlvatton.
RFA, rtght femoral artery pressure.
or the patient develops symptoms due to hypotension. In patients with abnormal His-Purldnje
conduction, block below the His bundle depolarization may occur during atrial pacing. as
noted in Figure 16-5.11 Atrial pacing should be continued until AV node block occurs, so that
both the AV node as well as the His-Purk:inje system can be evaluated.
We stress that, for accurate determination ofHis-Purkinje conduction, incremental atrial pacing
should be used-not the sudden onset of atrial pacing at various rates. The latter technique can
result in a sudden shortening of the atrial cycle length in a patient with a relatively slow heart
rate and subsequent block below the recorded His potential Block below the His in this contex:t
is a physiologic event, as previously reported.12 Block below the His recording can also occur in
situations in which there is sudden loss ofatrial capture during an incremental atrial pacing run
(Figure 16-6). In this patient, without interruption of the atrial drive train. Wenckebach block
occurred in the AV node during incremental pacing. but no block below the His depolariza-
tion was noted. However, in Figure 16-6, note that the second atrial stimulus fails to result in
an atrial depolarization, yielding a relatively long cycle length, and the third captured complex
demonstTates block below the His depolar:ization. Infra-His block here is physiologic and not
pathologic.
Incremental ventricular pacing to the point at which ventriculoatrial (VA) block occurs should
also be performed. In some patients without accessory pathways, there is minimal increase in
the VA conduction time until a paced cycle length 20 to 40 ms prior to block. This is a normal
finding and does not imply the presence of an accessory pathway. 13 Other patients demon-
strate a progressive increase in the VA interval until block occurs, and still other patterns of
II
Ill
350
HBE
RV
SH 170
ff t
160
t1 200 225
~ 235 190
t
i-------;
20orns
FIGURE 1H • Infra-His block due to long-short paced Interval during atrial cycle length of350 ms. The second a'Crlal paced
stimulus (S} falls to capture the atrium, allow1ng a sudden long Interval to occur, dosed by the third stimulus, which causes atria!
depolarization and conduction to the venuldes. The fourth stimulus results In block below the His deflection-not a pathologlc
tlndlng In this situation. Recurrence of block below the His can occur In subsequent beats (sixth stimulus) and Is also not abnonnal.
Note that AV node Wenckebach block also occurs at this cycle length, as evidenced by a progressive lnaease In the AH lntefllat
measured here for simplicity from the stimulus artefact to the His depolarization {SH).
conduction-such as intermittent VA conduction-can occur (Figure 16--7). In some patients

there is complete VA block during all paced cycle lengths, as noted in Figure 16-8, taken from a
15-year-old girl after successful radiofrequency endocardial catheter ablation of a left free-wall
accessory pathway. VA block at all p~ cycle lengths has no clinical relevance to anterograde
conduction over the AV conduction system and frequently occurs in patients with otherwise
normal anterograde AV conduction.
Programmed atrial stimulation is used to characterize AV node and His-Purkinje refractoriness.

Similarly, programmed ventricular stimulation is used to evaluate refractoriness of the VA con-
duction system. We recommend testing refractoriness during sinus rhythm as well as during at
least 1 paced cycle length. After 8 either sensed or paced atrial cycles, a premature atrial complex
is introduced, beginning in late diastole, and shortened progressively until atrial refractoriness
is achieved. In our experience, approximately one-third of patients will demonstrate AV node
refractoriness at relatively slow (e.g., 800 ms) atrial cycle lengths, and AV node block will occur
in another 30% to 40% at faster atrial paced rates. This is due to an increase in the AV node effec-
tive refractory period in the normal aduh AV node during faster atrial rates. However, approxi-
mately 20% to 30% of patients will not demonstrate AV node block at atrial pacing cycle lengths
of 400 ms or greater, because AV node refractoriness is less than atrial refractoriness at these
rates. An example of AV node refractoriness is demonstrated in Figure 16-9 in a patient who
had dual AV node physiology without initiation of tachycardia because of poor VA conduction.
Refractoriness of the VA conduction system is tested during ventricular padn.g at a constant
FIGURE 1..7 • Intermittent ventJia.lloa1Jfal conduction. Note that the first paced ventrla.llar complex does not conduct to the atria,
and this Is follD'tYed by a ventrla.ller fusion beat due to pertlel activation of the ventricles by a sinus-aJnducted complex. The third end
sixth pliKl!d beats conduct retrograde to the atria (A1 as noted bythe low-to-liigh atrial activation sequence (His bundle A' before HRAA,.
HRA~
HBE
FIGURE 1..8 • Complete ventr!ailoatrlel block. During ventrlcular pacing at a constant cycle length shorter then the sinus cycle
lengtfl, VA dissociation Is present and the f'ourth QRS complex Is a fusion beat. There Is a peulstent high-to-low atria I activation
sequence throughout.
v, . . . . . . . ..__...... ,...--...........___ ---...-- -----
HRA +-- 500

----.
Panel A PanelB
PlntlC PanelD
FIGURE 1H • Determination of refractoriness of the fast and slow AV node conduction pathway.s. The right atrium was paced at
SOO ms and a premature atrial complex of 440 ms conducted oveJ the AV node with a H,H2 of 475 ms (Panel A). An A,A,. of 430 ms
blocked in the fast AV node pathway, as noted by a sudden increase in H1H2 to 625 ms {Panel 8}. Conduction OCC\lrred over the
slow AV node pathway at A,A,. 390 ms (Panel O, but block was present at A,A,. 380 ms (Panel D).The effective refractory period
(ERP) of the fast and slow AV node pathways are 430 and 380 ms, respectlvely.
cycle length, with the introduction of progressively shorter premature ventricular complexes
until ventricular refractoriness is achieved.
Initiation ofTachycardla
Various pacing techniques can be used to initiate supraventricular and ventricular tachycardias
(VT). In some patients, especially those with AV reentry, incremental atrial or ventricular pac-
ing will initiate supraventricular tachycardia. Bursts of atrial pacing at rapid fi.ud cycle lengths
are also useful to initiate AV and AV node reentry and certain types of atrial tachycardia. Ven-
tricular pacing techniques often initiate AV reentry but are much less successful in inducing
AV node reentry. (see Chapter 7). Incremental and burst pacing from the atrium do not often
initiate sustained monomorphic VT, which usually requires pacing of the ventricle with intro-
duction of 1 to 3 extra.stimuli (Figure 16-10)14 (see Chapter 8). filustrated in Figure 16-11 is the
initiation of AV node reentry with the introduction of only I premature atrial complex during
sinus rhythm. In contrast, the patient shown in Figure 16-12 required 2 atrial extrastimuli to
cause block in the fast AV node pathway and initiate AV node reentry.
ENDOCARDIAL CATHETER MAPPING

Mapping during supraventricular and ventricular tachycardia is used to identify an area to tar-
get for ablation success. This is needed for both a focal site or reentrant circuit. An example of
mapping the earliest site of retrograde atrial activation in a patient with AV reentry is shown in
I
II
Ill
v,
HBE
RV
FIGURE 16-10 • Induction of sustained monomorphicventriculartachycardia during ventriadar pacing and double extrastimuli
(S2S,). There Is varlable VA conduction and a His depolartutlon Is not noted before each wntrlcular electro gram on the HBE tracing.
II
Ill
v,
Ve
HRA
HBE
RV
PCS
DCS
t-----i
200ms
FIGURE 16-11 • Initiation of AV node reentTy with 1 iltrial extrastimulu5 (S.J during sinus rhythm. Note the marked increase in AH
interval of S2 and the very short VA interval during tachycardia.
FIGURE 16-12 • Initiation of AV node reenlTy with 2 atrial extt7lltimulr (.AA) Introduced during sinus rhyttlm. A,HJ shOWl en
lnaease of 200 ms over AzH2•
Figure 16-13. In this example, the site of earliest VA conduction was 100 ms and ablation here
resulted in loss of conduction over the accessory pathway and inability to induce AV reen1ry.
Of note, the VA interval during mapping refers to the earliest recorded ventricular activation to
the rapid portion of the local atrial electrogram. Mapping techniques for supraventricular and
ventricular tachycardia are presented in Chapters 17 and 18.
DIAGNOSTIC MANEUVERS
Pacing techniques during tachycardia can be very helpful to uncovering its mechanism. and,
in some cases, the optimum site for ablation. Differentiating VT from other forms of wide
QRS tachyanhythmias is not usually a problem, but this is not so for various types of parox-
ysmal SVT, most notably atrial tachycardia (AT), AV node reentry (AVNRT}, and AV reentry
(AVRT). We find it helpful to employ a standardized approach to differentiate these 3 at EP
study, starting with the assumption that AV node reentry is the mechanism, and proceeding to
prove or disprove this assumption (see Tablet 16-1 through 16-4). Several pacing techniques,
including entrainment, are reviewed in Chapters 5, 6, and 18, and for WPW syndromes in
Chapter 7, and the reader can refer to them for more detail. Here we present several others that
will help to differentiate the mechanism ofSVT. As a general rule, key observations to differen-
tiate a narrow QRS tachycardia occur during ventricular pacing techniques, and for a wide QRS
tachycardia, during atrial pacing modes.
Table 16-1 begins the process of determining whether the patient has AV node reentry or not
Assuming a low to high atrial activation sequence during tachycardia, sinus node reentry is
Control CS pullback
1111 1 1
f r'
l' i·'i'l' 'l"' I" l'" l"'l:11:1·11i·1'l·'"l""I' l""l"''J'llll""J"llJ'111111111111,1nu1,,,111111uu1,111111111m,1111,1,,,,1,n111111p11•
II
Ill
V1
A' A'
HRA ~
HBE ~~
A'
PCS ~
DCS ~
FNA ---i..v ~I
Panel A PanelB
FIGURE 16-13 • Map of the left AV ring during AV reenny with right bundle branch block:. The earl lest VA Interval (100 ms} Is
noted on the proximal coronary sinus (PCS) electrogram In Panel A. Note that the VA Interval cm the dlstal (DCS) pole Is 110 ms. In
Panel 8, tile catheter In the CS Is withdrawn to a more proximal loc:Btlon and the VA Interval Is 105 ms on both the dlstal and proxl-
mal CS electrode pairs. Thus, the earliest retrograde atJial activity during tachycardia was at the previous PCS site; in this patient the
pathway was located in tile left free wall near the interatrial septum.
TABLE 16-1 Methods to diagnose AVN reentry at EPS.

I. Sinus nod!! reentry
• Excluded by low to high atrial activation
II. Atrial tachycardia
A. EllmlnateatJlal Involvement
1. V pace terminates tachycardia reproducibly without atrial activation
2. Pe~lstence of tachycardia without attlal actlwtlon
3. Tacyardla entTalnment during V pace with V-AN response

II. Atrial tachycardia
B. Prove AV node Involvement
1. Oianges in AH precede and predict M changes
2. Variable AH with fixed HA
3. PVC Initiates tachycardia wtth V-A-V response
4. Initiation with PAC requlnl!S c:cnductlon to His bundle {suggestive)
S. PVC Initiates tachycardia wtth long VA Interval (suggestive)
6. Critical AH Interval required to Initiate tachycardia (suggestive)
7. Reproduc!ble termination with Aand no His {suggative)

Ill. Atrioventricular reentry
A. Eliminate AP involvement
1. VA interval •too short"
2. VA dlssoclatlon for <?1 complex
3. Changes ln HV Interval do not affect subsequent HA Interval
4. Vr\."' -VART ~100 ms
5. Preexcitation index >75 ms with concentric atrial activation sequence
excluded, as is any AT with a similar activation sequence. However, if the lower atrial septum
is activated earliest, then AT needs to be considered. First, try to exclude AT. 15 If pacing the
ventricle terminates tachycardia without activating the atrium (see Figure 7-21) or SVT per-
sists on its own without atrial activation, AT is excluded.15 Next, during tachycardia introduce
PVCs and then trains of ventricular pacing typically starting at a cycle length (CL) about 20 ms
shorter than the tachycardia CL.15 Similar information can be obtained when a PVC captures
the atrium versus during constant ventricular pacing. As discussed in Chapter 7, a PVC that
preexcites the atrium when the His bundle is refractory from anterograde conduction demon-
strates that an accessory pathway is present but not necessarily used in the tachycardia circuit,
although practically it is invariably part of the circuit We showed that the difference in the VA
interval during AVRT and during the PVC that captures the atrium is typically less than 100 ms,
but with AVNRT the difference is 100 ms or more.1s.16 Further, one should also analyze the
response after capturing the atrium: the last ventricular paced beat (V) followed by an AV or
VAV response (Figures 16-14 through 16-16) is consistent with either AVNRT or AVRT15•17
and eliminates AT as the mechanism. In AT, the response is VAAV (Figures 16-17 and 16-18).
However, you need to be sure which atrial beat is last captured after cessation of ventricular
pacing, for a "VAAV" appearance can occur with long-captured VA intervals (Figure 16-19).
Thus, do not pattern read, but make the measurements!
Additional diagnostic information can be gleaned from differences in paced and tachycardia
VA intervals in the VAV response.1s.18 In 1 study, 18 the ventricular stimulus to atrial (S-A) inter-
val minus the VA interval during tachycardia (VA-RT) was more than 85 ms in all patients
with AVNRT but less than 85 ms in those with AVRT (Figures 16-15 and 16-16). The authors
also analyzed the post-pacing interval (PPI) minus the tachycardia CL (TCL) and a result of
>115 ms was consistent only for those with AVNRT. We prefer using the S-A minus VA-RT
interval, and use 100 ms or more to separate AVNRT vs AVRT. However, in patients with long

Ill. Atrioventricular reentry
B. Prove AP involved in tachycardia
1. VA prolongatfon with lpsrlateral BBB
2. HA prolongation with increase in HV interval
3. Tachycardia termination by PVC that occurs when His bundle is refractory and does not conduct to
atrium
4. Prolongatlon of AA Interval by PVC when His bundle ls refractory
5. VA - V~ <50 ms (highly suggestive)
AVFrr AVNFrr
V·A·V V·A·V
FIGURE 16-14 • Schematic at response to ventTlcular padng during SVT. After pacing ends, the last Impulse that has captured
the atrium mnducts retrograde over an accessory pathway {AP} on the left side or over the AV node on the right side of the figure,
with retum to the ventricle giving a V-A-V response. Avrrr, atrioventriculilr reentry; AVNRT, atrioventricular node reentry. (See text
for deta!ls.)
HBE l--~-1'--"'---~--<--1'._.~_,_-'"'-~~~~_,,..._...~~-"'tv--~~-.Jvv-~~--'1
HBE 1------1--..,i 1._,---.---1-...1 1....-~....---r---.11..-~--...-~~~--.111,-._._~~~1~--v~~__,,,,v-~~~-'1
PCS t--+-~~---'1r--~~-1r~~~-'r-~~~--'--'\r~~~__.,~~~~..,__~--t
300
N-6
FIGURE 16-15 • Response to ventricular pacing during AVRT. Afttr the last paced beat (51} there Is retrograde conduction over
a left-sided AP and AVRT contfnues with a VAV response. Note that the difference In the VA Interval at the S-A and VA-RT ls 70 ms,
consistent with Avrff. HRI\ high right alTium; HBE. His bundle efectrogram; PCS, proximal coronary sinus; MCS, mid CS; DCS, distal
CS; RV, right ventride. (See text for details.)
MCS5,81--~~+-~-+-~-+-~-1-~---t~--,,..__~+-~-t-~-r-~-t-~-+~-+~~1
MCS3,41--~'-~-+--~-+-~_,._~_,.~__,.__~r--~-r-~-t-~-r-~-+-~_..,,._~-r-~--u
DCS 1,21---(-~~~~-f-~-r-~---t~--,r--~-t-~""i"-~-r-~-r~-v-~-"l""~--f'~--1
RVA.i----ir-----v--~+-~...,......-iv~~~~~~~~~~~_,~~_,~~-.-.~~~..,.-~Jr-~--.-1
0 1000 2000 3000 4000
FIGURE 1..16 • Response to ventricular pacing during AVNRT. ~r the last paced beat then! Is a VAV response. The tachycardia
cycle length Is 316 ms and the paced CL Is 300 ms. Further, the difference In tf1e VA Interval of tf1e S.A and VA-RT Is nearly 200 ms,
typical for AVNRT. HRA. high right atrium; HBED, dlstal His bundle electrogram; HBEP, proxlmal His bundle electrogram; PCS, pr~
mal coronary sinus; MCS, mid CS; DCS, distal CS; RV, right ventricle. {See text f'or details.)
VA intervals over an accessory pathway during AVRT, both the delta SA minus VA-RT and
PPL-TCL measurements can be misleading, and one needs to use multiple maneuvers t.o be
sure ofthe diagnosis.111
Table 16-2 lists methods to prove the AV node is part of the tachycardia circuit, which would
eliminate AT as a possibility. The first 3 definitely implicate AV node involvement, an example
of which is shown in Figure 16-20. Note that there is wobble in the AH that results in changes
in the HH interval, and the changes in AH precede and predict the changes in AA interval Also,
the changes in AH are associated with a constant HA interval. Because the VA interval is too
short for AVRT, the diagnosis is AVNRT. If induced or spontaneous tachycardia reproducibly
tenninates with block in the AV node, it strongly suggests AV node dependence (Figure 16-21).
After AV node involvement in the tachycardia circuit is confirmed, the next step is to decide
whether AVNRT or AVRT is present Tables 16-3 and 16-4 list maneuvers and observations
at EP study that can either eliminate (Table 16-3) or prove an AP involvement in the circuit
(Table 16-4), and these are discussed in detail in Chapter 7.
Abtal Tachycardia
v v
V----- A------------------- A---- V
FIGURE 16-17 • Schematic of response to ventricular pacing during atrial tachycardia (AT). After the last ventricular beat the
atrium Is captured, shown here In a potenttal atriaI reentry drcutt. and the next atrfal complex conducts to the vennlcle, for a VMV
response. (See text for detalls.)
Use of a detailed systematic approach typically allows one to secure a diagnosis before start-
ing ablation. There are occasions where additional maneuvers may be needed, and in some
patients no one observation is diagnostic, but the cumulative responses to many will yield the
most likely mechanism. In some patients the differential diagnosis is between AVNRT and an
automatic junctional tachycardia. It is useful to introduce premature atrial complexes starting
late in diastole. If a PAC after His activation alters the subsequent His activation time (typically
shortens the H-H interval). then junctional automaticity is not present (Figure 16-22).20 While
AVNRT is almost always the diagnosis, a remote possibility is an AT with conduction over a
slow AV node pathway. However, if the HA interval remains the same, AT is essentially ruled
out This maneuver is shown schematically in Figure 16-23.
Responses to standard pacing techniques may not result in a diagnosis in some patients with
a long RP tacliycardia, especially with earliest atrial activation in the septum (Figure 16-24).
In such cases it is helpful to use differential right ventricular (RV) pacing from the apex
1000 2000 3000
II
Ill _ __,,__ _
.__~
V1
1000 2000 3000 4000
LB.10/02
FIGURE 16-11 • Response of ventricular pacing In AT. The last paced V that conducts to tile atrium (A) Is followed by anotller A
that conducts to the V, ylelding a VAAV response.
s, s,
J-2
FIGURE 16-19 • VAV response masquerading as VAAV. This patient has atypical AVNRT with a long RP Interval. Tachycardia CL Is
328 ms and the atrium Is captured during ventricular pacing {51) at CL 290 ms. The last captured atrial complex Is net the flrst A after
termlnalicn of pacing. but the next one as can be seen by the 290 ms interval. That A Is followed by the next beat of tachycardia, and
the actual response Is VAV, net VAAV. Tile S-A minus VA-RT Is about 170 ms.
389
Ii i------/
1111---- --'
v1 ,___ __...._,,_---~~--~.,----..,----~/---,~
v2 1---------~----"-----v-~--"'----"----.I\,-
V6t----__,'--~---A----A....-~-./\---..J ~---·'--
66ms
0 1000 2000
FIGURE 16-20 • lnlttation ofslow-fast form of AVNRT. There Is wobble In the tachycardia CL with changes In HH preceding and
predicting changes In AA Interval, with a constJlnt HA Interval. (See text for deta!lsJ
0 1000 2000
11 - - - - - / ' - - - - - - J ' - - - - - - J ' - - - - - J '---------1
111----.J .___ _ __, .___ _ _ __, ~---.../ '------- --1
1111----_.r'-----"-----'"'----~--------t
aVFi-----''-----''-----~-----''---------1
V1 i.---~--" ,.-,.---.. ,,..------. ,.---_.., , - - - - - - - --1
V61 - - - - - ' .__ _ ___, ..__ _ _ ___, ..__ _ _ _J ' - - - - - - - --11

230ms
HRA
S1 S1
0 1000 2000
FIGURE 16-21 • Initiation and termination of slow-fast form of AVNRT. (See text for detalls.)
11 1--~-----~~----~----~-~-----~---~
Ill
V1 t--__,.------_....,~-------'-----..--..._,r-
V2
-----..r -----1
A2.
Pcs ~~----_.,,,.,... ____ _,,~---1--------~._._------f
MCSt---J1------.i>------11------~------11------1
MCSt-----w''------w·----~v-------r-----~~-----t
DCS
RVl----"A.--------vv-------vv---~-'V\------Vv-----1
E4
FIGURE 16-:U • Response to PAC (A2) Introduced durfng AVNRT. The uchyardla CL Is 458 ms and A2. shortens It to 440 ms. (See
text for detallsJ
Respon• 1o PAC Dellwr9d When

JuncUon le Ref1ectory
AVN
H
FIGURE 16-23 • Schematic of response to
Panel A a prematureatrlal complex (PAQ Introduced
during either automatic junctlonal tachycardia
{A) or AVNRT (8). In Panel A, a PAC does not
affect the tachycardia CL (le). In hnel 8, the
A
PAC captures ttte slow AVN pathway (SP} and
shortens the CL (lc-n). A, atrfum; AVN, AV node;
AVN H, His bundle; FP. fast AV node pathway. {Repro-
duced with pennls.slon from Padanllam BJ, et al.
Differentiating junctional tachycardia and at~
H oventricular node re-entry tachyardia based
on response to atrial extrastlmUIU$ pacing. J Am
PanelB Col/C.Ordfol. 2008;52:1711-1717.)
FIGURE 16-14 • Twelve.fead ECG during long RP tachyardla.
and posterior wall (Figure 16-25). Figure 16-26 shows data from a patient with such an AP
that was ablated at the left posterior septum. During the study. atrial preexcitation occurred
considerably after His activation, and AVNRT could not be ruled out. The VA interval during
RV apex pacing is 262 ms (Figure 16-26, Panel A) and from the RV posteroseptal wall 214 ms
RVll*< VA< RVponir1or VA RVpoetar1or VA< RVIPflK VA

PanelA PanelB
FIGURE 16-25 • Schematic of dlfferentlel RV pacing technique. In Panel A., there ls no AP present end the VA Interval from the RV epex
(blue line) Is shortl!t' than the VA tntl!rvill from the RV posterior wall {green line). In Panel Bwith a slowly conducting AP present In the
septum, the VA intetval is shorterwflen pacing the RV posterior wall (green fine) than from the RV apex (blue line). (See text for detail5.)
10 RV APEX 11
PCS 1--~~~---.•~~~~~~.1.-~~~~~~~~~~~~~~~~
MCS t--~~~-1,~~~~~---.Jr-~~~~~.\.--~~~~~~~~~-'--!
Mcs 1--~~~--4~~~~~--'l~~~~~---'--~~~~~~~~~-J\--I
MCS l--~~~-1--~~~~~+-~~~==:=;:!t!--~~~~~~~~~~L....1
500 s, 500
Pa!MIA
37 RV POSTE SEPTAL 38
V1
HBEl----/~~"-~~~JV---~~~~../'-''----~~~-../"-"----~~~~---f
500 s 500
PanelB
FIGURE 16-26 • In a patient with a concealed left: posteroseptal slowly conducting AP, the VA Interval pacing the RV apex Is 262 ms
{Pan1I A) and 214 ms padng the RV posteroseptal region {Pan1I 8). (See text for detallsJ
II
Ill
V1
V2
HBED
PCS8, 7
MCS6,5
S2
MCS4,3
38ms
DCS2, 1
RV
Z-6
FIGURE 16-17 • lntTacardlac recording of the results of a premature atriaI sttmulus from the mid CS (S2) during antldromlc reentry
(ARD. (See text for detail$.)
(Figure 16-26, Panel B). A novel new pacing technique, introduction of premature His com-
plexes during SVT, is an excellent method to differentiate AVRT from AVNRT.21
In a patient with suspected antidromic reciprocating tachycardia, it is key to introduce atrial

premature complexes during tachycardia starting late in diastole near the presumed atrial inser-
tion site of the AP.15 In F.lgure 16-27, a PAC introduced in the coronary sinus (S2) at a time the
septal atrium has been activated pree:rcites the ne:rt ventricular complex (266 ms) with identi-
cal QRS morphology, confirming anterograde conduction over the AP. The subsequent atrial
complex is pree:rcited (272 ms) confirming participation of the AP in the tachycardia circuit.
Because the PAC was introduced after the septum was activated, this cannot be reset of AT, and
a "late" PVC cannot pree:rcite AVNRT-thus, this is antidromic reentry. A plus here is the ret-
rograde His recorded before the septa! A, and the H-H interval is also pree:rcited, ruling out any
concealed AP as part of the tachycardia circuit Flgure 16-28 is a schematic of this technique.
Para-Hisian pacing is most useful to determine whether retrograde conduction over a septal
AP is present.22 It can identify APs in other locations but typically they will also show eccentric
activation during routine RV apical pacing. Figure 16-29 shows schematics of the maneuver. A
catheter is positioned near the His bundle region and can be moved slightly back and forth to
capture the His bundle and RV or just the RV, or simply left in a position near the His record.Ing
Control PACnearAP
~'*"1
Alrlum
Ventrlcle
Atrium
Ventrfcle
AVN
His
tf
t
I
I
AP
~---·
t
Panel A PanelB
Returncyd&
Atrium
Ventrlcle
PanelC
FIGURE 16-21 • Schematic of PAC Introduced during ART. Panel A Is tfte control wltft the tachycardia cln:ult In red. In Pan1I B. a
PAC is introduced late in tfte tachycardia a. after the septum has been actimed and activates the ventricle over the AP shown in
blue. Panel Cshows the return cycle in the dotted blue line with preexcitation of the atrial septum.
and increase and decrease the pacing output, which we prefer to do. In Figure 16-29, Panel A,
a septal AP is present. The assumption is that retrograde conduction over the AP will be faster
than that over the AV node even when the His is captured. Thus, the VA is constant with the
wide (RV capture only) and narrow (RV and His capture) paced complexes. So, a W=N VA
demonstrates the presence of anAP. In Figure 16-29, Panel B, no AP is present Here the VA is
shorter with His capture than RV-only pacing. While a N<W VA is consistent with conduction
over the AV node, it does not rule out conduction over an AP as noted below. Figure 16-29,
Panel C, is an example of a N<W VA response with conduction over a left-lateral AP. In this
case there is poor or no retrograde conduction over the normal VA conduction system, and
when His is captured, conduction to the left ventricle is faster than if only the RV is captured,
resulting in a shorter VA interval This is the reason we do not like the term AV nodal response
and prefer simply stating what happened Figure 16-30 is an actual example of a N<W VA
response in a patient with a left-sided accessory pathway and poor retrograde AV node conduc-
tion. F.lgure 16-31 is another example ofN<W VA with an AP present. In Figure 16-31, Panel A,
note the VA interval is 94 ms with His capture and 132 ms with RV capture. Conduction is over
the AV node here but does not rule out the presence of a septal AP with retrograde conduction.
In fact, the patient had a concealed mid.septa! AP with slow retrograde conduction that was
only present during AVRT. In Figure 16-31, Panel B the ablation catheter (ABL) is positioned
Pant-Hlslan pacing wHh 8lplal AP
API
LBS
API API
WldeQAS NamrwerQAS
-with septa! AP. VA time doea not change.

Panel A
Para·Hl•l•n peeing - AV node only
Wldt QAS Ne.m>wer QAS

"With no AP, VA time la •horter whan 1her8 la HI• captul'8.
PanelB
FIGURE 16-29 • Schematic of Para·His pacing technique. Capture of the RV only is in blue and His and RV in red. Panel Ais with
a septa! AA Panel 8 wtth only AV node conduction, and Panel C Is when a left-sided AP Is present with poor AV node conduction.
(See text for detalls.)
396
Para-Hl•l•n pacing wllh Id 11'H wall AP
IAP
IAP
WideQRS NamJwarQRS
"With LFW AP, VA time may be llllor18r wllh Hla captul'9,
HBED
HBEP ~---1
PCS9,10 1-----~--........-----------......----------_,.,.__________..,,.._______,
MCS7,81----------1r-------~~,----------~1r----------1r-------i
MCSS, 61----------.,,----------_.,,..-----------w---------~1,-----1
MCSS,4i--------~--------~'tr---------~----------'v'-------i
BB
FIGURE 16-30 • Pa~H fsiin pacing in il Jmient with a left-sided AP and poor or no ret!Ogriide AV node conduction. The first 2 OAS
complexes are relatively narrow, and the VA conduction is shorter than in the last 2 wider OAS compleiaes that activate only the RV.
397
""l'"l'I"'~
2000
.'--~-----~-----~
DCB 1,21-----------~- - --+.- --f

FNAt--W'-----t""~~--;..;1..- --rJ'----
0 1000
"''l'"'l''''l"11111111111111n1p•••r ''l"''l'"'l '"'l"' l""P'"I' ''1''''1''''1'1111

ISOPROTERENOL 1000 2000
PCS e. 10.......,,_...,.._,,_ _,_,._~,.....,.......,..._._,._~-+--..-~+----i

MCS7,8 1-.1'-~.J--~J---~.J'-__..-.f'~-..1--....__,.~__,.._,._-J-..,._-.,11
MCS!S, a....,._.,.__,___,__.._........,_ __,____...__ _.__~-t
MCSS, 4~-i--...,._+-_,__i--.._..,~__,..---1,-1---1--~--i----11
ocs1,2~--------..--.---..-__,.. _ __,__ _,_~_,_--1
RVA ,___,,,~__,, _ _,.~~

s~ •·~_,.-....,.,~_..,.,~-.1~-~,__,
1000
PanelB
FIGURE 16-31 • Para-Hlslan pacing Is shown In Panel A. In Panel B, a PVC preexcltes the atrium with a VA Interval of 170 ms. {See
text for dmlls.)
in the His bundle region and records the earliest VA interval during tachycardia. A PVC (S2)
that preexcites the atrium has a VA interval of 170 ms during isoproterenol infusion, and this
is significantly longer than VA (132 ms) over the normal VA conduction system even in the
absence ofisoproterenol (Figure 16-31, Panel A). The short HV and minimal preexdtation is
caused by conduction over a fasciculoventricular pathway during AVRT. So, W=N VA response
demonstrates retrograde AP conduction, but N<W VA does not equate with the absence of AP
conduction.
REFERENCES
1. Dumr D, et aL The role of premature beats in the Initiation and the termination of supravtlltricular tachycardia
in the Wolff-Parkinson-White syndrome. Cimilation. 1967;36:644.
2. Scherlag BJ, et al. Cathetertedm.ique f'or recording His bundle actiYity in man. Circulation. 1969;39:13.
3. Prystowsky EN. Electrophysiologic testing. In Kelley WM, ed. Textbook of Internal Medicine; vol 1. Philadelphia:
Lippincott; 1989:344.
4. Gallagher JJ, et al. Bpicardial mapping in the Wolff-Parkinson-White syndrome. Circulation. 1978;57:854.
5. Prystowsky EN. The sick sinus syndrome-diagnosis and treatment. In: Donoso E, ed. Advances and Controversies
in Cardiology. New York: Thieme-Stratton; 1981 :95.
6. Mandel WJ, et al. Assessment of sinus node function in patients with sick sinus syndrome. Circulation. 1972;46:761.
7. Strauss HC, et al. Premature atrial stimulation as a key to the understanding of sinoatrial conduction in man.
8. Lange G. Action ofdriving stimuli from intrinsic and extrinsic sourcu on in situ cardiac pacemaker cells. Gire Res.
1965;17:449.
9. Browne KF, et al. Factors influencing specificity of sinus node recovery time in man. Circulation. 1983;68(III):
III-382.
10. Benditt DG, et al. Analysis of secondary pauses following termination of rapid atrial pacing in man. Circulation.
1976;54:436.
11. Dhingra RC, et al. Significance of block distal to the His bundle induced by atrial pacing in patients with chronic
bifascicular block. Circulation. 1979;60:1455.
12. Damato AN, et al. Functional 2:1 A-V block within the His-Purltinje system: simulation of type II second degree
A-V block. Circulation. 1973;47:534.
13. Prystowsky EN, et al. Electrophysiologic assessment of the atrioventricular conduction system after surgical cor-
rection of ventricular preexcitation. Circulation. 1979;59:789.
14. Prystowsky EN, et al. Induction of ventricular tachycardia during programmed electrical stimulation: analysis of
pacing methods. Circulation. 1986;73:II-32.
15. Klein GJ, Prystowsky EN. Clinical Electrophysiology Review. lst ed. New York: McGraw-Hill; 1997.
16. Miles WM, et al. The preexcitation index: an aid in determining the mechanism of supraventricular tachycardia
and localizing accessory pathways. Circulation. 1986;74:493-500.
17. Knight BP, et al. A technique for the rapid diagnosis ofatrial tachycardia in the electrophysiology laboratory. JAm
Coll Cardiol. 1999;33:775-781.
18. Marchand GF, et al. Differentiation of atypical atrioventricular node re-entrant tachycardia from orthodromic
reciprocating tamycardia using a septa! accessory pathway by the ruponse to ventricular pacing. /Am Coll Cardiol.
2001;38:1163-1167.
19. Bennett MT, et al. Entrainment for distinguishing atypical atrioventricular node reentrant tachycardia from
atrioventricular reentrant tachycardia over septa! accessory pathways with long-RP tachycardia. Gire Arrhythm
Electrophysiol. 2011;4:506-509.
20. Padanilam BJ, et al. Differentiating junctional tachycardia and atrioventricular node re-entry tamycardia based on
response to atrial extrastimulus pacing. JAm Coll Cardiol. 2008;52: 1711-1717.
21. Padanilam BJ, et al. Differentiating atrioventricular reentry tachycardia and atrioventricular node reentry tachy-
cardia using premature His bundle complexes. Circulation Arrhythmia and Electrophysiology. Accessed January,
2020. doi.orgl 10.116llcircEP.119.007796.
22. Hirao K, Otomo K, Wang X. et al. Para-Hisian pacing. A new method for differentiating retrograde conduction
over an accessory AV pathway from conduction over the AV node. Circulation. 1996;94:1027-1035.
Catheter Ablation of
Supraventricular Tachycardias
INTRODUCTION TO MAPPING AND ABLATION

The verb to abla~ means to destroy or remove functionality of a structure. Catheter ablation
involves delivering energy from a catheter to create a lesion eliminating a pathway or structure
causative ot or involved in the manifestation ot an arrhythmia. Ablation was initially done to
treat arrhythmias using surgical incisions. Seeking less invasive percutaneous treatment, direct
current catheter ablation was developed, but it was difficult to titrate and direct. Radio-
frequency ablation was first reported by Dr. Huang and c:olleagues1 and offered a much more
precise and targeted energy source. Radiofrequenc:y energy remains the most common energy
source, but cryoablation has been used for several arrhythmias and ac:c:ounts for over a third of
atrial fibrillation ablations. Laser ablation, using a balloon, is also approved for atrial fibrilla-
tion. Additional sources under investigation in.dude low-intensity ultrasound, elec:troporation
(pulsed field ablation),2 and stereotactic:, external X-beam ablation. Establishing the correct
diagnosis (see Chapters 6-9), and identifying the pathophysiologic and anatomic structure are
critical to ablation success. Ablation targets vary in scope from foc.al sources suc:h as atrial
tachycardia, accessory pathways, or atrioventricular (AV) nodal pathways to linear (or other-
wise extensive) ablation as in atrial flutter, other macroreentrant tachycardias, atrial fibrillation,
or structural heart ventricular tachycardia (VT) (Table 17-1).
Radlofrequency Ablation
Radiofrequenc:y energy is nearly always delivered in a unipolar fashion between the electrode
tip and a body surface grounding pad. The catheter tip electrode is usually platinum hidium
and about 4 mm (to up to -8 mm) in size. Being unipolar, current density at the distal elec-
trode greatly exceeds that for the much larger grounding pad. RF energy delivery occurs at
frequencies ofapproximately 500 kHz. This falls in the region of the radiofrequency spectrum
and is too rapid to depolarize cardiac or neural tissue. As energy dissipates from the electrode
tip. the tissue is heated up in a process called resistive heating (Figure 17-1). Current density
decreases by the square of the distance from the catheter tip resulting in the resistive heating-
generated lesion extending only 1-2 mm from the catheter tip. Notably, the predominant source
af the radiofrequency lesion occurs by conductive heating or passive thermal energy trans-
mission from the tissue heated resistively.3 Reversible effects on excitability and membrane
depolarization occur especially at -45°C (Figure 17-2). Irreversible lesions occur when the
tissue reaches about 50°C, likely related to phospholipid bilayer damage.' Pathologic analysis
AVRT AP(TAorMAJ AP potential and/or earliest 95% AV block (septa I pathways);

local V preceding surface Coronary injury (0.1%);
delta. Retrograde AP Tamponade 0.2%
potential (or earliest local A).
Endpoint no antegrade or
retrograde AP conduction.
AVNRT Slow pathway Empiric (V> >A between 98% AV block (0.2%-1 %);
CS os and TAJ. Junctlonal Tamponade 0.2%
rhythm (confirm retrograde
conduction). Endpoint
noninducibility.
AT(focal) Earliest A in AT Activation mapping shows Phrenic nerve injury for CT,
centrifugal spread. (Possibly LAA, or right superior PV.
pace mapping if no longer AVN injury for perinodal.
inducible.) Overdrive pacing. PV stenosis for PV.
shortest PPI. Endpoint: Tamponade 05%
nonlnduclblllty.
Atrial flutter CTI Activation map; 95% Coronary Injury (0.1 %);
(typical) entrainment; ablate from AV block (0.2%-5%);
TA at -6:00 to ER/IVC. Tamponade 05%
Endpoint bidirectional CTI
block.
AtriaI PVfocl; Wide circumferential PV 1-year, single-procedure Tamponade 1%
fibrillation other foci isolation. Other triggers if success rates: -65%-80% Stroke/TIA 05%-1 %
identified. Possibly other for paroxysmal with near ACE2%-10%
substrate. normal LA size; 50%-70% PV stenosis 1%
Endpoint PV entrance and for persistent; 40%-50% Atypical flutter 2%-10%
exit block. for longstandlng Atrloesophageal fistula
persistent. 0.05%-0.2%
All ablations carry !he following possible risks: (1) Vascular access-related complications (hem atom a, arterial pseudoaneurysm, arterio11enous fistula, relTO·
peritoneal hematoma); (2} cardiac tamponade due to myocardial perforation; (3) 11enous tflrombosis or pulmonary embolism; (4} arterial embolism or slTO~,
if LA ar LV access or if LAA or other thrombus (e.g.. LVapex afterMl) is present; (5) anesthetic complications; (6} ffuoroscopic~lated radiation injury (skin injury
from excessi11e exposure on subacute basis tflot muy require skin graft; late risks ofmalignancy}.
Abbreviations: Accessory patflwoy, AP; ER, eustachian ridge; IVC, inferior 11ena covo; TA, tricuspid annulus; MA, milTOI annulus; CTI, covotricuspid isthmus;
PPI, post pacing interval; PV, pulmonary 11ein; AT, atrial tachycardia; AVNRT, atrio11entricular nodal reentrant tachycardia; AVRT, atrio11entricular reentrant
tachycardia; ACE, asymptomutic cerebral embolic lesions.
of radiofrequency ablative tissue shows coagulation necrosis with a slightly irregular border.
Hemorrhage and edema are present in acute lesions and replacement fibrosis occurs after about
4 weeks. If the catheter tip temperature reaches about 100°C, blood coagulates and coats the
electrode. This limits energy delivery and poses an embolic risk. Consequently, thermocou-
ples or thermistors have been used in the electrode to avoid extreme increases in temperature.
Temperature-mode ablation varies the power output to achieve the set target temperature. On
the other hand, the power-controlled mode delivers a fixed power (halted automatically for
greater than desired temperatures or impedances). With RF ablation, lesion size is propor-
tional to power delivery, tip temperature, ablation duration, catheter contact force, electrode
orientation, blood pool or catheter tip cooling (with saline), electrode size, I/impedance (for
CHAPTER 17 • Catheter Ablation of Supraventrlcu la r Tachyca rdlas 403
Convective heat
loss to circulating
~ bloodpool
Resistive (volume)
heating of blood
and tissue
Conductive heating
exchange into tissue
Convective heat
loss to epicardial
coronary artery
FIGURE 17-1 • PrlnciplH « n1dlafnlqu1ncyttnergyablltfon. The electrode dellvers energy in un!polar fashion
with a body surface grounding pad. Resistive and conductive heating ocan. (Modlfled with pennlssion from Nath S,
DiMarco JP, Haines DE. Basic aspects ofradiofrequency Ciltheter ablation. JCardiOllOsc Electrof)hysiol. 1994;5:863-876.)
power-controlled mode), and catheter stability.5 Limitations of the temperature-control mode

include discrepancies between temperature at different portions of the electrode tip, whether
it is in contact with the blood pool of the tissue or embedded in the tissue, and discrepancies
between electrode temperature and temperature deeper in the tissue. With irrigated catheters,
the power-control mode is used because both electrode and tissue surface temperature, cooled
by the saline, are not representative of tissue temperature, which peaks at a depth of 1-3 mm.~ 7
Irrigated catheters have been developed to minimize charring and coagulum on the electrode
tip, thus delaying the onset of impedance rise, and allowing greater lesion size. Irrigated abla-
tion facilitates energy delivery most notably when there is absent or diminished blood pool
cooling (e.g., in epicardial space or in the coronary sinu.s). The region of res.isti.ve heating is
increased with irrigated catheters, just as it is for larger electrodes (provided current density is
maintained, i.e., power is increased).~ Closed irrigation catheters were used initially, but open
48- r--1
37-_J L_
FIGURE 17-2 • Potentlal transient effect of radlofrequency energy abladon. The top shows a guinea pig papll-
lary muscle preparation paced continually and exposed to transient Increase In perfused blood temperature. The
bottom shows membrane depolarization from resting of ~5 to -50 mv, reduction in action potential amplit\.lde,
then transient loss of excitability at 48"C (pacing spikes below baseline continue) followed by recovery upon return
to baseline temperature. This illustrates tne reversibility of ablation wnen tissue temperatures do not exceed SO"C.'
(Reproduced wltn permission from Natnan S, et al.Cellular electropllyslologlcal effects of nypertnermla on Isolated
guinea pig papillary muscle. Implications fur catneter ablation. Circulation. 1993;88:1826-1831.)
irrigated catheters are now more common; prolonged ablation with open irrigated catheters
may lead to volume overload, however. The lack of temperature feedback with irrigated cathe-
ters increases the chance of extreme tissue heating several millimeters subsurface. In fact, steam
pops can occur at tissue temperatures above 100°C and may lead to myocardial perforation.
Cryoablation
Cryoablation catheters contain 2 lumina within the catheter shaft for delivery and removal
of the nitrogen oxide refrigerant, respectively. This energy was developed in part to provide
a slower onset and some ablation reversibility for risky areas. To that end, a cryo-mapping
mode is present in some applications. Based upon the Joule-Thompson principle, compressed
nitrogen oxide is allowed to expand at the catheter tip; this causes cooling of the electrode
to temperatures of - 70°C or lower.9•10 As the electrode cools, an ice ball forms and the tip
becomes adherent to the tissue. Cryothermal injury has several components. First, extracel-
lular ice forms beginning at about -20°C leading to loss of intracellular water. Second, with
further cooling to -40°C, intracellular ice forms, which leads to cellular death (Figure 17-3).
Third, damage to blood vessels in the area can cause tissue necrosis as well. Tissue warming can
result in additional injury. The effects of cryoablation can be reversible with brief, modest cool-
ing or permanent with longer excursions to lower temperatures. Cryoablation has been used
with intraoperative probes for decades.11 Percutaneous catheters (7-8 French) with 4-8 mm
electrode tips for focal ablation became available in the early 2000s. They are used most often
for AVNRT and septal accessory pathways. Cryoablation lesion size is proportional to electrode
size, electrode orientation (horizontal greater than vertical), tissue contact, surrounding blood
flow, time, and refrigerant flow. 12 Presently, the most frequent application for cryoablation is via
balloon catheters used for pulmonary vein isolation.
ABLATION OF ACCESSORY PATHWAYS

Accessory pathways (APs), of several types, are the pathologic substrate for ventricular preexci-
tation and for atrioventricular reciprocating tachycardia (AVRT) (Figure 7-2). The physiology
and arrhythmias associated with APs are covered in detail in Chapter 7. According to several
CHAPTER 17 • Catheter Ablation of Supraventricular Tachycardias 405
Cryosurgical Mechanisms of Injury (Immediate) Overview:
Cryosurgical Cryosurgical
kill zone probe
:!:-40"C
_ _ !_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ __
Radial Position
-0.5°C
-20°c
lceball
--- ~~~!~~~~-----------~l~~~-----
Edge llF Vascular Injury
(Stasis & thrombosis)
(-0.5°C)
Injury Mechanisms
FIGURE 17-3 • Cryoablation mechanism. Temperature declines with distance from the cryoprobe. Irreversible injury occurs at
about-40°C.'0 Abbreviation: llF: intracellular ice formation. (Reproduced with permission from Avitall B. Kalinski A. Cryotherapyof
cardiac arrhythmia: from basic science to tne bedside. Heart Rhythm. 2015;12:2195-2203. Copyrignt e Heart Rnytnm Society.)
detailed anatomic dissections,13 APs are usually about 1-3 mm wide and 5-10 mm in length.
They usually course across the AV annulus in an oblique fashion (Figure 17-4). APs are found
at any location around the tricuspid or mitral annulus, except for the mitral aortic continuity.
As such, the ventricular insertion is close to the annulus, i.e., basal, for typical AV pathways.
Branching at the insertion has been observed pathologically and may explain the not infrequent
clinical challenge in eradicating them. Left-sided APs usually lie epicardial to an intact annu-
lus fibrosis, sometimes on the very outer wall (Figure 17-4). Right-sided APs course through
the epicardial fat between atrial and ventricular myocardium. Less common atypical pathways
include longer pathways with either or both insertion sites more distant from the AV ring. Such
atypical APs have been ablated from either atrial sites such as the atrial appendage or ventricu-
lar sites off the rings including epicardial sites or adjacent to the normal AV conduction system.
Careful mapping of both atrial and ventricular insertions, when possible, (ie., for bidirectional
pathways) prior to ablation is important as ablation will interfere with interpretation of electro-
grams. The preexcited electrocardiogram {ECG) provides useful clues to AP location (Chapter 7}.
Regarding mapping the ventricular insertion, the optimal electrogram includes an atrial, AP,
and a local ventricular potential that precedes the onset of the surface delta wave by 15-30 ms
{Figure 17-5). Merely having a "fused" A and V signal does not predict success as this could
represent a relatively late atrial signal with a moderately early ventricular signal some dis-
tance from the ventricular insertion. The unipolar ablation electrogram can provide useful
PllnelA PanelB PllnelC Panel D
FIGURE 17-4 • Hlstologlc Hdlons ofa left posterior aca.uory psthway (AP). Panel A Illustrates the atria I Insertion of1he AP
(arrow). The AP Is on the eplcardlal side of the annulus fllxosis, which ls the dark staining tissue In the anter. The annulus attadies
to 1he mltral valve, ls located above the ventricular myocardium (VM) and below tfle atrial myocardium (AM} and rightward of the
epicardial fat (EF). In Paneli 8-C, the AP bundle travels tflrough the AV groove as.soc:iated with a nerve, arteiy, and vein labeled
in Panel C. Panel D shows insertion of 1 root of the connection to the myoardium relatively removed from the endocardium.
Because the sections were perpendl<:\llar to 1he annulus, 1he oblfque course of tfle AP Is establlshed.u (Modlfled wtth permission
from Bedcer AE, Anderson RH, Ourret' D, Wei lens HJ. The anatomical substrates ofWotff-Parlclnscn-Whlte syndrome. Acllnlcopatflo-
loglc correlation In seven patients. arculation. 1978;57:870-879.)
'\_____--
avl
Hlem
Hisp
RV
CSd
CSm- - - - '1
Panel A
FIGURE 17-5 • Mapping llCGISIOl'Y pathway during antarograd• canductlon. Plnal Ashows mapping a right lateral AP taking
advantage of Intermittent preexcl!Artlon. Compare the ablation catheter slgnalsshowlng an Aand widely delayed Vcomponent on the
first beat as opposed to 1he fused Aand Vwith possible intervening AP potential on the second beat. The V(or APP) precedes the delta
wave (QRS onset) by 30 ms. The AP wu ablated successfully at 1hls site (not shown). Panel Balso Illustrates a premising efectrogram
during mapping of a ventrklllair Insertion In a dlfferet'ft patient. An A, APP {AP potential), andV are labeled; 1he APP p~es tfle QRS
onset by 25-30 ms. Panel C shows mapping and ablatlon of a left lateral AP that exhibited robust anterograde conduction down to a
220 ms. The flrst 2 beats are preexclted.The RF map catheter records an A. APP, and Vwi1h 1he APP preceding the~ onset by 28 ms.
Ablatfon energy delivery begen just before the tracing shown, and led to loss of preexclttltion on 1he 1hlrd beat, about 25 sea:mds
after the onset of energy delivery; note 1he prolongiltion of intracardiac AN intef'Vals especially on the RF map ca1heter.
CHAPTER 17 • Catheter Ablation of Supraventrlcular Tachycardias 407
CSp
Abl
\v
Pan.IB
P9nelC
FIGURE 17-S • (Conrfl'lued)
confirmatory evidence with a QS pattern. A consistent beat-to-beat signal indicative of a stable

catheter position is critical. Sufficient contact pressure is important as well. Ablating at the
site of an AP potential is theoretically beneficial because APs commonly cross the AV groove
obliquely (Figure 17-6). Consequently, changing the atrial pacing site and thus activation
wavefront may result in separation of the atrial, AP, and ventricular potentials, thereby making
the thning easier to measure and the AP potential more obvious. Explanations to consider
when troubleshooting an unsuccessful ablation include misinterpretation of signals. incorrect
diagnosis, oblique directionality, and catheter contact or stability. The operator should search
fur the earliest near-field electrogram, and not be distracted by interesting. fractionated signals
occurring later, after ventricular depolarization.
Mapping retrograde conduction, ie., the atrial insertion, follows similar principles. It can be
performed during orthodromic AVRT (Figure 17-6) or during ventricular pacing (from vari-
ous locations) (Figure 17-6). AVRT ensures that the activation sequence being mapped derives
RF map p1----...r
CSp t----1--J--..,,v-~~~~--1--J--..,1v-~-1-J-~--1'~~~~~~~~~~~~--i
•
CS7-8 t--~_,,,,..._,,,..-~~~~~_,,,,..._, ..-~~-.r-~---.r;~~~~~~~~~~""""r1~
cs51 1--~~r--;1.1-~~~~~~r--;i.-~~-./"~---;1i---~~~~~~~~~--u1t-""\
(:$3-4 1--~~~'--~~~~~_,."-:ll '--~~f-~~· ~~~~~~~~~~~~~-.....-t

CSd l-----...---__,.._,lf~~~~~--....---__,.._,lf~~--,,,-__,-~---111'--~~~~~~~~~----t1r---f
800
Panel A
FIGURE 17-6 • Mlpplng accessory pathway during retrogr11de conduction. Panel Adlsplays RV pacing wl1fl fusion of AV node
and left latl!ral AP conduction; note the V, probable AP potential (arrow}, then Aon the mapping catheter wltti change In morphology
on the PVC when the AP blocks retTOgradety; note that dte Aon map occurs much later. On dte next sinus beat thl!fe Is preexc!trtlon
widt dte mapc:atheterreccrding an A. probable AP potential (ctlTOW), then V, moments bef'oredte tracing shown in Figure 17-SC.
Panel B Is a tracing during AVRTwtth the abladon c:adtetef on dte posterior mltral annulus showing an Aearlier than CS and an AP
potenual between dte Vand retrograde A. Mapping during AVRT avoids the potential that the activation Is generated fully or partly
via retrograde AV nodal conduction. This consideration Is especially crttlcal for septal APs. Panel C shows abletlon of a left letera~
retrograde-only AP during RV peeing with retrograde AP block on fourth beat, resldual conduction on fifth beat (vs possible
automatlclty) and then block on sl:xth and seventh beats. The fourth and sl:xth ventricular beats conduct tetrogradelyvfa dte AV node.
L~ ·~
_/\
. A_____
avF
V1 v
CSd
CSp --'~----t---
Abl
PIMIB
Mapd2- ,~~~vv
CS e11n- --11r - - - ----: - - ~.,.._,11,.......-~~-t~'-- -----t1r - ~
Page: A1111t1on Spead; S7 mrMI

PanalC
FIGURE 17-6 • (CotltfnUC!d)

from AP conduction. Conversely, mapping during ventricular pacing could represent either
AP or AV nodal conduction; this is especially problematic with septal pathways. Theoretically
parahisian pacing can dissect out AP versus AV nodal conduction.
Pathway location determines success, as well as complications. Approaches vary to some degree
too. Success rates average about 90%-95% (Table 17-1). They are slightly higher for left free wall
pathways, versus lower for posteroseptal ones. Recurrence rates tend to be higher if cryoab-
lation is used (primarily for midseptal or anteroseptal ones) and for right free wall pathways.
Left free wall APs are approached most often using transseptal access (Figure 17-6), but the
retrograde aortic approach occasionally affords advantages. Septal pathways may often require
mapping the tricuspid valve, mitral valve, and within the coronary sinus before determining
which is best. A coronary sinus venogram is helpful when a pathway is found to be related to
the venous system, e.g., middle cardiac vein, because a diverticulum (possibly harboring the
pathway) needs to be excluded or localized. For right free wall pathways, many operators favor
a deflectable sheath.
Complications related to transseptal access including stroke are relevant for left-sided pathways
(Table 17-1). AV nodal injury resulting in AV block is the focus of concern for septal pathways
(especially midseptal or anteroseptal ones). Coronary artery injury is possible with epicardial
pathways, particularly those adjacent to the middle cardiac vein. Before ablating, angiogra-
phy should be considered. Overall, major complications from experienced centers are less than
2%-3%, with AV block less than 1%, and tamponade occurrence also under 1%.
ABLATION OF AV NODAL REENTRANT TACHYCARDIA

Anatomy and Proposed Circuits
The exact anatomical circuit for AV node reentrant tachycardia (AVNRT) remains unknown.
The initial debate centered on whether the reentry was confined to the AV node or utilized
perinodal tissue. The ability to advance most of the atrium with premature stimulation without
perturbing the tachycardia and occasional demonstration of AV dissociation argued for the
atrium not being part of the circuit although a small rim of protected atrial tissue in the circuit
could not be excluded. •4-16 The ventricle can be dissociated from AVNRT as well; specifically,
2:1 AVNRT with block below the His is frequently observed. More rarely seen is block above
the His, again usually 2:1, implicating a turnaround point above the His. This has been con-
ceptualized as the lower common pathway, although there is no anatomical basis for such a
division. Current understanding of the circuit(s) for AVNRT postulates a compact AV node
with 1 or more perinodal extensions providing the dual pathways for reentry (Figure 17-7).
Right inferior and leftward inferior AV nodal extensions were actually described in Tawara's
seminal book,17 and confirmed by more recent anatomical study. 18-20 Fast pathway(s) lack clear-
cut anatomical correlation. The AV node is located in the AV septum between the RA and LY.
It is positioned in the middle of Koch's triangle whose boundaries are formed by the central
fibrous body (and His bundle) superiorly, the tendon of Todaro posteriorly, the septal leaflet
of the tricuspid valve anteriorly, and the coronary sinus os inferiorly. The rightward inferior
extension, found in -95% of specimens, lies anterior to the CS and posterior to the tricuspid
valve averaging about 4 mm (as long as 9 mm and thus sometimes extending inferior to the
CS). The leftward inferior extension projects toward the CS and mitral annulus, is not as uni-
versally present (-67%), and is shorter (1-4 mm).
FIGURE 17-7 • Anatomical basis for AV node reentry: Inferior extensions of AV node. Aschematic model (In white) suggesting
the locatlon of the compact AV node within the triangle of Koch Is projected onto the surface of a gross anatomlal Image of the
right atrium and atrlovenulcular tissue. The fossa ovalls Iles to the far left The triangle ls bounded by the tendon of Todaro (on the
left side of the CS os), the septal leaflet oftrlcuspld valve to the right of the AV node. and a llne pe1pendlcular to the septa I leaflet
of trlcuspid valve at the height of the CS. Two Inferior extensions of the compact AV node are lllumatl!d, lndudlng the Oongef)
right inferior coursing between the CS and the 5ef)tal leilflet of tlicuspid valve, and the (shorter} left inferior (toward the CS roof).1•
(Modified with permission from Inoue S, Becker A£. Posterior extensions of the human compact atrioventriculilr node: a neglected
anatomic feature of potential cllnlcal significance. Orculatlon. 1998,'97:188-193.}
Typical AVNRT (Slow-Fast)

As denoted by the name. this version of AVNRT accowrts for about 80% of AVNRTs observed.
Slow-fast AVNRT exhibits an AH greater than HA, with HA usually< 70 ms. In typical AVNRT,
the earliest A may be recorded near the His A, but is somewhat heterogeneous and is discussed. fur-
ther below. The anterograde limb involves a slowly conducting pathway. possibly involving the right
inferior AV nodal extension in most cases. Less frequently, the anterograde pathway might be the
leftinferiorAVnodalextension,orrarely(05%),apathwaythatmayrequirea1eftsidedapproach.21
The retrograde aspect of the circuit is the fast conducting pathway that probably has both
right septal and left septal exits emanating from the superior (anterior) aspect of the AV node.
These may consist of the uansitional cells. This may help explain why retrograde conduction
presumably over the fut pathway during ventricular pacing or typical AVNRT may show earlier
activation in CS electrodes beyond the ostium and yet not be due to an AP. n-~ Despite years of
analysis, controversy remains as to the exact anatomical components of the AVNRT circuitry.
Earliest efforts at AVNRT ablation targeted the fast pathway but AV nodal injury requiring a
pacemaker occurred in excess of 5%, and otherwise the long PR interval sometimes caused
a pacemaker-like syndrome. Consequently, slow pathway ablation (just anterior to the CS os
and posterior to the septal leaflet of the tricuspid valve) was pursued (Table 17-1). Electrogram
characteristics (e.g., atrial fractionation) have been described and may stem from anisotropic
conduction. The slow pathway approach proved highly successful, has less than a 1% incidence
of AV block, and has supplanted the fast pathway approach.27
Atypical AVNRT Circuits

At least 2 types of atypical AVNRT circuits have been described, including fast-slow and slow-
slow, but the anatomical properties remain even more controversial than for slow-fast AVNRT,
and some atypical AVNRTs fit neither category. In fact, the term slow-slow is misleading
because the actual AH and HA intervals may not be that long. Rare cases have been reported
with a superior, retrograde slow pathway that has been ablated near the fast pathway or even
from the noncoronary cusp.28
In fast-slow AVNRT, the HA interval is substantially longer than the AH, and the AH is usually
<200. The earliest retrograde atrial activation typically is recorded in the posteroseptal area
(ie., between the CS os and septal tricuspid leaflet or within the proximal CS especially the
roof). In the so-called slow-slow AVNRT, the AH is longer than the HA, but unlike slow-fast,
the HA is relatively long (i.e., >70). Despite the name, slow-slow AVNRT does not have a longer
cycle length, on average, than other AVNRT types.
In terms of ablating atypical AVNRT, a recent multicenter case compilation found that empiric,
anatomic slow pathway ablation (targeting the right inferior extension, between CS and TA)
was successful in 110 of 113 patients, whereas 3 were ablated in the left posteroseptal region. 29
RF Ablation Methodology
Radiofrequency energy using a 4 mm nonirrigated tip catheter is used most often, but some
experience has been presented using irrigated catheters.30 Adequate clockwise torque on the
catheter is used to provide sufficient contact force on the septal structure being ablated. If cath-
eter reach, contact, or stability is problematic, a long fixed curve or deflectable sheath can be
used. A large V/A ratio usually >3 is commonly sought, and ablation is almost always done
in sinus rhythm. If isoproterenol was needed for induction, it is usually washed out before
ablation to optimize catheter stability and facilitate recognition of junctional beats. Ablation
should be avoided in the anteroseptal region at the His bundle and also in the midseptal region
harboring the compact AV node. Successful sites are usually between the CS os and the TA,
below the upper extent of the CS os. Typically a good starting point is at the height of the
lower edge of the coronary sinus and between it and the tricuspid annulus (Figure 17-8). Deep
inspirations and/or intermittent airway obstruction due to deep sedation can cause danger-
ous catheter excursions upward resulting in AV nodal block. Careful attention to the airway
(oral or nasal airway, LMA or ET tube) or minimal sedation may be needed. Before initiating
RF energy, careful delineation of the EP lab team's roles is vital. These include watching for
catheter stability on fluoroscopy or electroanatomic mapping, observing native PR inter-
val, recognizing junctional beats and whether retrograde conduction occurs, and immediate
cessation of RF energy on command. With a nonirrigated 4 mm catheter, RF is started at
10-30 Wand titrated upward manually (or automatically by the generator) to 30-40 W seeking
a temperature target of 55°C-60°C. A gradual impedan~ drop of 10 ohms or more is strong

evidence of lesion creation. If tip temperature is not at target and/or an impedan~ drop is not
noted, the power can be titrated up to 50 W. If accelerated junctional rhythm is not observed
despite evidence ofeffective RF (temperature target and decline in impedance) by about 20 sec,
RF should be stopped. Rarely, ablation is successful despite not eliciting junctional complexes.
Thus, reevaluating inducibility and/or slow pathway conduction after lesions is reasonable.
Durlngjunctional ectopy, catheter stability needs to be c:arefully monitored because the change
in rhythm and rate may cause catheter displacement. Retrograde conduction during juncti.onal
cse_oi--1-,1 r~~-i1r-..n-~~-....---.11--~~-11-~ 1t~~~1r-,1 r~~-lt\.1 1-~~-----1.1r~~-....11-1r--1

CS7Jl l--.._~ 1 ~~~---11Br---11'-~~-c---1 11'--~~---11 ~~~-------11.'--~~11-1 1 t~~~-s.111--~~~ 1~.-.
css_s 1--...--~1~~~-1i.-i1 r--~~-10-1 1r---~~----~ 1 ~~~11,-~1~~~-.111--~~--1~1~~~--t1ra--1
cs3_4 1--11---~ 1~~~---1r--"~~~-1.-..: 1'-~~--+--.. 1 '--~~+-~1'~~--u-i ;:-~~---1~1~~~----11H1--1

CS1_2 t---""'--..;1·~~~1r-~ 1~~~--i.--..J'-~~_,~.........,,.__~~....-...-...;1'~~-11 1J~~~~1~-~~--.i~·.-.
PanelA
FIGURE 17-1 • AV nod1I r•rrtnlnt 1ac:hycardl1: 1bh1tlon of the slow piathway (With RF). Panel A shows ablatlon of the slow
pathway of the AV node. The patient has a baseline LBBB, with Inducible typlcal AVNRT. CL 350 ms, and QRS to ea rifest Aof 0 ms. A
VAV response with long PPI had been noted with ventricular entrainment Note that the bipolar map r.atheter electrogram features
a small fractionated atrial and large ventricular electrcgram. RF is turned on after the third ORS (see the upward artifact on the map
catheter).The flnal 3 beats represent accelerated Juncttonal beats. AVNRT. however, remained lnduc:lble. Panel Bshows another
ablatlon lesion. again lea ding to accelerated junctional beats (second through last QRS complexes). Note that the AIs delayed for
the second junctlonal beat {third QRS complex) and absent on the third junctlonal beat. RF ls promptly turned off (see artlfact).
Panels C and Dshow RAO and LAO views, respectively, ofthe electroanatamlc map of a different patient with AVNRT. The orange
doD mark sites with His potentials. Note the ablation dots {Teet pink, and blue) anterior to the CS (green) but posterior to the TA
(purple a.rtout). lhe blue dot denotes the successful site where inducibility was eliminated. The coronary sinus is in green with the
catheter seen inside it in Panel D. The His catheter is seen in Panel Dtco. Ablation just below the His points and at or above the top
of the CS would rtsk Injury to the compact AV node. Tagging multtple His locatlons, especlally those more lnfedor and posteflor,
helps the operator minimize the risk of Inadvertent AV block.
Mopa_ o JI.- A ,I, j1,-- f"-------i

')
I \ j \ I \ (\ (
Map1
------~·"~r--- 1---11,__._, 1 - - - - \tr- - - - - - - - . 1 1..11---+-+---- l
·~~.~~,~-·---·~~~~·~~~
I
PanelB
PanelC
FIGURE 17-t • (Continued)
PanalD
FIGURE 17-e • (Continued)
beats confirms lade: ofdamage to the compact node and fast pathway. Conversely, ifa junctional
beat fails to conduct retrogradely RF should be halted. If junctional beats occur, the lesion is
continued for a total of 30-60 seconds. Fast junctional beats (<350 ms) portend possible AV
nodal injury and usually warrant cessation of energy delivery. If junctional beats do not occur
(and/or if AVNRT remains inducible) additional lesions may be placed closer toward or in the
CS, and more superiorly, while however avoiding the compact AV node. If retrograde conduc-
tion is absent under baseline autonomic conditions, monitoring retrograde conduction during
junctional beats may likewise be problematic; energy may be delivered during atrial pacing to
ensure intact antegrade conduction.
If AVNRT remains inducible despite ablating the (right-sided) slow pathway region, one should
consider a left-sided (especially left posteroseptal or left posterior) slow pathway. The transsep-
tal route is preferred to ablate such left-sided "slow"' pathways, but this is needed in less than
about 2% of ablations.21
Cryoablation Methodology
Cryoablation is an alternative energy source for AVNRT. It is used preferentially by most pedi-
atric centers and by some adult electrophysiologists. Still other operators use cryoablatio.n in
select cases especially when the risk ofAV bloclc: appears higher, for example, ifablation at more
inferior sites is unsuccessful or if the vertical height of the triangle of Koch is small
Several aspects of the procedure are different for c:ryoablation.31 First, junctional beats do not
occur during ablation. Second, the catheter will exhibit excellent stability after reaching about
-10°C, a property termed cryoadherence (Figure 17-9). If the fixed position proves subopti-
mal due to momentary catheter movement before the critical freezing level was reached, the
ablation should be terminated, and the catheter repositioned. Third, the risk of AV block is
undoubtedly lower with cryoablation. Given the absence of junctional beats to help identify
a successful site during ablation, and using the cryoadherence property, it is helpful to deliver
I .........,.........1"'"""t''"""'l'"'"""'""''"'l '""'"'l"" '""l'"'""'l""''"'l""' ""t""'""l"""'"t'""'"''"''""'l'""""l'""'"'l""''"'l"""'"l"""'"''"'"""'""''200'iT.8'""""'''" '""'
avFtt-------' \ , . - - - - - - - - - ' ' v - - - - - - - - - - - ' \,------../\,-----../
V1 .---~ , . . - - - - - - - - - - . . ,..---~---------..,..-------.. ,.---- -----
His t---"--'"----..lllr-----~___,,-~ ~-./'-------"-..JI'--------. · ~-----.
PanelA
.. ..
''"'' " ' l ' " '"'"l"""""l""'""l'"'"'"l"'' " '"l'' " ' ' " ' l' '"''"'l'"'"'"l" ' ' " '"l"'"""'l""' " " l"''"'"l""""'l" '"" ' ' l'"'""'l"'"''"l"'" ' " ' l"""''"l"''"l""""""l""'""l"""l"''"'""'I' '"""'
200 . .
aVF
V1
HISd
HISm
HISp
PanelB
I
Bl:18 """"'l" '"""l""'""l"'"'"'l'""""l".."'"l"'"'" 'l' '"'"''l"''"'"l'" " '"'l"'"'"'l'""""l"'"' '"l""""'l""' '"'l'"'""'l'""'"'l""' '"'l"'"""l"''"f"l"'"''"l""'""l"""t"''"'""'I"'"'"'
\Y
...
aVF
V1
HISd
HISm
HISp
PanelC
FIGURE 17-9 • CrJ011blation of 5IDW pathway. Panel A shows induction of typical AVNRT with a jump in A2H2. Panel Bshows an
atrial extrastimulus with coupling intenral of 380 ms after a 600 ms drive train; the extrastimulus conducts over the slow pathway
with a jump in A2H2 time. This stimulus sequence is delivered just prior to the start of a cryoablation lesion. Panel C shows the
same Sl-52 sequence during the cryoablation lesion and shows block in the slow pathway. Later during the lesion, and afterward,
the AVNRT was no longer indudble. Junctional ectopic beats are not observed during ayoablation.
stimulation sequences that either induce AVNRT or elicit slow pathway conduction once the
catheter is cryoadherent. If the tachycardia remains inducible or slow pathway conduction per-
sists, ablation can be stopped_ If PR (AH) prolongation (or AV block occurs). ablation must
be stopped immediately. The cryoadherence property even allows safe ablation during iso-
proterenol infusion to readily identify ablation success during the cryoablation lesion. Also,
if AV nodal injury occurs, it is almost always reversible, provided that ablation is immediately
stopped. whereas for RF it is often not reversible. Fourth. whereas the continued presence of
a jump and an echo (single conducted impulse down slow pathway) results in a similar long-
tenn freedom from AVNRT recurrence after RF ablation, some strive for elimination of slow
pathway conduction with cryoablation.n More recent studies have usually used the 6 mm
cryoablation catheter rather than the 4 mm one, and at least 1 study found favorable results
with the 8 mm catheter. In a meta-analysis including 5 RCTs and 9 observational studies with
1262 RF ablation and 1078 cryoablation procedures, the recurrence rate after cryoablation
was 9.1% versus 3.5% for RF ablation. Many labs now describe lower recurrence rates though.
Transient AV block was noted more often with cryoablation (8% vs 4%). However, the risk
of permanent AV block was 0% for cryoablation and 0.87% for RF. The increased transient
Focal atrial tachycardia Centrifugal spread from focus.

Typical atrial flutter Cavotricuspid isthmus (CTI) dependent; counterclockwise; -80% of CTI
dependent flutters.
Reverse typical flutter Clockwise CTI dependent; -20% of CTl-dependent flutters.
Lower loop reentry Circulates around IVC: CTI dependent, but lack of complete line of block
ln crlsta termlnalls; rare form ofCTl-dependent flutter.
Upper loop reentry Circulates around SVC (lack of complete line of block in crista terminal is);
also rare.
lncisional tachycardia Post-surgical incisional tachycardia (right atrial or other incision or
around ASD patch, etc.).
Mltral annular flutter Mltral annular flutter (counterclockwlse more common); seen most
often after AF ablation.
Roof-dependent flutter Reentry up posterior wall and down anterior wall of LA or vice-versa;
seen most often after AF ablation.
Note: The mechanism for these arrhythmias is macro-rttntry, exapt for focal atrial tachycardia, whose mechanism is usually either
micm-mmtrant or triggered.
AV block stems from the need, in most cases, for ablating more superiorly in the triangle of
Koch, and the near absence of risk of permanent AV block despite it occurring transiently
(if ablation is halted immediately)."
ABLATION OF ATRIAL TACHYCARDIA

Atrial tachycardia may exhibit a focal pattern or a macroreentrant one (defined as >2 cm size
of the circuit).34 (See Chapters 5-6 for more detail.) Focal atrial tachycardia ablation will be
discussed in this section. On the other hand, typical atrial flutter is an example of a macroreen-
trant atrial tachycardia. (See Table 17-2 and next section.) Concerning atypical flutter, the left
atrial flutters are addressed with atrial fibrillation ablation, because most arise after prior atrial
fibrillation ablation. Post-surgical atrial tachycardias, or incisional, macroreentrant tachycar-
dias have been reviewed elsewhere.35
Diagnosis of atrial tachycardia may be obvious in some cases with an abrupt onset, a p-wave
distinct from sinus rhythm, and AV dissociation. Other atrial tachycardias (especially with
inverted inferior p-waves) may be challenging to sort out from atypical AVNRT or AVRT. Sim-
ilarly, a high crista terminalis atrial tachycardia may mimic sinus tachycardia in appearance.
The general rules for differential diagnosis of SVT apply including AV dissociation excluding
AVRT and AV node dependence implying either AVNRT or AVRT. (See Chapter 16.)
Atrial tachycardia arises preferentially from certain regions, due to embryologic, anatomic,
ion channel makeup, and/or other characteristics.34,36,37 The most common sites, in decreasing
order of frequency, include the crista terminalis, tricuspid annulus, pulmonary veins, perinodal
region, CS os, mitral annulus, and then left or right atrial appendage (Figure 17-10). The P-wave
morphology allows a preoperative prediction of the AT focus location (Figure 17-11) provided
Anatomic dil!ribution of mi11111 and tl'i~icl annullll' atrial tachycatcliu
Tl'i~icl annul~ (22%) Mttra1 annu (4%)
LorRM!)tal (4%)
Panel.A Panel B
FIGURE 17-10 • Atr11I tachycardl1 fad distribution. Plnel A shows 1he right and left atria viewed from anterlorfy w11h the ven-
tricles and AV an null cut away. Common AT focus sites are the crfslll tennlnalls, pulmonary veins, trlcuspld annulus, and perlnodal
region. PaMI B shows 1he relatlve dlsttlbution of AT f'ocl 1hat OCOJr along 1he AVannun.:i. (Reproduced with pennlsslon from Lee G,
Sanders P, Kalman JM. artheter ablation of atria Iarrhythmias: state of the art. The Lanret. 2012;380:1509-1S19.)
V1 neg posllieg neg/pos iso pos

180/pos
V2-4
pos
lG l l aVL
R.Septum
Perlnodal
l
bifid in II
&/orV1
7 ~o "i ~ yes/ ~o
0 neg in all
inf.leads I SMA I I r:os I neg in all
inf.leads
sinus rhythm
Pwave
yes/ \ no ~1 l no posl "\'-

~ 1~1 ~U[J~ LAA RPV
I RPV I
FIGURE 17-11 • Algorithm for ECG id1ntlfic:ation of dlff'tlrll"lt 1tr11I t1chyc:ardl1 foci. P-wave algor11hm for ldentfficatlon of atrial
tachycardia focus locatlon. Owing to lndl\tldual anatomy and other facto!S:r variations oc:cur so these algorlthms are a starting point;
intracardiac mapping is the gold standard." (Modified with permission from Kistler PM, et al. P.w.we morphology in focal atTial
tachycardia: development of an algorithm to predict the anatomic site of origin.J Am Coll C4rdiol. 2006;48:1010-1017. Copyright c
American College of Clrdfology Foundation.)
25
QRS
FIGURE 17-12 • Mapping olatrial tachycaAiia. When the p wave is obscured bythe Twave (or QRS), the morphology {Figure 17-11)
cannot be easily assessed. Single, or In this case dual, premature ventrk:ular stimulation during AT allows separation of the Pwave
from the Twave In order to examine the morphology and evaluate the timing of lntracardlac electro grams with respect to the
onset of the p wave. Care must be taken to ensure the AT has not terminated.
it is not buried in the T-wave (or QRS).38.39 Premature ventricular stimulation during AT allows
separation of the P-wave from the T-wave (Figure 17-12). A positive p-wave (or negative/
positive) in Vl suggests a left atrial origin and a negative one (or positive/negative) a right atrial
origin. lsoelectric p-waves in Vl component are seen with perinodal or septa! tachycardias.
Although pace mapping has been reported,40 AT ablation generally requires inducibility and
activation mapping (Table 17-1 ). If the arrhythmia fails to occur spontaneously. burst pacing.
programmed stimulation, and graded doses of isoproterenol should be tried. Reducing seda-
tion may facilitate AT induction too. A nonsustained AT can usually be mapped with cur-
rent electroanatomic mapping systems. Besides activation and pace mapping. atrial overdrive
pacing can be used to localize the site of origin of AT.41 Although nonreentrant arrhythmias
(predominantly triggered and other automatic ones) do not exhibit resetting with fusion they
can nevertheless be reset. and this aspect can be utilized to localize them similar to post-pacing
intervals after entrainment.
Crista terminalis ATs are notable for: (1) originating near the sinus node, (2) double potentials
in the area due to the anatomy, and (3) the need to exclude phrenic nerve overlying the site by
high output pacing prior to ablation. An exemplary case is shown in Figure 17-13. It is critical
to recall the anatomic relationships because an AT from the right superior PV may mimic an
SVC region one.
AT from the PVs often arise from the ostium. and can be ablated focally; more distal sources
should be ablated with circumferential ablation to avoid PV stenosis. Interestingly in a series of
28 such patients, all but I had only 1 focus and no patients developed atrial fibrillation in 6-year
follow-up.42 A more recent, larger series confirmed the lack of progression to atrial fibrillation
and used both cryoballoon and RF circumferential ablation as well as focal ablation sue<:ess-
fully.~ Some unusual, autonomic nervous system-related, usually nonsustained, atrial tachycar-
dias, associated with respiration and deglutition, have been predominantly localized to the right
pulmonary veins. In contrast to multifocal atrial tachycardia, rare patients have 2-3 foci of AT
and may have good outcome with a modest chance ofsubsequently develop.Ing additional fod"
H ssms
H 98ms
CS9J1nt-~---1v--~~~~.,...,...~~~~-"'~~~~__.,--~~~~~ ..,..~~~~_,.~~~~~
CS7~ 1-./'-~~· ~~~-.J.__~11 r--~--...r--~~L~~~....r-~.-......~~-...J.__~1~~---.r-~~~~-r-1
Panel A
FIGURE 17·13 • Crista terminalis atriilll tach)'cardiill. P.lnel A shows the ablation siteelectrogram onset to pwave of 58 ms and
ablatlon site elec:trogram to cs-os electtogram of 98 ms. The CS A Is used as the reference for Umlng In P.lnel B. Panel Bshows the
activation map with earliest site In ted compared to the CS electn>gram reference; ablatlon sites are ted, successful site blue; phrenlc
stlmulatton sites orange (postedor to ablation site) and His sites omngr at TA. Plnel Cshows ablation onset and termination of the
tllchycardla In -25 sec. Ablation more posterlorly (at sites with phrenlc stimulation) would pose a risk of diaphragmatic paralysis.
When geneJal anesthesia Is wed, one needs to reverse or wait for offset of paralytlc agents.
PanalB
H60m•
H 1ooms
---
PanalC

Perinodal ATs are characterized by narrow p-waves with the His A appearing earliest (at least
until detailed mapping of the LA or aortic cusps is performed). These ATs have been challenging
due to the risk of damaging the AV node. The p-waves typically exhibit a negative direction infe-
riorly, but various reports show considerable variability. They can be mapped from the right and
left atrial septum, but recent reports suggest the noncoronary cusp (NCC) as the preferential site
often with earlier activation times (25-50 ms before the p-wave), absence of a His potential at the
earliest site, lack ofjunctional ectopy during ablation, and a lower risk ofAV block..s-t7 The NCC
lies slightly superior and posterior to the His bundle anatomically. If the NCC is not successful,
within or below the LCC, or aortomitral continuity should be considered. One should be atten-
tive, however, to the possible risks of aortic valve injury, coronary artery injury if manipulating
in the left or right cusp, as well as atheroembolism from the aortic root.
The coronary sinus is a relatively uncommon location for focal AT. The tachycardia p-wave is
inverted in the inferior leads with Vl varying by location within the CS, being negative for ATs
originating from near the ostium and positive for more left-sided sources deeper into the CS.
For those foci near the ostium, the superior and posterior aspects are favored. Foci within the
CS may lie 2-4 cm deep, exhibiting a diffuse endocardial breakout near the posterior mitral
annulus (slightly later than the CS itself). Of note, AVRT with retrograde conduction earliest
in the CS can mimic an AT and maneuvers need to be performed to differentiate this from AT.
ATs from the atrial appendages are relatively rare (1 %-5% of ATs) and have been reported to
often require surgery for cure. The RAA is involved somewhat more often than the left. In a
large recent series, thoracoscopic surgery was required in nearly 30% of 42 patients, was suc-
cessful in all, and needed only when the focus was in the distal appendage. A percutaneous
epicardial approach has also been reported. The trabeculated nature and markedly thin walls
in spots makes mapping and ablation challenging and associated with a risk of perforation.
Angiography has been used to help understand the source and guide mapping.~ In another
case series, RAA ATs made up 3% of all ATs, were often incessant, and most localized to the
inferolateral base of the appendage. 49 Another report found 3% of ATs mapped to the LAA,
equally distributed to base, mid, and apex, and these were amenable to ablation.50 Yamada et al
found a predilection for the LAA base, more often on the medial side.51
ABLATION OF CAVOTRICUSPID ISTHMUS-DEPENDENT ATRIAL FLUTTER

Typical atrial flutter is a macroreentrant rhythm circulating in a counterclockwise direction
around the tricuspid valve including through the cavotricuspid isthmus (CTI), defined as the
region from the eustachian ridge to the tricuspid valve annulus (Figure 6-11). The clockwise
variety is also CTI-dependent (Table 17-2).52 Its ablation started with surgical approach,53
evolved to direct current ablation," and then to RF ablation (Figures 17-14 through 17-16 and
Table 17-1) owing to lower complication rates.55 Initially, success was gauged by noninducibility
but recurrence rates exceeded 20% until confirmation ofbidirectional block with pacing became
the endpoint.56.s7 Various criteria for identification of block have been proposed, including both
the presence of double potentials along the entire CTI ablation line and a timing differential
between the 2 double potentials of at least 90 ms with proximal CS pacing (Figure 17-16).53 The
goal is to confirm lack of conduction through the ablation line with activation on the distal side
progressing toward the line (rather than away from it) using differential atrial pacing maneuvers
and/or recording from several points opposite the pacing location (Figure 17-16).
PanalA
FIGURE 17-14 • ActMltlon mapping and 411'ltralnmt!l'lt ofcavotrlcuspld lsthmus-d1penclent atrial flutter. Panel Ashows an
electroanBtomlc activation map of countefclockwlse atrial flutter. The activation proceeds from red (lateral TA) toward the en, then
up septum to purple adjacent to red area on map. Note that the early meets late (red/purple) is arbittary and depends on the refer-
ence and the window chosen. The cycle lengtti of the fluttef' is accounted f'or in the chamber mapped, as expected f'or a macroreen-
ay arrhythmia (upper right). Panel Bshows entrainment from a different patient,, also wfth courrterclockwlse atria! flutter. Note the
high to low O.e. proximal to dlstal) activation on the lateral RA (crim arthet@r). The tachyardla CL (TCL) Is about 238 ms. Pacing
the proximal CS has a retum or post-padng Interval {PPI) of 266 ms, within 30 ms of the KL and conslrtent but borderline for being
within the cl!t:Ult. In Panel C, similar entrainment from the late1al RA (alsta 1-2) has a PPI equal to KL In Plln1I D, however, pacing
the distal CS produced a much longer PPI demonstrating that it was out of the circuit. Panel Eshows AFL termination during abla-
tion; note it terminates aftet' activating the lateral wall but before activating the CS consistent with termination in the en.
16 17
aVF
V1 1-----...____....._
V6t----------'
Crista 9-0,___ ___,,,___ _ _ , ""_ ____, ------~ ' -----r------.r-----J'---~.r---
Crista 7-S,___ _.,.____ _ _...,.,,..___ _ __ _ __..,,,__ _ __ __ ______ __ __ _......,.__
Crista H 1 - - -- 111'-- ---..i1' - - ------1
Crista 3-41--- -,r ' - -- ---.r'--- -""•'--- -----11 '--- --.11 '-"-- -..,1 '-"-- -••'--- ----"'\
Crista 1-21'--4----'11'----111'---_.,,,. ,'-..-------'l1'------'1t'-----111''--- - - '11''--- - - 't 1!'--
I· 2aa ms ·I I· 238ms
Retum R1
CS9_0
CS7_8 i--.r"---~~-~__,r----A"'"--~--r------¥"------'
CS5_61-1'11...__ _-n..__--...__..,r---n'~~-1~'-----11'-"~--~~-----u---~
CS3_4 ........,.,1"------M.f'.--A..--~r'----M~-"'---_,~1'----___.,,~---·r------.1'-----
cs1_21-+-v-------+-,,.....,v-_ _,_,.r----1-V"'--' \,--- - - 1 - v - . . - - - - - , J V - ---v...___ _--11,_ _ __
PanelB
22 23
aVF
V1
V6
Crista 9--0
Crista 7-8
Crista5-6
...
N
"'
CS9_0 \\ #- .f,
CS7_8
CS5_6
CS3_4
CS1.....2
PanelC
FIGURE 17-14 • (Conttnued)
I I I I I I • I • I I I I I I I I I I I I I I I I I I I I
31 32
Crista 9-0r-------,. I --------..1·~----- I -------..! '------.. ~----.f'----
Crista 7~ ~--___,1--_ _ _...,.__ _ ~--v---~-1---~-~,.-..,_---_,,_--~
336 ms
~1
PanelD
I I I I ' l I r I r I I I I I I I I I I I I I I I I r r I I I
49 50
Panel E
Par.IA
ParwlB
FIGURE 17-15 • Atrial flutter 1bi.tfon.The ablatlon In this patient Is guided by lntracardlac edtocardfography and electroana-
tomlc mapping. Lower left shows lead V1 displaying sinus rhythm, small Aand large Vslgnal on mapping catheter positioned near
the tricuspid annulus (TA) aspect of the cavolTicuspid isthmus (CTI). Upper left and upper right panels show electroanatomic map
images in RAO and LAO caudal respectively of ablation catheter coming from the IVC with tip near TA side ofen. Note the shaft
and tip of the ultrasound catheter In the RAO view In mid right atrium. The contact fo~e Is measuring 14 grams and Impedance 92
ohms as shown. The orangtt dots show sites where His .signals wen! recorded. The green /Ina are ultrasound contours drawn of the
en. Lower right shows ulttasound Image of ablation catheter tip nearTA side ofCTI (with gtHn dot mamr). Panel Bshows ablatlon
In the mid-Isthmus In small pouch or anatomic depression, with the same layout as In Panel A. In addition, red dots show prior abla-
tion lesions from TA back toWclrd the location for Panel 8. Panel Cshows ablation at eustachian ridge junction of CTI, again with
the same format ;is in P8nel5 A-8. In lower right pane~ the eustachian ridge is at the upper edge of the ultrasound image going
upward and to the right; see the green ultrasound contour in RAO view too. The electrogram shows only an atTial signal.
428
Panel C
Larger tip (especially 8 mm) and irrigated catheters have facilitated more efficient and successful
creation of CTI block. Utilizing such catheters renders CTI ablation successful in 95% of cases
with a recurrence rate of 3%-5%.59AO Overall complication rates are 2%-3%, including vascular
0.4%, AV block 0.2%, pericardial effusion 0.3%, and stroke 0.05%. One dataset had no procedural
deaths but anothe.r found a 0.08% in-hospital death rate. Complications we.re much higher in
patients ove.r 80 years of age as well as in low-volwne labs.57.s9.61 Very rarely the distal right coro-
nary artery or posterolateral branch can be injured or even occluded needing acute intervention.61
Challenges to successful atrial flutter ablation include an incorrect diagnosis, arrhythmia tran-
sition or double loop reentry,6' anatomical complexity; catheter instability, and confirmation
of endpoint. The relevant anatomy has been studied pathologically; angiographically; by 3-D
imaging, and by intracardiac ecb.o.64 A:ngiographic anatomical. variation is immense and con-
tributes to ablation difficulty.64 en length varies from 17 to 54 mm, and angulation with respect
to the IVC ranges from 68 to 114 degrees. Other anatomic distinctions include the following:
presence of a eustachian valve (25% of patients), a depression or pouch on the atrial side of
the eustachian ridge up to 4 mm in depth (50%), and a concave versus convex shape. It may
be preferable to ablate in the mid isthmus (about 6 o'clock in the LAO view) because thicker
tissue is common more laterally and a deeper pouch more likely encountered medially.65 A
small randomized study found a higher success rate with the posterior versus septal approach;
furthermore, AV block occurred in 1 patient treated with the septal approach.66
A meta-analysis examining atrial fibrillation occurrence at 1.5 years after CTI ablation found
about 25% occurrence of atrial fibrillation in patients without prior documentation ofit, versus
over 50% in those with atrial fibrillation noted before the CTI ablatl.on.57 Patient characterlstl.cs,
including younger age, left (and right) atrial size, and indudbility ofatrial fibrillation, can pre-
dict development of atrial fibrillation after CTP7
To minimize stroke. therapeutic anticoagulation should be confirmed for about a month before abla-
tion, or, alternatively a transesophageal echocardiography (TEE) can be performed. Uninterrupted
anticoagulation is commonly used in the periprocedural period. Post ablation, anticoagulation
should be continued for at least a month. (See Chapter 9 for long-tum anticoagulation guidelines.)
Ifthe patient presents in atrial flutter, entrainment and activation mapping (Figure 17-14) should
be done to confum the diagnosis. Ifthe patient is in sinus, but has had confirmed typical flutter by
Panel A
FIGURE 17-16 • O.monstmlon ofbkflrectlonal C11 block. Pln1I Ashows pacing from proxlmal CS and recording from map
catheter sllghtly lateral to tfle CTI ablation llne at 7:00 (referenced to tfle LAO view); the stimulus to A Is 162 ms. The Impulse needs
to travel around the TA counterdockwise to reach the CS. When the catheter was placed more laterally (further from the pacing
site) the stlmulus to Awas shorter demon mating that conduction was blocking at the en. Panel Bshows pacing frcm tfle abla-
tion catheter just lateral to the en ablation line, as It was positioned for Panel A. Recording from tfle proximal CS the st1mulus to
AIs 172 ms. In this situation, the Impulse needs to travel around the TA clodcwls• to reach the CS (l.e~ to reach the septal side of
the CTI ablation llne). Pan1I C shows activation timing measured during pacing from tfle proxlmal CS electrode, just as In Pln1I A.
The activation times from stimulus at CS proximal to -8:00TA are 140 ms (see activation time legend upper right of eltfler panel).
Activation immediately lateral to ablation line (fed dots} in purple region is 172 ms. Activ.ttion is counterclockwise toward the line
Indicating complete block In the clockwlse direction. In Panel D (same patient as Figure 17-148-D) the pacing maneuver demon-
strated In Panel A Is shown wtth a clsta catheter In place. With pacing from the proximal CS, thefe Is high to low activation seen
on tfle crista catheter.The map catheter, situated just lateral to the en ablation llne, activates next with a long stlmulus to A. This Is
supportive of an absence of conduction across the llne, with only counterdockwise propagation. Nate tfle wldely spaced double
patentlals (142 ms} on the map catfleter {from activation on eltfler side of the llne}.
7 o'clock TA to CS
172ma
PanelB
PanalC
FIGURE17-16 • (Continued)
I I I I I
I I'+
aVF .-----r-v
V1 -
IV
V6 - ~
(\
Crista 9-0
Crista 7-8
Crista 5-6
Crista 3-4
•1 ~
"
Crista 1-2
'
Map 3_4
I I~
.
I
Map 1_2 ~\ ""-

Jvv ·- - ·-
J42 ms_
~ -
CS9_0
I
CS7_8
... .
CS 5_6 .I
CS 3_4
r
CS 1_2
l -
PanelD
FIGURE 17·16 • (Continued)
ECG, proceeding straight to CTI ablation is reasonable, because induction often produces atrial
fibrillation inswad, or perhaps a nonclinical flutter. However, ifprior ECGs are not diagnostic. or
ifthe patient has had prior surgery or ablation. the.n induction and mapping are warranted
Many operators use an irrigated, force-sensing. RF catheter and deliver 30-35 Win power-control
mode with 5-20 grams of force for 20-30 seconds seeking to achieve a 10 ohm impedance drop.
Others choose a nonirrigated 8 mm tip catheter with a 40-50 W energy setting. The catheter
can be dragged from the TA to eustachian ridge in 3-5 mm increments or discrete lesions can
be deployed. An alternative, more focal, voltage-based approach has been described too.67 To
avoid perforation or AV block, energy delivery should be halted if the impedance or tempera-
ture rises unexpectedly, or the catheter moves or drops into IVC. Reduced time, power, and/or
contact force should be used in pouches (Figure 17-lSB). An electroanatomic mapping system
increases cost, but reduces fluoroscopy time; we therefore favor it. Intracardiac echo is not used
routinely by most, but can help the operator understand the reasons for lack of success and the
anatomic characteristics such as the exact location of the tricuspid valve, the eustachian ridge
size and orientation, and presence of pouches or diverticula (Figure 17-15).
If the rhythm terminates, bidirectional block should be confirmed by both CS pacing and lat-
eral TA pacing (Figure 17-16). If the line is "completed" without achieving CTI block, the isth-
mus should be explored for promising electrograms (preferably with CS pacing. rather than in
flutter). Orientating the catheter such that it is retroflexed back toward the IVC often identi-
fies residual unablated tissue (Figure 17-lSC). If AFL persists, entrainment should be repeated
because the arrhythmia circuit might have shifted (even without a CL change).63
ABLATION OF ATRIAL FIBRILLATION

Ablation of atrial fibrillation (AF) primarily relies on isolation of the pulmonary veins
(Figure 17-17, Table 17-1, Table 17-3), stemming from recognition of their triggering role
in the arrhythmia.68.69 (See Chapter 9 for background.) Other targets are pursued less fre-
quently and/or have a less solid evidence base. It should be appreciated that AF ablation
bears dissimilarities to the other supraventricular targets discussed so far. AVRT, AVNRT,
focal AT, and atrial flutter have well-defined, either focal sources or consistent circuits
with stable beat-to-beat activation whereas atrial fibrillation is a polymorphic arrhythmia.
Although gaps in our understanding of the former arrhythmias exist, especially for AVNRT,
AF remains more poorly understood. Moreover, for AVRT, AVNRT, and atrial flutter, the
ablation target is the circuit maintaining the arrhythmia, not the trigger, whereas for AF
trigger ablation occurs foremost.
Seeking to reduce complications and improve efficacy, pulmonary vein isolation (PVI) evolved
from focal ablation inside the PVs to segmental ostial isolation, and then to the current stan-
dard of wide, circumferential ablation to achieve PVI. Efforts to further improve the success
rate for AF ablation have included 2 major thrusts: ( l) creating more durable and permanent
pulmonary vein isolation; and (2) identifying and treating sources of or substrates for perpetu-
ation of AF beyond the pulmonary venous antra.
The methodology for PVI is detailed below. Figure 17-17 shows a CT scan of the left atrium
and pulmonary veins, and thereafter, a 3-dimensional mapping representation of the LA and
pulmonary veins with the superimposed RF ablation lesion set. The lesions circle the left and
right vein pairs. Figure 17-ISA shows ongoing ablation at the time entrance block into the
right inferior PV occurs owing to completion of the lesion set around the veins (similar to
Figure 17-17B). Note the delay in the PV potentials on the second and especially third beats
before entrance block develops. Other recordings immediately afterward showed entrance
block into the right superior PV as well, and exit block from both right PVs. Figure 17-ISB
illustrates why PVI may be successful in preventing AF. After PVI (shown for this patient in
PllnelA
PanalB
FIGURE 17·17 • Anatomic ref)resentatlon of wtde clrcumfererrtial pulmonary vein lsolltlon for ablatfon of atrial flbrtllltfon.
Panel A shows a CT anglogram In PA view showing LAA (upper left), LSPV, LIP\/, RSPV, and RIPV. Panel B shows electroanatomlc
map of same patient after completing PV lsolatlon; dte leslon set Is shown. Voltages below 0.1 mv are red, above 05 mv purplt.
Wittlin the PVs 0.e~ the red area), detASlled mapping demonstrated dtat In fact no signals were detectable, due to absence of con-
duction into PVs [l.e~ entrance block). Pacing within the PVs also demon mated exit block (not shown). The patient's ejection frac-
tion improved from 25% to 55%.
Figure l 7-18A), isoproterenol was administered in an effort to identify other possible AF trig-
gers. None was found, but the drug helped provoke right PV ectopy and a run of an AF-like
arrhythmia confined to the right PVs (Figure 17-18B). Note entrance block on the first beat
(no signal on circular 20-pole catheter in vein) and toward the end when the firing ceases (as in
Figure 17-lSA); exit block is demonstrated during the firing because sinus tachycardia (from
the isoproterenol) continues unperturbed. In terms of recurrences after initially successful PVI,
SVC foci HRA before His A or CS A; upright P wave Isolate SVC (Figure 17-21 ); avoid phrenic nerve
inferiorly, Vl positive-negative or negative. injury.
Crista terminalis foci Similar to SVC; see Figure 17-13. Map and ablate focus; avoid phrenic nerve injury.
Coronary sinus foci Negative p waves inferiorly. Ablate focus; isolate CS but could create substrate
for reentry.
Posterior wall Posterior LA early activation, after PVs Isolate posterior wall or ablate focus.
isolated.
Atrial septal foci His A, Cs proximal and CS distal similar Focal ablation; avoid AV node injury.
timing. From RA or LA side.
LA appendage May originate near ostium or deep in LAA. Isolate LAA. Safety related to thromboembolism
risk Increase Is unclear.
Rotors LA or RA; may be stable or migratory. Phase or other mapping; focal or regfonal ablation.
Complex fractionated atrial Rapid or highly fractionated and/or nearly Ablation has not been proven to be beneficial.
electrograms continuous electrograms.
Ligament of Marshall Focal activation near LSPV and LAA. Ablate LA ridge; rarely cannulate vein from CS
and ablate.
Other Adjunctive Ablatlon Lesion Sets
Ratlonale and Characteristics
Ganglionated plexf, fncludfng Autonomic triggers of AF. Fractionated electrograms Identify by triggering vagal response to
Marshall tract GP, superior left high-frequency pacing or by highly fractionated electrograms in suspected areas. Ablation trials
GP. anterior right GP, inferior have suggested benefit, but surgical trial was negative."'
left GP. and inferior right GP
LA roof line Linear lesion between RSPV and LSPV; used to treat roof-dependent atrial flutter; may also
prevent reentry near PVs; ff Incomplete {Inltlally or after healing) may actually promote roof-
dependent AT; confirm block by pacing LAA and noting low to high activation on mid and upper
posterior wall.
Posterior wall Consider if low voltage in posterior wal I or ectopic foci from posterior wall. Roof line plus line
connecting RIPV and LIPV. Confirm entrance and exit block in region.
Mltral Isthmus line Treatment for m ltral annular flutter. Linear leslon between LIPV and posterolateral mltral annulus;
or between RSPV (or roof llne) and anterior mltral annulus. If Incomplete {lnftlally or after heal Ing)
may actually promote mitral annular flutter. Confirm bidirectional block by pacing on either side.
Low-voltage zone Electrograms identifying presumed scar by low voltage (or MRI showing delayed hyperenhance-
isolation ment); ablation lesions deployed to encircle the abnormal tissue.......
one could imagine if (exit) conduction resumed and thereafter PVs fired again. This concept
highlights the critical (if challenging) goal of durable PVI.
Correct identification of electrograms and their sources is vital to accomplish successful PVI
and to minimize complications. Catheters in the PVs can record local (near-field) PV potentials
from the musculature extending into the PVs but additionally they may record far-field signals.
Predominant far-field sources include: (1) the left atrial appendage (LAA) (for LSPV and less
prominently the LIPV) and (2) the superior vena cava (SVC} and/or right atrium (RA) with
regard to the RSPV. The timing for SVC or RA far9field signals for the RSPV is characteristi-
cally within the first 30-40 ms of the p-wave. Conversely, local RSPV potentials occur later.70
Figure 17-19A showstheinitiallyfusedfar-fieldandnear-field PV potentials (arrows) separating
1•1• 1•1• 1• 1 • 1• 1 ·1·1·1·1•1•1•1• 1 •1• 1 •1•1•1•1•1•1•1•1•1•1•1•1•1•1•1•1•1•1•1•1•1•1· 1·1·1•1• 1•1•1•1•1 •1•1• 1 •1 •1 •1•1•1•

u ~ ~ ~ ~ ~
20POLE817t--t-~~~~~~--1t--~~~~~~~-i'--~~~~~~~~~~~~~~~~
20POl.£B1 &l--+~~~~~~--l,._~~~~~~~--+~~~~~~~~~~~~~~~~~
20POLEB1 3l--~~~~~~~--i~~~~~~~~--.~~~~~~~~~----~~~~~~~-
20PQ..EB 1
211POl..EB~~...,...,.~~---~---~~~~~~.-..._~--..~~~_,,.-...--~~~~~~~~~~~~~-
20POl..EB711--+-~~--_,._--~-{.~~~~--~~~-+-...._,-----~~~~-...~~~~~~~~
20POl..EB~~--.11--~~~~~~1._~~~~~~~~4,-~~~~~~~~~~~~~~~~-
20POLEBW~---''--.-..~~~~~.._~~~~~~~~~~~~~~~~~~~~~~--~~-
20POLEB17 1--~--~~~----~~~~--~.---....~~------.....~~-....-.-.~.-...~~~~~~~~
20POlEB15 1--~~~~~~~~~~~~~~~~~~~~~~~~~~--~..-.~~~~~
20POl..EB13 1--~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
20POLEBt1 1--~~~-.r~.....__,__._~~__.,......._...._...,_.._....._,.._...__.,._.,._..._,_..,.._~..._....._.._...~~~~~--1,___._
20POLEBfllr - - - - - + - + -.,n...,·- t-fl1----ti'I' I I 1'

20POLEB7/ ~r T ..
20POLEB~ t--~~~~~~~~~~~~~~~_,.~~~-.-~~~~~~~~~~~~~~
20POLEB~ ..-~~~~~~~~~~~~~~~~~~~_,,..~~~~~~~--~~~~._..-~
20POLEBd t---....--~"-'"~.-....-----.....~~._,..~.-.....--__...._~~~-------~--_,...~----...,,..._,,.'-~,,....._.__,-...~
FIGURE 17·11 • Pulmonaryvefn liolltlon. Panel A shows ablation posterior to the RIPV completing the lesion set encircling the
RSPV and RIP\/ with isolation of both veins Oast 2 beats). Panel 8, after P\11, shows a vay rapid, irregular PV tac:hycardia (about 152 ms)
confined to the RSPV. See text for details.
CHAPTER 17 • Catheter Ablation of Supraventrlcular Tachycardias 437
, ..···· ___......... ............ x

2DPOLEB201r-~~~~---~~~~~~~--t~.....--.-r-~.....-~~~~-.-~~~~~~~~----'
20PCLEB191t--~r-~~..,._~~~~~~~--j'--~~~~~~~~~---~~~~~~~~----'
ll!OPOL.EB191r-~r-~~-r-~~~~~~~---1v--~~~~~~~~.,._~~~~~~--t-~~------,
20PCLEB14.t--~r-~~-r--~~~~~~~~-1-~~~~~~~~.,._~~~~~~-i-~~---,
20POLEB1,2-~-u--~~~~~~~~~~~+-1,--~~~~~~~-11---<'--~~~~--,~~~-'
20POl..EB101 t--~t-~~*"-~~~~~~~--1,..+~~~~~~~~-;--i-~~~~~--+~~----'
20POl..EBS-
20POl..EBS- t--~~~~~~~~~~~~--t~--._._...._~~~~~~-+~~~~~~~~------:
20POLEB~ i--~~~~--~~~~~~~--.~~~~~~~~~~_,..~~~~~~~~------:
PanelA
.....
.. v
I
I I . ... .
\
I •
19
I
~
I I I
/\
I I
~
I I I • I
20
I I • J I
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I I I
•
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ve -
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I
_,
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M11p 112 v
'
f'ltni.17- 18
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l'lani.1&-18
l'lanta 13-14
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FIGURE 17-11 • Nur.fleld vs far-field potll!ntfals In left superior PY. See text for details.
during ablation around the LSPV; on the last beat, immediately after achieving entrance block,
only the far-field potential from the LAA remained. Pacing maneuvers can help differentiate
these near-field vs far-field electrograms. Figure 17-19B shows LAA pacing via the 20-pole
catheter ("Penta"). The signal recorded from a map catheter in the LSPV was diagnosed as far-
field because its timing coincided with the stimulus similar to those seen on the LAA catheter.
On the other hand, PV potentials would occur 100 or more ms after the stimulus. With respect
to distinguishing RSPV near-field PV potentials from SVC ones, the SVC/RA junction could
be paced. Far-field potentials will be seen immediately after the stimulus, but RSPV local sig-
nals will be delayed. If conduction into and out of the PVs persists despite completion of the
encircling lesion set, various mapping approaches may identify the gap. 71
Randomized trials of PVI in patients with paroxysmal AF, employing either RF or cryoablation,
have demonstrated freedom from AF recurrence of 60%-80% at I-year, with results signifi-
cantly better than found with antiarrhythmic drug treatment (Figure 17-20). Quality of life
outcomes have been superior for ablation too. AF recurrences continue to accrue after 1 year,
however, owing to previously unrecognized PV conduction recovery, other triggers, and/or
evolving substrate in the LA and/or RA.
Recent and ongoing efforts to improve RF-based PVI and its durability have been extensive and
multipronged. These have included: (1) a waiting phase (since PV to LA conduction sometimes
RF AAD CAYO AAD
I Thermocool AF I STOPAF
FIG URE 17-:ZO • Results of atrial fibrillation ablation in select. pivotal, randomized, clinical trials. The y-axis is freedom from
any recurrent AF, atrial flutter or tachycardia after a 3-month blanking period. The freedom from atrial arrhythmia recurrence for
the randomized RF ablation arm (66%) versus the antlarrhythmlc drug treatment arm (16%) Is dlsplayed on the left.91 On the rig nt,
freedom from atriaI arrhythmia recurrence for the randomized cryoballoon ablation arm (69.9%) versus the antlarrhyth mlc drug
treatment arm (7.3%) is shown.74
B c .
- .... - " ~ -- ..( .,_ -

,;,,,..,.....,.,.,.,..,_....,.~\_,,~· .,,._,.)-.,•\ ......
_ _..__,_,_~--~-~---_...,....,....~~--
- ,y)\i~/r.tt""""i°JW.~',,... 'l<T:r·~(l'f'rrnktf'I
- .,,....: .i.,.r.._?·""""-..,...,..,,....,,tt•""._,...,.,:,.fY; \:1• !"""-~""""'
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D• '----• ·-- E -
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FIGURE 17-21 • AVjunction 1bl11fon. A pattent with refractory, permanent AF, suboptimal rate control, LBBB and an EF of 40%
underwent a blventricular pacemaker Implantation. Several weeks later we performed an AVJ ablatfon after suboptlmal blventrfcular
pacing percentage was confirmed. The AVJ ablation was perfonned as a staged procedure to ensure stablllty of both leads and acute
healing of the pocket. Panel Ashow5 the His recording in AF; the HV is 64 msec; note the LBBB. Panel 8 is the electrogram recorded
just prior to ablation. Note that the atrial signals are much larger than seen in Panel A. and a His potential is not apparent The cath-
eter had been deffected lnfeflorly and withdrawn~ from the trlc:uspld annulus sllghtly (I.e., ~ay from the His bundle toward
the compact AV node). Ablatlng at a large His potential and small atria! potential (e.g~ Panel A) frequently causes RBBB Instead of
complete AV block. Panel C Is recorded during onset of block with one paced beat then Junctlonal beats. Plnll Ddisplays Junctlonal
rhythm at about 45 bpm {-1300 msec) about 30 minutes afmf ablation. Panel E presents the 12-lead during blventTlcular paced
rhythm. Panel F (a different patient) shows the His bundle recording sites in orange and ablation site IO'Wet' (blue dot); a His potential
was still noted at the ablation site, albeit smaller in amplitude than that recorded more superiorfy. (An electroanatcmic mapping sys-
tem Is Infrequently used for AVJ ablaUon but provides a good demonstration In this use.)
resumes minutes after PVI is first achieved); (2) use ofadenosine to demonstrate latent PV recon-
nection by virtue ofits ability to transiently repolarlze injured and partially depolarized tissue; (3)
assiduously seeking to achieve a 10 ohm or greater impedance drop with each lesion; (4) careful
titration and localization of individual RF lesions using more advanced lesion tagging based on
stability. contact force. energy, and time; (5) composite scores logging these same factors to pre-
dict an adequate lesion; and (6) exploring higher energy. shorter duration lesion delivery modes.
Cryoablation
AF cryoablation employs a 28 mm (rarely the smaller. 23 mm) cryoballoon to deliver cryoenergy
at each PV ostium. Only a single fJ:ansseptal sheath is needed but it is larger (12F ID) than
that used for RF (8.5F ID). Catheter positioning uses fluoroscopic guidance, and usually not a
3-dimensional mapping system. Before ablating, contrast is injected tluough the lumen to con-
firm a seal; otherwise, energy 1ransfer is often insufficient and ablation ineffective. Alternative
methods for confirming occlusion of the vein before freezing include noting a pressure wave-
form change distal to the balloon from LA to PA, or color flow intracardiac ICE. One or more
3- to 4-minute lesions are delivered for each vein. Isolation can be monitored real time (similar
to RF) by advancing a small multipolar catheter into the PY via the catheter lumen. Work to
optimize the duration and number of lesions, possibly depending upon how quickly isolation
occurs during the initial freeze, is ongoing. In parallel with improvements in RF ablation, bal-
loon cryoablation has benefited by improved technology allowing quicker, more reliable, and
possibly wider PYI to be achieved. A large randomized trial demonstrated equivalent results
for RF and cryoballoon.n
Persistent Atrial Fibrillation, Nonpulmonary Vein Foci and Adjunctive Ablation

It has been appreciated that the ablation success rate is lower for nonparoxysmal AF, including
persistent and especially for long-standing persistent AF. The higher recurrence rate has been
attributed partly to a greater prevalence of non-PY triggers or substrate (Table 17-3). This con-
tention has been difficult to prove, however, since durable PVI has been elusive. An important
randomized 3-arm trial compared PYI alone to PYI plus complex fractionated atrial electro-
grams and to PYI plus linear LA lesions. Neither adjunctive approach was better than PYI alone.
Nevertheless, non-PY foci certainly exist. Indeed, repetitive ectopic firing or actual AF trigger-
ing can sometimes be demonstrated, either spontaneously or during isoproterenol infusion.
In such cases, the ectopic heat's p-wave morphology (Figure 17-11) and activation mapping
guide ablation. Nevertheless, the intermittent nature undoubtedly makes definitive mapping
challenging. More often, however, these adjunctive sites are empirically ablated. Table 17-3 lists
the potential targets.
Currently cryoballoon ablation is approved only for paroxysmal atrial fibrillation in view of it
being designed for PVI alone. However, in light of trial results supporting PYI alone as a rea-
sonable strategy in persistent AF, it is sound to consider cryoballoon ablation for such patients.73
AF Ablation and Impact on Mortality and Other Outcomes

Early AF ablation studies focused on elimination of the arrhythmia and resultant impact
on quality oflife as noted above. Most enrolled a relatively youthful population.74•91 Subse-
quent studies suggest that select AF patients with reduced EF and heart failure may have
a reduction in hospitalization and mortality with ablation. 75 AF patients with a low EF but
not LY scar by MRI may be especially likely to respond with an improvement in EF. 76 The
recently completed CABANA trial (The Catheter Ablation vs Antiarrhythmic Drug Ther-
apy for Atrial Fibrillation Trial) is by far the largest AF ablation trial. It enrolled a higher
risk, older AF population; most had a preserved EF. By intention to treat analysis, the pri-
mary endpoint (total mortality, disabling stroke, serious bleeding, or cardiac arrest) was
not reached (HR = 0.86 [95% Cl, 0.65-1.15]; p=0.30). However, 10% of those assigned abla-
tion never underwent the procedure (patient or physician refusal). Analysis by treatment
received demonstrated a significant 33% reduction in the primary endpoint along with a
significant 40% reduction in total mortality. 77
Complications
Complication rates are higher for AF than other SYT ablations, in part due to more extensive
catheter manipulation and/or more widespread ablation energy delivery. Superimposed on AF
patients' preexisting thromboembolism risk are those of prolonged LA catheter dwell time,
sheath or catheter exchanges, the thrombotic potential of extensive LA endocardial lesions

and possible cardioversion. Aggressive measures to counteract thromboembolism, by using
uninterrupted oral anticoagulation plus intraoperative heparin, pose potential for vascular and
hemorrhagic complications.
Notwithstanding the above concerns, uninterrupted anticoagulation, especially with direct oral
anticoagulants, has actually reduced both vascular and thrombotic complications. Femoral vascu-
lar complications such as pseudoaneurysm occur in under 1% of procedures in most labs. Ultra-
sound-guided puncture has gained favor and may help minimize such problems. Stroke or TIA
event rates have fallen below 0.5% for experienced operators. Careful sheath management is crit-
ical to prevent thrombus or air embolism. Notably, asymptomatic cerebral events can be detected
by MRI (several days post ablation) in approximately 5%-15% of patients. Their etiology seems
multifactorial and not just related to char or thromboembolism but also to microbubbles, sheath
exchange, and other factors either with RF or cryoablation. Follow-up studies usually demon-
strate the majority of these lesions have resolved, but the long-term implications of these MRI
lesions are unclear because they have been associated with cognitive dysfunction in other settings.
Owing to the use of 3-dimensional mapping and/or intracardiac echocardiography with RF

ablation, low (5-10 minutes) fluoroscopic exposures have become typical, and even zero or
near-zero use is possible. Whether zero fluoroscopy reduces risk for the patient, or only the
operator, remains unclear however.
Cardiac tamponade, along with stroke and atrioesophageal fistula, causes most of the rare
deaths related to AF ablation. Tamponade may stem from intracardiac catheter manipulation,
transseptal puncture, or ablation. Late tamponade could develop due to pericarditis and antico-
agulation. Accurate transseptal puncture (especially guided by intracardiac echocardiography)
and careful catheter manipulation can help avoid cardiac tamponade. Theoretically, the use of
contact force-sensing catheters may help prevent excessive force and thus avert tamponade.
Recent trials report an incidence of tamponade of 1% or less. Like many complications, these
are related to operator experience and AF ablation volume. If tamponade occurs, it must be
recognized and managed quickly to avert a fatality.
The incidence of pulmonary vein stenosis has declined, stemming from ablation further from
the PV ostium. As a consequence, and because it usually presents weeks to months after the
ablation with nonspecific symptoms (e.g., dyspnea), the diagnosis is often missed or delayed.
A recent study showed a 1% incidence of significant pulmonary vein stenosis although fewer
needed treatment. Diagnosis is best established using contrast CT or MR. Quantitative perfu-
sion scanning of the lung plays an adjunctive role. Most labs do not perform follow-up imag-
ing to screen for PV stenosis. However, we have a low threshold for repeat PV imaging in the
patient with unexplained dyspnea.
Although atrioesophageal fistula is rare (-0.1 %-0.3%), nearly 90% are fatal. A related injury,
esophageal perforation into the mediastinum or pericardium (as opposed to the LA), exhibits
a lower fatality rate. Evolving evidence points to a transmural, thermally mediated esophageal
injury for RF or cryoablation. Atrioesophageal fistula has been reported with other energy
sources, too. A mucosa! ulcer, evident in the first week post ablation, may be a precursor. 78
Gastric reflux, esophageal nerve injury, pericarditis, and/or LA wall necrosis may facilitate the
progression.79 Atrioesophageal fistula usually presents between 2 and 4 weeks after AF ablation,
but can be seen as early as 7 days and as late as 60. Premonitory symptoms {chest pain, dyspha-
gia, or odynophagia) are unfortunately nonspecific. With overt fistula development, manifes-
tations include fever, polymicrobial sepsis, 1 or more cardioembolic neurological deficits, and/
or massive hematemesis. Nevertheless, quick recognition and emergent cardiothoracic surgical
repair can be lifesaving. Contrast-enhanced CT may demonstrate air in the mediastinum, peri-
cardium, heart, or brain. However, CT may be nondiagnostic at first, and should be repeated if
suspicion persists. In the setting of a suspected atrioesophageal fistula, upper endoscopy or TEE
can result in severe complications (e.g., due to air insufflation). Surgery should not be deferred
if the diagnosis is likely. Regarding prevention, esophageal luminal temperature monitoring
is often employed, but remains unproven. Esophageal deflection or movement has recently
been invoked to reduce exposure to the thermal ablation injury, but definitive data are not yet
available. When ablating with RF on the posterior wall overlying or adjacent to the esophagus,
a reduction in power and/or time is advisable.80.&1 For cryoablation, avoiding extremely low
esophageal temperatures (possibly below 10°C) may be protective, especially while ablating the
left inferior PV, but a validated cutoff does not exist.79.&2
Transient or even permanent injury to the right phrenic nerve may occur via ablation anterior
to the RSPV or less often the RIPV. Despite improvement, the recent incidence remains higher
with cryoablation (-1 %-3%) than for RF {about 0.5%).72 With cryoablation, most injuries
resolve by 1 year. During RSPV or RIPV cryoablation, the phrenic nerve should be paced (via
the SVC) and diaphragmatic contraction scrutinized. Optimal methodology emphasizes proxi-
mal deployment ofthe balloon, especially for the RSPV, diaphragmatic compound motor action
potential monitoring, and immediate, active balloon deflation if contractile force declines. 83
Additionally, bronchial thermal injury has been reported with cryoablation. With irrigated RF,
volume overload with pulmonary edema may occur. In addition, extensive left atrial ablation
can produce a stiff LA syndrome with large v-waves in the absence of mitral regurgitation.
ABLATION OF OTHER SUPRAVENTRICULAR TARGETS

Sinus Tachycardia
Inappropriate sinus tachycardia (IST) is defined as a resting HR >100 and 24 hour average
HR >90 bpm (in adults) with symptoms of palpitations (see Chapter 6).84 Although a logical
treatment, sinus node modification unfortunately exhibits only modest success rates. More-
over, symptom relief is infrequent and complications (phrenic nerve injury, transient SVC
syndrome, and need for pacemaker) are appreciable.15-a7 Ablation therefore does not have an
evidence-based role for appropriate sinus tachycardia (Class III indication), and may be harm-
ful in the related condition postural orthostatic tachycardia syndrome (see Chapter 6).
Junctional Tachycardia
Junctional tachycardia is a rare primary arrhythmia, usually occurring in infants or children,
often after congenital heart surgery. It should be distinguished from AVNRT and especially
from a concealed, retrograde nodofascicular or nodoventricular pathway. Amiodarone has been
used and recently ivabradine has been reported. Ablation without incurring AV block is chal-
lenging but has been described by targeting the posteroseptal area, or possibly the anteroseptal
area using either RF or cryoablation.88- 90
REFERENCES
1. Huang SK. et al. Closed chest catheter desiccation of the atrioventricular junction using radiofrequency energy-a
new method of catheter ablation. J Am Coll CardioL 1987;9:349-358.
2. Reddy VY, et al. Pulsed field ablation for pulmonary vein isolation in atrial fibrillation. J Am Coll CardioL
2019;74(3).
3. Nath S, DiMarco JP, Haines DE. Basic aspects of radiofrequency catheter ablation. J Cardiovasc ElectrophysioL
1994;5:863-876.
4. Nath S, Lynch C, Whayne JG, Haines DE. Cellular electrophysiological effects ofhyperthermia on isolated guinea
pig papillary muscle. Implications for catheter ablation. Circulation. 1993;88:1826-1831.
5. Barkagan M, et al. Effect of baseline impedance on ablation lesion dimensions. Circ Arrhythm ElectrophysioL
2018;11:e006690.
6. Nakagawa H, et al. Comparison ofin vivo tissue temperature profile and lesion geometry for radiofrequency abla-
tion with a saline-irrigated electrode versus temperature control in a canine thigh muscle preparation. Circulation.
1995;91:2264-2273.
7. Demazumder D, Mirotznik MS, Schwartzman D. Biophysics of radiofrequency ablation using an irrigated
electrode. l Interv Card Electrophysiol. 2001;5:377-389.
8. Langberg JJ, Lee MA, Chin MC, Rosenqvist M. Radiofrequency catheter ablation: the effect of electrode size on
lesion volume in vivo. Pacing Clin Electrophysiol. l 990;13:1242-1248.
9. Andrade JG, Khairy P, Dubuc M. Catheter cryoablation: biology and clinical uses. Circ Arrhythm ElectrophysioL
2013;6:218-227.
10. Avitall B, Kalinski A. Cryotherapy of cardiac arrhythmia: from basic science to the bedside. Heart Rhythm.
2015;12:2195-2203.
11. Klein GJ, et al. Reaction of the myocardium to cryosurgery: electrophysiology and arrhythmogenic potential.
Circulation. 1979;59:364-372.
12. Wood MA, et al. Determinants of lesion sizes and tissue temperatures during catheter cryoablation. Pacing Clin
13. Becker AE, Anderson RH, Durrer D, Wellens HJ. The anatomical substrates of Wolff-Parkinson-White syndrome.
A clinicopathologic correlation in seven patients. Circulation. l 978;57:870-879.
14. Janse MJ, van Capelle FJ, Freud GE, Durrer D. Circus movement within the AV node as a basis for supraven-
tricular tachycardia as shown by multiple microelectrode recording in the isolated rabbit heart. Circ Res.
1971;28:403-414.
15. Mendez C, Moe GK. Demonstration of a dual A-V nodal conduction system in the isolated rabbit heart. Circ Ru.
1966;19:378-393.
16. Josephson ME, Kastor JA. Paroxysmal supraventricular tachycardia: is the atrium a necessary link? Circulation.
1976;54:430-435.
17. Tawara S. Das Reizleitungssystem des Siiugetierherzens (The conduction system ofthe mammalian heart). Verlagvon
Gustav Fischer: Jena, Germany; 1906.
18. Anderson RH, Beck.er AE, Brechenmacher C, Davies MJ, Rossi, L. The human atrioventricular junctional area: a
morphological study of the A-V node and bundle. Bur J CardioL 1975;3: 11-25.
19. Inoue S, Beck.er AE. Posterior extensions of the human compact atrioventricular node: a neglected anatomic fea-
ture of potential clinical significance. Circulation. 1998;97:188-193.
20. Katritsis DG, Beck.er A. The atrioventricular nodal reentrant tachycardia circuit: a proposal. Heart Rhythm.
2007;4: 1354-1360.
21. Stavrakis S, et al. Slow/fast atrioventricular nodal reentrant tachycardia using the inferolateral left atrial slow
pathway. Circ Arrhythm Electrophysiol. 2018;11:e006631.
22. Sung RJ, Waxman HI., Salcsena S, Juma Z. Sequence of retrograde atrial activation in patients with dual atrioven-
trlcular nodal pathways. Circulation. 1981;64:1059-1067.
23. Katritsis DG, Ellenbogen KA, Becker AE. Atrial activation during atrioventricular nodal reentrant tachycardia:
studies on retrograde fast pathway conduction. Heart Rhythm. 2006;3:993-1000.
24. Dandamudi G, et al. A novel approach to differentiating orthodromic reciprocating tachycardia from atrloventric-
ular nodal reentrant tachycardia. Heart Rhythm. 2010;7:1326-1329.
25. Lockwood D, Nakagawa H, Jackman W. In: Zipes DP, Jalife J, Stevenson W. eds. Electrophysiological characteris-
tics of atrioventricular nodal reentrant tachytardia. Cardiac Electrophysiology: From Cell to Bedside. Philadelphia,
PA: Elsevier; 2018.
26. Chua K, et al. High-resolution mapping of the triangle of Koch: spatial heterogeneity of fast pathway atrionodal
connections. Heart Rhythm. 2018;15:421-429.
27. Jackman WM, et al. Treatment of supraventricular tachycardia due to atrioventricular nodal reentry by radiofre-
quency catheter ablation of slow-pathway conduction. N Engl I Med. 1992;327:313-318.
28. Kaneko Y, et al. Atypical fast-slow atrioventricular nodal reentrant tac.hytardia incorporating a "superior" slow
pathway: a distinct supraventricular tachyarrhythmia. Circulation. 2016;133: 114-123.
29. Katritsis DG, et al. Catheter ablation of atypical atrioventricular nodal reentrant tachycardia. Circulation.
2016;134:1655-1663.
30. Chrispin J, et al. Current management and clinical outcomes for catheter ablation of atrioventricular nodal
re-entrant tachycardia. Europace. 2018;20:e51-e59.
31. Budzik.owaki AS, Tisma-Dupanovic S, Kroening D, Daubert JP. How to perform cryoablation for atrioventricular
nodal reentrant tachycardia. Cardiol]. 2007; 14:597-604.
32. Eckhardt LL, Leal M, Hollis Z, Tanega J, Alberte C. Cryoablation for AVNRT: importance of ablation endpoint
criteria. I Cardiovasc BlectrophysioL 2012;23:729-734.
33. Santangeli P, Proietti R, Di Biase L, Bai R, Natale A. Cryoablation vmus radiofrequency ablation of atrioventricu-
lar nodal reentrant tachycardia. I Interv Card E/ectrophysiol. 2014;39: 111-119.
34. Liu CF, et al. Unifying algorithm for mechanistic diagnosis of atrial tachycardia. Circ Arrhythm ElectrophysioL
2016;9.
35. Scaglione M, et al. Very long-term results of electroanatomic-guided radiofrequency ablation of atrial arrhythmias
in patients with surgically corrected atrial septa! defect. Buropace. 2014; 16: 1800-1807.
36. Ip JE, et al. Unifying mechanism of sustained idiopathic atrial and ventricular annular tachycardia. Circ Arrhythm
Electrophysiol 2014;7:436-444.
37. Yamamoto M, et al. Extended atrial conduction system characterised by the expression of the HCN4 channel and
connexin45. CardiovascRes. 2006;72:271-281.
38. Lee G, Sanders P, Kalman JM. Catheter ablation of atrial arrhythmias: state of the art. Lancet. 2012;380: 1509-1519.
39. Kistler PM, et al. P-wave morphology in focal atrial tachycardia: development of an algorithm to predict the ana-
tomic site of origin. I Am Coll CardioL 2006;48:1010-1017.
40. Hayashi K, et al. Pace mapping for the identification of focal atrial tachycardia origin: a novel technique to map
and ablate difficult-to-induce and nonsustained focal atrial tachycardia. Cin: Arrhythm BlectrophysioL 2016;9.
41. Mohamed U, et al. A novel pacing maneuver to localize focal atrial tachycardia. I Cardiovasc ElectrophysioL
2007; 18: 1-6.
42. Teh AW, et al. Long-term outcome following successful catheter ablation ofatrial tachytardia originating from the
pulmonary veins: absence of late atrial fibrillation. I Cardiovasc BlectrophysioL 2010;21:747-750.
43. Wei HQ, et al. Long-term outcome of cryoballoon ablation versus radiofrequency ablation for focal atrial tachy-
cardias originating from the pulmonary veins. I Interv Card Electrophysiol. 2019.
44. Hillock RJ, et al. Multiple focal atrial tachytardias in a healthy adult population: characterization and description
of successful radiofrequency ablation. Heart Rhythm. 2007;4:435-438.
45. Yang JD, et al. Focal atrial tachytardi1111 from the parahisian region: Strategies for mapping and catheter ablation.
Heart Rhythm. 2017;14:1344-1350.
46. Pap R, et al. Should the aortic root be the preferred route for ablation of focal atrial tachycardia around the AV
node? JACC: Clinica/BlectrophysioL 2016;2:193.
47. Wang Z, et al. Focal atrial tachytardia surrounding the anterior septum: strategy for mapping and catheter abla-
tion. Circ Arrhythm ElectrophysioL 2015;8:575-582.
48. Guo XG, et al. Management of focal atrial tachycardias originating from the atrial appendage with the combi-
nation of radiofrequency catheter ablation and minimally invasive atrial appendectomy. Heart Rhythm. 2014;
11:17-25.
49. Roberts-Thomson KC, et al. Focal atrial tachycardias a:rising from the right atrial appendage: electrocardio-
graphic and electrophysiologic characteristics and radiofrequency ablation. I Cardiovasc ElectrophysioL 2007;18:
367-372.
50. Wang YL, et al. Focal atrial tac.hyta:rdia originating from the left atrial appendage: electrocardiographic and elec-
trophysiologic characterization and long-term outcomes of radiofrequency ablation. J Cardiovasc BlectrophysioL
2007; 18:459-464.
51. Yamada T, et al. Electrophysiologic and electroca:rdiographic characteristics and radiofrequency catheter ablation
of focal atrial tachycardia originating from the left atrial appendage. Heart Rhythm. 2007;4:1284-1291.
52. Waldo AL, Feld GK. Inter-relationships of atrial fibrillation and atrial flutter mechanisms and clinical implica-
tions. J Am Coll Cardiol. 2008;51:779-786.
53. Klein GJ, Guiraudon GM, Sharma AD, Milstein S. Demonstration of macroreentry and feasibility of operative
therapy in the co=on type of atrial flutter. Am J CardioL 1986;57: 587-591.
54. Saoudi N, Mouton-Schleiffer D, Letac B. Direct catheter fulguration of atrial flutter. Lancet. 1987;2:568-569.
55. Feld GK, et al. Radiofrequency catheter ablation for the treatment of human type 1 atrial flutter. Identification of
a critical zone in the reentrant circuit by endocardial mapping techniques. Circulation. 1992;86:1233-1240.
56. Nakagawa H, et al. Role of the tricuspid annulus and the eustachian valve/ridge on atrial flutter. Relevance to
catheter ablation of the septa! isthmus and a new technique for rapid identification of ablation success. Circulation.
1996;94:407-424.
57. Perez FJ, et al. Long-term outcomes after catheter ablation of cavo-tricuspid isthmus dependent atrial flutter: a
meta-analysis. Circ Arrhythm ElectrophysioL 2009;2:393-401.
58. Tada H, et al. Double potentials along the ablation line as a guide to radiofrequency ablation of typical atrial flutter.
J Am Coll Cardiol. 2001;38:750-755.
59. Spector P, et al. Meta-analysis of ablation of atrial flutter and supraventricular tachycardia. Am J CardioL
2009;104:671-677.
60. Feld G, et al. Radiofrequency catheter ablation of type 1 atrial flutter using large-tip 8- or 10-mm electrode cath-
eters and a high-output radiofrequency energy generator: results of a multicenter safety and efficacy study. J Am
Coll Cardiol. 2004;43:1466-1472.
61. Patel NJ, et al Contemporary utilization and safety outcomes of catheter ablation of atrial flutter in the United
States: analysis of89,638 procedures. Heart Rhythm. 2016;13:1317-1325.
62. Pothineni NV, et al Coronary artery injury related to catheter ablation of cardiac arrhythmias: a systematic review.
J Cardiovasc Electrophysiol. 2019;30:92-101.
63. Shah D, et al. Dual-loop intra-atrial reentry in humans. Circulation. 2000;1O1:631-639.
64. Heidbuchel H, et al. Right atrial angiographic evaluation of the posterior isthmus: relevance for ablation of typical
atrial flutter. Circulation. 2000;101:2178-2184.
65. Asirvatham SJ. Correlative anatomy and electrophysiology for the interventional electrophysiologist: right atrial
flutter. J Cardiovasc ElectrophysioL 2009;20: 113-122.
66. Passman RS, Kadish AH, Dibs SR, Engelstein ED, Goldberger JJ. Radiofrequency ablation of atrial flutter: a ran-
domized controlled study of two anatomic approaches. Pacing Clin ElectrophysioL 2004;27:83-88.
67. Jacobsen PK. et al. Voltage-guided ablation technique for cavotricuspid isthmus-dependent atrial flutter: refining
the continuous line. J Cardiovasc Electrophysiol. 2012;23:672-676.
68. Callcins H, et al. 2017 HRS/EHRA/ECAS/APHRS/SOLAECE expert consensus statement on catheter and surgical
ablation of atrial fibrillation. Heart Rhythm. 2017;14:e275-e444.
69. January CT, et al 2019 AHA/ACC/HRS Focused Update of the 2014 AHA/ACC/HRS Guideline for the Man-
agement of Patients With Atrial Fibrillation: A Report of the American College of Cardiology/ American Heart
Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2019.
70. Shah D, Burri H, Sunthorn H, Gentil-Baron P. Identifying far-field superior vena cava potentials within the right
superior puhnonary vein. Heart Rhythm. 2006;3:898-902.
71. Martins RP, et al. Localization of residual conduction gaps after wide antral circumferential ablation of pulmonary
veins. JACC: Clinical ElectrophysioL 2019;5:753.
72. Kuck KH, et al. Cryoballoon or radiofrequency ablation for symptomatic paroxysmal atrial fibrillation: reinterven-
tion, rehospitalization, and quality-of-life outcomes in the FIRE and ICE trial. Eur Heart]. 2016.
73. Tondo C. et al. Pulmonary vein isolation cryoablation for patients with persistent and long-standing persis-
tent atrial fibrillation: clinical outcomes from the real-world multicenter observational project Heart Rhythm.
2018;15;363-368.
74. Packer DL, et al. Cryoballoon ablation of puhnonary veins for paroxysmal atrial fibrillation first results of the
North American Arctic Front (STOP AF) pivotal trial J Am Coll CardioL 2013;61:1713-1723.
75. Marrouche NF, et al. Catheter ablation for atrial fibrillation with heart failure. N Engl l Med. 2018;378:417-427.
76. Prabhu S, et al. Catheter ablation versus medical rate control in atrial fibrillation and systolic dysfunction: the
CAMERA-MRI study. J Am Coll CardioL 2017;70:1949-1961.
77. Packer DL, et al. Effect of catheter ablation vs antiarrhythmic drug therapy on mortality, stroke, bleeding, and
cardiac arrest among patients with atrial fibrillation: the CABANA Randomized Clinical Trial. JAMA. 2019.
78. Daly MG, Melton I, Roper G, Lim G, Crozier IG. High-resolution infrared thermography of esophageal tempera-
ture during radiofrequency ablation of atrial fibrillation. Gire A"hythm Electrophysiol. 2018;1 l:e005667.
79. Kapur S, Barbhaiya C, Deneke T, Michaud GF. Esophageal injury and atrioesophageal fistula caused by ablation for
atrial fibrillation. Circulation. 2017;136:1247-1255.
80. Bhardwaj R, et al. Esophageal deviation during atrial fibrillation ablation: clinical experience with a dedicated
esophageal balloon retractor. JACC Clin Electrophysiol. 2018;4:1020-1030.
81. Parikh V, et al. Feasibility, safety, and efficacy of a novel preshaped nitinol esophageal deviator to successfully
deflect the esophagus and ablate left atrium without esophageal temperature rise during atrial fibrillation ablation:
The DEFLECT GUT study. Heart Rhythm. 2018;15:1321-1327.
82. John RM, Kapur S, Ellenbogen KA, Koneru JN. Atrioesophageal fistula fonnation with cryoballoon ablation is
most co=only related to the left inferior pulmonary vein. Heart Rhythm. 2017;14(20):184-189.
83. Kulkarni N, Su W, Wu R. How to prevent, detect and manage complications caused by cryoballoon ablation of
atrial fibrillation. Arrhythm Electrophysiol Rev. 2018;7:18-23.
84. Sheldon RS, et al. 2015 heart rhythm society expert consensus statement on the diagnosis and treatment of
postural tachycardia syndrome, inappropriate sinus tachycardia, and vasovagal syncope. Heart Rhythm. 2015;
12:e41-e63.
85. Ibarra-Cortez SH, et al. Strategies for phrenic nerve preservation during ablation of inappropriate sinus tachycar-
dia. Heiirt Rhythm. 2016;13:1238-1245.
86. Olshanslcy B, Sullivan RM. Inappropriate sinus tachycardia. Europiice. 2018.
87. Rodriguez-Manero M, et al. Ablation of inappropriate sinus tachycardia: a systematic review of the literature.
JACC Clin Electrophysiol. 2017;3:253-265.
88. Kusterer N, et al. Junctional ectopic rhythm after AVNRT ablation: an underrecognized complication. Piicing Clin
89. Piericlc AR, Law IH, Muldonado JR, Von Bergen NH. Junctional ectopic tachycardia localization and procedural
approach using cryoahlation. Piir:ing Clin Electrophysiol. 2017;40:655-660.
90. Brochu BD, Abdi-Ali A, Shaw J, Quinn FR. Successful radiofrequency ablation of junctional ectopic tachycardia in
an adult patient. HeartRhythm Cwe Rep. 2018;4:251-255.
91. Wilber DJ, et al. Comparison of antiarrhythmic drug therapy and radiofrequency catheter ablation in patients with
paroxysmal atrial fibrillation: a randomized controlled trial. JAMA. 2010;303:333-340.
92. Kottkarnp H, Schreiber D, Moser F, Rieger A. Therapeutic approaches to atrial fibrillation ablation target-
ing atrial fibrosis. JACC Clin ElectrophysioL 2017;3:643-653.
Catheter Ablation of Ventricular
Tachyarrhythmias
INTRODUCTION
General Features ofVentricular Tachycardia Ablation Patients
Patients undergoing ablation for ventricular arrhythmias have somewhat ofa bimodal distribu-
tion, including those with severe structural heart disease versus other patients with idiopathic
ventricular tachycardia (VT) having a structurally normal heart. First, characteristics of the
structural heart VT patients include: (1) a very high medical acuity with most being inpatient
and often in an intensive care unit (ICU); (2) frequent need for urgent ablation; (3) severe
structural heart disease due to 1 o.r more prior, often large, myocardial infarctions (Mis),
or severe nonischemic cardiomyopathy (NICM); (4) most have been implanted with ICDs;
(5) many have had cardiac arrest and/or VT or VP storm (~3 episodes within 24 hours) having
re<:eived multiple shocks; (6) many are being managed with intravenous antlarrhythmics;
(7) consideration for hemodynamic support (intra-aortic balloon pump. percutaneous left
ventricular assist device, or extracorporeal membrane oxygenation) is common. On the other
hand, a substantial number of VT ablation patients1 have idiopathic ventricular arrhythmias,
lacking appreciable structural heart disease. The relative distribution will depend on referral
patterns. Origins include the outflow tract region, the conduction system, and papillary mus-
cles. Sustained VT occurs with these foci, but many have PVCs or nonsustained VT.
Indications for Ventricular Arrhythmia Ablation
In general, ventricular arrhythmia ablation is indicated when medical therapy has failed or is not
tolerated or not preferred by the patient (Table 18-1). Medical treatment for sustained reentrant
VT with dilated (ischemic or nonischemic) cardiomyopathy includes amiodarone or possibly
sotalol (ifthe heart failure or EF depression is not severe). For normal heart ventricular arrhythmia.
medical options comprise beta blockers, nondihydropyridine calcium channel blockers, or Class I
or III antiarrhythmic agents. Verapamil can be uniquely effective for fascicular VT (see Chapter 8).
ABLATION OF VENTRICULAR ARRHYTHMIAS IN THE STRUCTURALLY NORMAL HEART

(SEE ALSO CHAPTER 8)
..................................................................................................................................................
Idiopathic Outflow Tract Arrhythmias: PVCs and VT
Idiopathic outflow tract (OT) arrhythmias, from either the RVOT or LVOT, may manifest
as isolated PVCs, runs of nonsustained VT (NSVT), or sustained monomorphic VT. Some
OT arrhythmias present during exercise. PVCs may be asymptomatic or cause palpitations,
Sustained monomorphic VT (post-infarct); failure of amiodarone or sotalol; frequent VT or VT storm

Sustained monomorphicVT (post-infarct); failure ofamiodarone or sotalol; single or occasional episodes llA
Sustained monomorphic VT (NICM); failure of amiodarone or sotalol llA
Polymorphic VTNF; no reversible cause; not controlled with medications; Identifiable PVC triggers
RVOT/LVOT PVCs or VT; normal heart; antlarrhythmlc medications Ineffective, not tolerated, or not preferred
RVOT/LVOT PVCs or VT; with suspected PVC cardlomyopathy (usually>15% PVCs); antlarrhythmlc medications
ineffective, not tolerated, or not preferred
Fascicu lar VT; antiarrhythmic medications ineffective, not tolerated, or not preferred
Papillary muscle PVCs or VT; antiarrhythmic medications ineffective, not tolerated, or not preferred
(Note: Guidelines from Al-Khatib SM, et aL 2017 AHA/ACC/HRS Guidl!linl! for Management ofPatients With Ventricular Arrhythmias and the Prl!vention ofSud·
den Cardiac Df!ath: ExecutiveSummary: A Report ofthe Ameriron CDJ/ege ofCardiology/American Heart Association Task Force on GiniaJI Practice Guidelines
and the Heart Rhythm Socif!ty.J Am Coll Cardiol. 2017J
lightheadedness, or fatigue; bigeminal PVCs sometimes result in low cardiac output-related

symptoms. Most patients display a single morphologic pattern. As implied by the name,
patients generally are devoid of other heart disease, but ventricular arrhythmias arising from
arrhythmogenic right ventricular cardiomyopathy (ARVC), cardiac sarcoidosis, or other non-
ischemic cardiomyopathies sometimes arise from these areas.2 Tipoffs include ventricular dys-
function, atypical PVC morphology, multiple foci, or polymorphic arrhythmias. Cardiac MR
is very hdpful in this scenario. (See also Chapters 8, 11, and 15.) Complicating matters, when
PVCs are frequent(> 10%-20% burden), patients may devdop a PVC-induced cardiomyopathy
(PIC). Suppression or elimination of the frequent ectopy with medications or ablation often
resolves the PIC, as discussed in Chapter 8.
The OT region's anatomy is challenging due to complex rdationships and variable terminol-
ogy (Figure 18-1). The stakes are high given the proximity of critical coronary arterial origins,
valve leaflets, and conduction system {Figures 18-2-18-5). Intracardiac echo and dectroana-
tomic mapping are invaluable real-time guides. The RV can be divided into 3 components, the
inflow tract starting at the tricuspid valve, the apical and trabeculated portion, and the outflow
tract region {Figures 18-2).M Most idiopathic RV sources originate in the OT and exhibit a
rightward (inferior) axis (Figure 18-6). Some ectopic foci are located less superiorly, near the
His bundle or the ventricular infundibular fold, or supraventricular crest, (Figures 18-2 and
18-6) and have a slightly less inferiorly directed axis. Less common RV sources include the
moderator band and papillary muscles {see bdow regarding papillary muscles). In ARVC,
typical VT or PVC sites include the free wall of the RV especially near the tricuspid valve and
theRVOT.
Anatomically, the RVOT courses in front of the LV becoming leftward and anterior to the
aortic valve and LVOT. The pulmonic valve (PV) plane is situated higher than the aortic
valve plane in the thorax. It lies horizontal, whereas the aortic valve plane angles down-
ward (front to back). The RVOT has rightward, anterior, leftward, and posterior surfaces,3-5
CHAPTER 18 • Catheter Ablation of Ventricular Tachyarrhyth mlas 449
FIGURE 1&-1 • Anatomy of RV and RVOT. Right anterior oblique view of a adaverfc specimen. Inlet portion Is outlined In glffn,
and ventrlculolnfundlbular fold Is outlined In red. Abbreviations: AA, ascending aorta; CS, coronary sinus; IVC. Inferior vena caw;
MPA, main pulmonary artery; SVC. superior vena cava; Tv, tr!aispld valve. {Reproduced with permls.slon from Sareml F, Ho SY,
Cabrera JA, Sanchez-Quintana D. Right ventJicular outflow tJact imaging with CT and MRI: part 1, morphology. AJRAm J Roentgenol.
2013;200:W39-WSO. Copyright c American Roentgen Ray Society.)
The posterior RVOT (sometimes called "septa!") abuts the LVOT, and more superiorly the
right and left coronary cusps (RCC, LCC); the LAD runs just anterior and leftward. Con-
sequently. RVOT and LVOT ECG patterns may differ substantially for disparate locations
(anterior RVOT vs aortomitral commissu.re) but some overlap considerably (Table 18-2 and
Figure 18-6). Some foci are most easily ablated above the PV; importantly, the left main lies
deep to the posterior aspect.
The LVOT is even more complex than the RVOT. Left-sided sources include those that origi-
nate (or can most easily be ablated) from the RCC or LCC, the RCC-LCC commissu.re. endo-
cardial tissue below the coronary cusps, the aorto-mitral continuity area, the left side of the
interventricular septum, epicardial sources close to the great cardiac vein or anterior interven-
tricular vein, and the left ventricular summit bounded by the bifurcations of the left main LAD
and circumflex vessels. LVOT is dearly an anatomical misnomer for some of these foci. The
coronary artery ostia arise superiorly within the LCC and RCC, whereas the ectopic foci typ-
ically originate from myocardial extensions in the inferior aspects of the cusps or below them
FIGURE 11-2 • Rel1tloruhtp between RVOT and LYOT. Superior view through the base of the heart shows the pulmonary valve
cusps induding the anterior (A), left posterior {Lp), and right posterior (Rp). closest to right coronary cusp, R). The aortic valve cusps
Include the right coronary cusp (R), closest to the right pulmonary cusp, left (I..} closest to the left pulmonary cusp, and the noncor-
onary cusp (N) situated most postedorty. (Reproduced wfth permission from Sareml F, Ho SY, cab~ra JA, Sanchez-Oulntana D.
Rlghtventrfcular outflOW' tract Imaging with er and MRI: part 1, morphology.AJRAmJ Roentgenol. 2013;200: W39-W50. Copyright o
American Roentgen Ray Society.)
(Figures 18-4-18-5). The RVOT is muscular in its circumference, thickest posteriorly abutting
the LVOT. Conversely. the aorto-mitral aspect of the LVOT is fibrous.u
The ventricular-arterial junction marks the start of the aorta. The aortic sinuses end superiorly
at the sinotubular junction. Critically, it is important to understand that there is not a clean
separation between the uniform layer of ventricular muscle and a fibrous ring at the aortic or
at the pulmonic valve annulus. Myocardium in most hearts extends superiorly. to a variable
degree within and between different aortic and pulmonic cusps.' The inferior recesses of the
RCC and LCC overlap the ventricular myocardium below the ventricular-arterial junction and
are in continuity with parts of the RVOT myocardium. This myocardial tissue may be reached
from a supravalvular, retrograde aortic approach or below the cusp (retrograde or transseptal).10
Unfortunately some of these ventricular arrhythmias originate from intramural sources and
others from more epicardial aspects of the left ventricular summit, most easily mapped via the
coronary venous system (Figure 18-5).
I~
lllDClenllon
D.F.
I
CMA'\ID
2010
FIGURE 18-l • Myocardial tissue in right and left outflow tracts. P.lnel Ashows myocardium extending into RCC {but not LCC
In this parttc:ular heart). On the right Is a schemattc: demonstrating these extensions. Panel BshOW$ an example of RV myocardium
extending above the pulmonlc valve. Panel C shows a sagltal section of the RV outflow tract, J'1V root. LVOT, and aortic root. The
proximity of muscle flbers to the base of the rusps Is apparent as Is the close relationship of the RVOT and LVOT. Abbreviations: L.
=
left aortic sinus; L-PSV right posterior pulmonary sinus ofValsalva. (Reproduad with permission from Gaml AS, et al. Anatomical
correfates relevant to ablation above the semilunar valves for the cardiac electrophY5iologist: a study of 603 hearts.J lnt.ervCard
Electrophysiol. 2010;30'5-15 and Sanchez-Ouintana 0, Doblado-calatrava M, Cabrera JA. Macias Y, Sarani F. Anatomical basis for the
cardiac lnterventlonal electroPhY5lologlst. Blomed Res tnr. 2015;2015:547364.)
FIGURE 1H • Left wntrkular summit. Three-dimensional reconstruction of coronary Cl anglogram showing relationship of
left main coronary artery bifurcation, great cardiac vein, and anterior interventticular vein, right and left aortic cusps, and RVOT.
Viewed from a aanlal right anterior oblique view, the LV summit, outllned In yellow, Is deflnect as an eplcardlal triangular structure
whose apex Is formed by the blfuratlon of branches of the left main Into LAD and LCx. The right and lek ASV are outlined (tight
yellowdashf!d llM). Abbreviations: AIV, anterior lnterventrlcular vein; GCV, great cardiac vein; LM, left main coronary artery; R-L
Comm, commlssure between right and left ASV; RVOT, right ventTlcular outflow tract; Summit CV, communicating veins of the
GCV. (Reproduced with pennlsslon from Cheung JW, Andefson RH, Markowttz SM, lefman 88. Catheter ablation of arrhythmias orig-
inating from the left ventricular outflow tract.JACCClin Electrophysiol. 2019;5:1-12. Copyright C Amefican College of Ciirdiology
Foundation.)
PanalA Panel B Panel C
FIGURE 11-5 • 'fyplcal QRS morphology mcamples for dlfftirent RVOT sources. Panel k RVOT septal /posterior. Plln1I B: RVOT
anterior. Panel C: Parahlslan PVC.
ECG characteristics suggest specific RVOT or LVOT foci (Table 18-2). but given anatomic
variability and the potential for lead malpositioning. these traits do not substitute for detailed
mapping. RVOT foci display an LBBB pattern and a precordial transition at V3 or later. Located
most superiorly, RVOT sites exhibit a QS pattern in aVL and aVR. Arrhythmogenic foci from
the LVOT. on the other hand. feature either a LBBB pattern with early transition (V2 or V3)
or a RBBB pattern. Thus. an LBBB with precordial transition in V3 may occur with RVOT or
LVOT sites (Figure 18-7). Ifthe precordial transition occurs later for the PVC than for the sinus
beats, then an LVOT source is very unlikely. The relative amount of R wave in V2 for sinus vs
PVC beats can generate a V2 transition ratio to predict RVOT versus LVOT.U For RVOT foci
in the posterior region. the QRS is relatively narrower. the precordial transition is earlier (ie..
V3). and the inferior leads are very positive and lack notching. RVOT foci from the free wall
display a later precordial transition (e.g., V4 or V5) and exhibit notching in the inferior leads.
Parahisian ectopics show some positivity in lead I and possibly aVL. and less overt positivity
inferiorly. Supravalvular RVOT sites sometimes feature more negativity in aVL than AVR. and
very tall inferior R waves. Considering Figures 18-2and18-3, a progressively earlier transition
occurs with more posterior location (greater distance from Vl), respectively, for the anterior
RVOT, posterior RVOT, RCC, LCC, and lastly. the aortomitral continuity (AMC), and left ven-
tricular summit.1:i."
.,.,.,.,.,.,.,.,.,.,·r··
~
~ ~ ~ ~
4 ~ ~ ~
~ ~ ~~
~ ~ ~ ~ ~
-1)"- ~
~
~ ~
~ ~ ~ ~
v-y-
-v-v-- ~ ~ ~
x rt ~ ~ ~
~
v-\r -L-flv
± -LL ~~
~
~ ~ ~
. 1. 1.1.1.1. 1.1.1.1. 1. 1.1.
Panel A Panel B PanalC PanelD PanelE
FIGURE 1H • 'fyplc:al QRS morphology examples for different LVOT sources. Panel A:. Right coronary cusp. Panel B: PVC from
RCC/LCC commlssure. Panel C: Left coronary cusp. Panel D: Aortomltral contfnulty. Panel E: Epfcardlaf perlvenous source mapped
to dte great cardiac vein-anterior lnterventrfculer vein junction.The lead display Is dte same as Figure 18-S.
An algorithm for efficient mapping derives from these ECG considerations (Figure 18-8).
Mapping guided by activation timing is more accurate than pace mapping. If ectopy is infre-
quent, options include pharmacologic challenge (isoproterenol or epinephrine), burst pacing,
reduced sedation, preprocedural sleep deprivation, and possibly. preprocedural body surface
mapping. Given the <Xlmplexity of anatomy and proximity of multiple structures. it is advisable
to continue mapping until an optimal ablation target is identified. Ideal sites are identified by
early activation (S25 ms before PVC onset). along with a QS in the unipolar electrogram, and
often demonstrate a fractionated or prepotential. Notably. unimpressive pace mapping may be
present at a favorable activation-map location, and this alone should not deter ablation. Open
irrigated ablation catheters are strongly preferred in the CS or AlV. generally used in the cusps
and LVOT and either these (with limited power) or solid-tip 4 mm catheters used in the RVOT.
Intracardiac echocardiography has now replaced coronary arteriography in most electrophys-
iology laboratories for guidance of ablation in the aortic sinuses,15 but arteriography is needed
for evaluating ablation targets in the epicardial coronary veins.
RVOT, anteroseptal LBBB Right inferior rS Transition V3 or V4; I, avL negative

RVOT, free wall LBBB Right inferior rS Transition V4 or VS, notching in
inferior leads, I may be positive;
avL negative
Parahlslan LBBB Right Inferior as I positive; avL positive or lsoelectrlc
RCCofASOV LBBB Right Inferior rSorRS Transition In V3; broad r (or R) In V2
LCCofASOV LBBB Right inferior RS or rS Mor W in V1;transition in V3
RCC-LCC commissure LBBB Right inferior Multiphasic
ofASOV
GCV, AIV (LV summit) LBBB or RBBB Right inferior rSorR Early transition V2 or V1 . Broad QRS
with late peak; MDI >0.55
LVOT,AMC RBBB (or LBBB) Inferior RorQR RlnV2-V6
LVOT, anterolateral MA RBBB Inferior R I negative; notching Inferior leads
LV, inferobasal, endocardial RBBB or atypical LBBB Left superior RsR'orrS rS in inferior leads; V2-6 positive
(•posterior superior process")
LV, inferobasal, epicardial Atypical LBBB or RBBB Left superior R<S QS in inferior leads; higher MDI;
c·crux1 V2-6 positive; may be approached
via CS
Papll lary, anterolateral RBBB Inferior R II positive usually; Ill positive; rS In
V6 and I; transition to S>R in V4-6
Papillary, posteromedial RBBB Superior R II, Ill negative; rS in V6; transition to
S>RinV3-4
Maximum deflection index (MDI} is defined as the shortest time to maximal positive or negative deflection in any prerordia/ lead divided by the total ORS
duration."
Soutr:e5: Haqqani HM et a{ J Cardiovosc Electrophysio{ 2009;20:825-832, U A, et al. Heart Rhythm. 2018;15:1356-1362, and Kowomura M, et al. Heart Rhythm.
2015;12:1137-1144.
If after exhaustive mapping (Figure 18-8), an ideal site has not been identified, it is reasonable
to ablate a safe region that has the earliest activation. For these intramural and LV summit foci
ablating on either side, as close as possible, while avoiding coronary artery proximity, some-
times succeeds. If the optimal site is too close to a coronary artery (~5 mm), then the closest
RVOT or LVOT endocardial site, RCC, or LCC location should be considered. Investigational
approaches such as needle ablation and radiation therapy are on the horizon too. Percutaneous
or surgical epicardial approaches have been tried but often fail as well due to coronary proxim-
ity and exuberant fat.
Complications related to RVOT/LVOT ablation include cardiac perforation, aortic dissection,

symptomatic or asymptomatic cerebral embolism, and injury to an aortic, pulmonic or mitral
valve leaflet, or coronary artery (possibly resulting in MI). Retrograde and transseptal approaches
exhibit slightly different complication profiles. Major complications occurred in 2.4% of patients
in a large multicenter study, with specific rates of 0.8% for cardiac tamponade, femoral vascular
complications 1.3%, AV block 0.1 %, and another 0.3% had other complications. There were no
periprocedural deaths or strokes. 16
lntrafasclcular VT ("'fasdcular VT9' or Idiopathic LVVT [ILVTJ)

Several forms of reentrant VT utilize the LBBB fascicles (Figure 1-2) (Table 18-3). (Bundle
branch reentrant VT is related and discussed in Chapter 8, and below in Section 18-4.) ILVTs
are normal heart arrhythmias, exhibiting verapamil sensitivity. Infarction may elicit VT (or
VF) from the fascicles as well, however (Section 18-S). The RBB-left axis type (Figures 8-39
and 8-40) uses the left posterior fascicle (LPF) as part of the reentrycircuit (Figure 18-11) and
accounts for about 90% ofILVTs.11•21 Nogami's group reported on ablation for 6 patients with
the rare RBB-right axis type of ILVT, that uses the left anterior fascicle (LAF) as part of the
reentry circuit, and also exlu1>its verapamil sensitivity.12
PlntlA
FIGURE 18-7 • Outflow tract c.ase. Panel A, left side, shows activation timing at the earliest site in LVOT or cusp region at 20 ms
before the PVC onset; the'"vlslon"traclng ls In the CS recording from the AIV and Is relatlvely late; the right top shows the ICE Image
with cusps open and catheter {arrow) prolapsed through aortic Vlllll'e and conactlng the lower aspect of RCC-LCC commlssure;
bottom ICE Image Is Just later with cusps closed; cathmr tip Is marked grnn on ICE and location Is Indicated by arrow. Panel B
shows electro anatomic map views, right lamal cranlat PA cranlal and left lateral cranlat from left to right LCC Is purple, RCC blur--
green, and NCC yellow. Catheter is at RCC-LCC commissure as in Panel Aadjacent to the RVOT posterior surface. The RV is in mesh,
LV chamber solid gray, and CS displayed as mesh also. The middle image shows the catheter vector toward the RVOT from below
RCC-LCC ccmmissure. The right image best displays the early ac:tivation in ml at RCC-LCC commissure. After ablation at that site.
the PVC was suppressed but returned. Remapping the RVOT showed a signal about 20 ms before the PVC onset s!m!lar to Panel A.
RVOT ablation at the bottom shows ellmlnat!on of the OT PVCs. The proiclm!ty of RVOT, LVOT, and CS/ArY Is evident
Panela
FIGURE 1•7 • (Continued)
Nakagawa, Jackman, and colleagues perfonned ablation at the site of presystolic fascicular
potentials.:u Nogami and colleagues studied ILVT with a decapolar catheter along the LV sep-
tum (Figure 18-12C).24.2 5 Optimally positioned, the LPF can be tracked from base to apex in
sinus rhythm. During VT, the LPF activates retrogradely. with fascicular potentials (termed P2).
Outflow tract PVC

pmcordlal transHlon
Map RVOT Sinus V2

and PV -----1 1ransition in transition
cusps V2 (earlier) ratio
MapRCC, Map CS,

LCC, LVOT GCV,AIV
FIGURE 1 •a • Sugguted algorithm of priority for mapping ofoutflow tnid arrhythmias.The flowchart presents an approach
for whether to mep tfle right or•1ett• OT regions first Abbreviations: LVOT, left ventricular outflow tract; RVOT, right ventrlculer
outflow tract; GCV, great cardiac vein; Arv, antl!flor lnterventricular vein. The V2 transition ratio ls found In Reference 11. The MDI
(maximum deflection index) derives from Reference 12.
CHAPTER 18 • Catheter Ablation of Ventricular Tachyarrhythmias 457
Verapamil-Sensitive Idiopathic LVVTs: I ntrafascicular VT

Left posterior Healthy individual. RBBB, LAD, L posterior fascicle exit; LPF Mid to dista I P1
fascicularVT Verapamil sensitive. QRS 120-140 ms retrogradely (P2 component); fiber; empiric
{Belhassen VT) nearby Purklnje flber conducts transection of LPF
base to apex {P1 component)
and has decremental properties,
verapamil sensitivity
Left anterior Healthy individual. RBBB,RAD, L anterior fascicle and other Midseptal
fasclcular VT2 6 Verapamil sensitive. QRS120-140ms Purkinje fiber diastolic Pl
potential near LAF
Upper septal Healthy individual. Narrow QRS (<120) Septal fascicle retrogradely and Midseptal
fascicular VT Verapamil sensitive. LAF and LPF antegradely diastolic Pl
{very rare, After prior LPF ILVT potential
1% offascicularVT) ablation.
Macro Reentry In Bundle Branches or Left Fascicles
Bundle branch NICM; AR; AVR; LBBB Antegrade RBBB, retrograde RBB(orLBB)
reentrantVT conduction system LBBB; HV longer than SR;
disease. His activated retrogradely.
Bundle branch NICM; AR; AVR; RBBB Antegrade LBBB, retrograde RBB(orLBB)
reentrant VT conduction system RBBB; HV longer tnan SR;
{atypical) disease. His activated retrogradely.
/nterfasclcular VT After RBBB ablation? RBBB; RAD or LAD Antegrade over LAF produces Either LAF or
RAD; antegrade over LPV and LPF depending
retrograde over LAF produces upon conduction
LAD; HV snorter tnan SR in SR
Earlier, mid-diastolic potentials, termed PI, activate base to apex during ILVT. The PI fiber
represents the decremental, verapamil-sensitive Purkinje tissue fiber (Figure 18-9). The optimal
ablation site has been described as two-thirds from base to apex and where the Pl signal is
approximately 60 ms before the QRS; more apical may fail and more proximal ablation could
damage the LBBB.2s Entrainment must be interpreted carefully since local myocardial capture
and/or fascicular capture may occur.26 ILVT is sometimes noninducible or may become non-
inducible due to mechanical injury from mapping. Empiric ablation perpendicular to the LPF,
about 10-15 mm proximal to the VT exit, has been reported. 27
The very rare upper septal ILVT is noteworthy for exhibiting a QRS less than 120 ms. It accounts
for I %-10% ofILVT but at least half of the patients had undergone prior ILVT ablation for the
more common LPF variety.28 The HV interval averaged 25-30 ms, shorter than that observed in
sinus rhythm, and the QRS during VT averaged about 15 ms longer than that in sinus. Upper
septal VT may exhibit a normal or right axis and incomplete RBBB. Recordings and ablation
were described recently. 28
Papillary Muscle Sources Including Mitral Valve Prolapse Ventricular Arrhythmias

The papillary muscles represent a unique and important source of both monomorphic and
polymorphic, ventricular arrhythmias in normal hearts, post-infarction, mitral valve prolapse,
Sinus Rhythm CommonlLVT

iiu ' i i " ' l ' i i ii ii i i j i i " ' ii iijii
I~ ~~----......~--~~~~---......
II~
111- - - - " ' - - - - -
FIGURE 1H • Recordings from lntr~cularVT (ILVT) ablation. A deapolar catheter Is po$ltloned along the LV septum
with dlstal electrodes being aplcal. During sinus rhythm the LPF Is recorded actlvaUng from base to apex and labeled Pl. During
common ILVT (RBBB, superior axis) P2 activates from apex to base and a P1 potential ls tracked from base to apex. Note His poten-
tial burled In QRS. (Reproduced with permission from Tallb AK, et al. Verapamll-sensltlve upper sepml ldlopathlc left ventrlcular
tachycardia: prevalence, mechanism, and electrophysiological characteristic:s.JACCCfin ElectrophyJiol. 2015;1 :369-380. Copyright C
American College of Cardiology Foundiltion.)
and other structurally abnonnal VT substrates. Both. PVCs and ventricular tachycardia are
observed. Anatomic sources include the posterior septal papillary muscle (PSPM), the anterior
lateral papillary muscle (Al.PM). with. the form.er more common (Figures 18-10 and 18-11).
Less frequently, the Rv•s papillary muscles (anterior or posterior, but especially the septal) may
harbor PVC or VT foci. The moderator band connecting the RBB to the anterior PM is another
arrhyth.mogenic structure.2 ~31 Foci have been mapped to th.e base (attachment site to the LV
[or RV] wall). more often than the middle or apex (attachment to chords).3 1.U Papillary sources
may mimic II.VT (see above). but often have beat-to-beat variability or are frankly polymor-
phic, tend to exhibit a nonsustained or single ectopic pattern rather than a sustained one, do
not respond to verapamil, and have a wider QRS complex (averaging about 160 ms). Due to
the anatomical substrate, they are challenging to map and ablate. The PM arrhythmias were not
inducible with programmed stimulation and could not be entrained. Mapping reveals a focal
pattern and successful sites exhibit a local activation about 30 ms before the QRS onset Pace
mapping is useful ifectopy is scarce but exits may vary and activation mapping is optimal. Cat-
echolamine infusion or burst pacing (not programmed stimulation) can help elicit th.e arrhyth-
mia. Enriquez et al have provided a detailed description of these arrhythmia foci and their
PanalA PanalB
FIGURE 11-10 • Panel A; ECG morphology of Antenor letenil paplll1rymuscle(Al..PM)focus. Panel B: Postetforseptll paplll1ry
musde (PSPM) focus. With PSPM leads I~ II~ and avF are negattve. whereas for ALPM, leads Ill and avF are pcsltlve with lead II being
variable. (The lead display Is the same as Agure 18-5.}
ablation.33 Presystolic Purkinje potentials are often identified at the PM base ablation sites, as
these tracts tend not to extend more distally toward the PM apex. Detailed mapping is impor-
tant, and multiple exits can confuse the operator. The mobility and narrow structure ofthe PMs
poses major challenges for catheter stability. Intracardiac echocardiography is most helpful for
appreciating the catheter location with respect to the various surfaces of the PM. The vector
directionality in contact force-sensing RF catheters is synergistic with the ultrasound images
as well as the actual force applied. Although inferior for mapping. the stability due to cryoad-
herence (Chapter 17} makes cryoablation uniquely well-suited for ablating PM sources.3 J.M It
is preferable to map with the more maneuverable RF catheter prior to introducing the cyroab-
lation one. The operator should be prepared to employ either the transseptal or retrograde
approaches to optimize success and safety. Nevertheless, in a recent multicenter series, PM foci
exhibited the lowest long-term su.ccess rate (65%) among all anatomic sources.16 Worsening
MR, VF during ablation and catheter entrapment are unique complications requiring vigilance.
Chapter 8 details the interesting association of malignant arrhythmias with mitral valve
prolapse. The most common PVC site in this syndrome is the PSPM, followed by the ALPM,
I
I I I
- I I I I I
37-
I I
!....
I I I I I I I I
38-
av-
V1
... -
·~~
H1:,.. v v ~"
HIS,,.,
v -
HIS-d r>/ J~
~~
~
RFm ap,.
RFm apd
~r ~
H36ms
CS ,.
CS 7~
-
~
CS
CS ::
CS d
__,,
Rv.~c . _
I I I I I I I I I
' I I I I
' I
Pan.. A
Pan1IB
FIGURE 11-11 • ALPM and PSPM PVC abi.tfon cans. Panel Ashows 2 sinus beat5 then the same ALPM PVC from Figure 18-1 OA.
Note the fractionated sign al on the RF map dlstal preceding the PVC onset by 36 ms. Ablation Jn this area was successful. Panll B
shows the PSPM PVC from Figure 18-1 OB. The pace-map from the early, and successful, site shows >95% match except in V3 82%
match (not shown). The electroanatomic map (middle) of the PSPM region in RAO view displays the early activation site in red. The
right image shows an ICE image still frame with the catheter (green dot) in contact with the PSPM; note its brightness due to ablation.
fascicular-related foci, mitral annulus, and then the OTs.35 Those MVP patients with prior
SCA had PVC/VF site ablated at either a PM with a Purkinje potential or a fascicular site
most often. RF ablation at these Purkinje potential sites triggered VF in nearly half of
patients.36
POST-MYOCARDIAL INFARCTION VENTRICULAR TACHYCARDIA ABLATION

Understanding the Pathology
Reimer and Jennings' wavefront theory of cell death explains the stepwise progression of cor-
onary occlusion-related MI from subendocardium outward, owing to greater subendocardial
region wall stress impeding epicardial to endocardial collateral blood flow. A rim of subendo-
cardial tissue deriving oxygen directly from the chamber is often spared.37 Patients dying from
VT post infarction characteristically exhibited large infarcts that bore this spared subendocar-
dial rim. 31 Patchy surviving myocardial bundles course through infarct scars and subendocardial
or other border zones. Tissue in these channels exhibits impaired cell-to-cell conduction due to
interdigitating fibrosis thus yielding a zigzag pattern of activation. Multiple such slowly conduct-
ing, interconnected channels provide a rich substrate for reentry (Figures 18-12 through 18-14).
Panel A
loop
PanelB PanelC
FIGURE 18-12 • Schematic representation of postinfarction VT circuit. This shows a central isthmus (heavy wavy arrow), exit to
relatively normal tissue (giving rise to the onset of the QRS), and figu re-of-8 reentry with 2 outer loop components, entrance to
the Isthmus (proxlmal), and bystander (Bys) regions. The dense, lnexcltable scar ls the hatched zones. (Reproduced with permission
from Stevenson WG, Friedman PL. Sager PL, et al. Explorlng postlnfarctlon reentrant ventrlcular tachycardia with entrainment map-
ping. J Am Coll Cardiol. 1997;29:1180-1189. Copyright «:I American College of Cardiology.)
Pacing during VT
I
Entrain with
concealed fusion
1 i·-·-
QRSfusion
PPI = VTCL +I- 30 ms PPI = VTCL + /-30 ms

or
S-QRS = EG-QRS + /-20 ms
No Yes
Yes Remote Outer

No bystander loop
(S-QRSNTCL) X 100
<30% 31-50% 51-70% >70%

Adjacent
~
bystander
1J.,.,1 1J...,1 Inner loop
Isthmus sites
FIGURE 18-13 • Entrainment responses during VT. Before analyzlng, the operator must confirm that the VT Is advanced to the
pacing rate. The first step then is to analyze the QRS and determine whether it is identical to the native VT QRS complex (entrained
with concealed fusion) or whether it has {manifest) fusion (to the right side). Then the return cycle or post pacing interval (PPI) is
measured on the pacing channel electrogram and compared to the VT cycle length {CL). This step helps identify the site of pacing
as shown. Sites where pacing entrains tachycardia with QRS fusion and the post pacing Interval exceeds the tachycardia cycle
length are remote bystanders. Next the stimulus to QRS (S-QRS) during pacing and/or the electrogram at the pacing site (EG) to
QRS onset {during VT) interval is measured. The S-QRS should be essentially equal to the EG-QRS for critical parts of the circuit,
but not at an adjacent bystander. Expressed as a percentage of the VT CL. the S-QRS wil I be short near the exit and progressively
longer moving back toward the entrance of the central isthmus (proximal), and long at inner loop sites. See also Figure 18-15 for
anatomic schematic. {Modified from with permission from Stevenson WG, Friedman PL, Sager PL, et al. Explorlng postlnfarctlon
reentrant ventricular tachycardia with entrainment mapping. J Am Coll Cardiol. 1997;29:1180-1189. Copyright «:I American College
of Cardiology.)
The pathologi.c substrate explains why an endocardial ablation approach yields benefit for the
majority of postinfarction VTs. In contrast, nonischemic cardiomyopathies have a higher pre-
dilection for subepicardial and intramural circuits.
Activation and Entrainment Mapping

Activation and entrainment mapping are complementary techniques for identifying the reen-
try circuit during ongoing VT. Substrate mapping is often considered an opposing approach,
but in reality the two can work in tandem.
The VT QRS morphology derives largely from the location of the reentry channel exit, where-
upon a substantial mass of tissue then begins to become activated. The data contained in the
ECG pattern combine with the infarct location (identified by Q waves, coronary occlusion,
akinesis, and/or delayed enhancement on CMR) to guide mapping.
Creation of an activation map in a very abnormal, infarcted milieu is much more challenging
than generating one for a focal arrhythmia source in normal tissue. The electrograms in impor-
tant areas display low amplitude (often approaching the noise threshold), double potentials,
and fractionation defying easy determination of an activation time.
Information can also be gathered to identify the critical aspects of the reentry circuit during VT
by entrainment mapping. Each has its pros and cons. Entrainment'P utilizes a train of pacing
from different locations slightly faster than the VT cycle length. The first step is to dete.nnine
whether capture has occurred (ie., excluding an isorhythmic situation). Thereafter, using sev-
eral criteria, as illustrated in Figures 18-12 and 18-13, the pacing site's relationship with the
reentry circuit can be defined. Next. by comparing the paced QRS morphology with the VT
morphology, one identifies the presence of either manifest fusion or, if the QRS is identical,
entrainment with concealed fusion. The timing from the last stimulus to the Brst native return
activation at the pacing site (post pacing interval, or PPI) is compared to the tachycardia cycle
length. In addition, the interval from the local site's electrogram to QRS is compared with the
stimulus to QRS.39
II
aVR
aVF
V1
V2
V4
vs
V6
Pa!Mll.A
FIGURE 18-14 • Patient with reemrant VT post myocardlal lnfarctlon. Panel A shOW5 the baseline ECG (left) demonstrating a
Q-wave inf'erior myocardial infarction and 3 ofs distinct monomorphicVTs that were induced. Panel 8 (left) shows mapping in the
scar region with a S-Spllne mapping catheter with closely spaced electrodes during 1 of the VTs In hnel A. Note the multlple dla-
stollc potentlals vlrtually spanning the entrance, mid, and exit regions of the Isthmus. In the middle Is an electroanatomlc voltage
map In RAO-caudal view. The scale shows that red Indicates bipolar voltage <0.5 mv (I.e., the scar mne), purpk >1.5 mv {relatively
normal tissue), and border zone Intervening colors. On the right Is the same map viewed from PA caudal; the mltral valve Is cutout
The aorta and cusps defined by ICE are shown. The ablation lesions are red dots in and surrounding the scar region. Panel C{left) is
an example of entrainment from a aitical isthmus with a post pacing interval {PPI) essentially equivalent to the tachycardia CL
(544 ms). The stimulus to QRS (136 ms) matches the local electn>gram to QRS (132 ms). The entrained QRS Is ldentlc:al to the
native VT (template matching software percenaiges of 9996 etc.; I.e., concealed entrainment). The right hand tracing shows
entrainment from the scar region, and as on the I~ thefe Is concealed en1.Talnment However,the PPI Is longer than the tachycardia CL
(596 vs 522 ms), and the stimulus to QRS (234 ms) ls longer then the local electro gram to QRS (162 ms}. This ls compatible with an
adjacent bystander (Figures 18-12 and 18-13).
I
a.VF
V1
VB
P01Jl2
POO..G4
P05_0S
P07_08
POUO
p 11_12
P13_14
P15_19
p 17_18
PUl...20
RVd r
PanelB
POS
p 07.
I-
132n
H
ff./ I l I _i:-:::::_ t___:;,__
1 544,..
j I l~.--J-
I
""' ll!!!!/
p.29 ~
1118 RV
Pan.. c
Substrate Mapping and Ablation

The activation and entrainment mapping approach seeks to identify and eliminate "the clin-
ical VTs" critical .isthmus. Limitations include: (1) noninducibility of the clinical tachycardia,
(2) hemodynamic instability during the VT. (3) spontaneous or pacing-induced conversion
from one VT morphology to a different one, and (4) the potential, even likelihood. that mul-
tiple different clinical vrs exist. The substrate approach does not depend upon VT induction
or its hemodynamic stability, and furthermore endeavors to eliminate all the potential VT cir-
alits. One study randomized 118 patients with mappable vrs to the activation-entrainment
strategy vs substrate ablation. Seeking to eliminate all abnormal potentials in the scar region,
the substrate group received about twice as much ablation, but had a shnilar procedure dura-
tion. vr recurrence was 15.5% for substrate approach vs 48% in the mapping group.'° With
regard to abnormal potentials in the scar and border region, the initial emphasis was on late
Steps VT Ablatlon Procedure

Substrate mapping
CC entrance identification
2 CC elimination
Remapping
3 Residual CC ablation
lnducibility
4
Residual VT ablation
FIGURE 18-15 • Conducting channel approach to substrate ablatlon. Schematic of substrate-based, postinfarction VT ablation
using selective ablation of conducting channels (CC, white with dotted lines) through scar tissue (the blue area) rather than ablation
of the entire scar (homogenization) or all the LAVA potentials. Note the 6 local idealized electrograms show large far-field compo-
nents and smaller, fractionated local, near-field components that may be continuous with the far-field component or widely spilt.
The temporal relatlonshlp wlll depend on the direction of activation via the CC, I.e., the pacing site. Ablatlon Is locallzed to the crit-
ical entrance and exits from the scar, i.e., the CCs. The step-by-step chart suggests 1 possible workflow where a voltage map with
identification of fractionated potentials and relative activation time of the near-field components to identify the CCs. The CCs are
ablated to eliminate conduction, then remapped to confirm. Finally, if the patient's status permits, inducibility can be tested and
additional mapping and ablatlon performed as tolerated. (Modified with permlsslon from Berruezo A, et al. Scar dechannellng: new
method for scar-related left ventricular tachycardia substrate ablation. Circ Arrhythm Electrophysiol. 2015;8:326-336.)
potentials. Recent investigation led to the term LAVA for local abnormal ventricular activ-
ities within either dense scar (<0.5 mv bipolar voltage) or border zone (0.5-1.5 mv bipolar
voltage), defined as sharp, near-field signals during or after far-field potentials. (See example
of these electrograms in Figures 18-14 and 18-15.) Not unexpectedly, LAVA signals from the
septum occurred temporally earlier than those from the lateral wall (during sinus or RV pac-
ing). Changing the activation wavefront direction or using premature stimulation will make
the LAVA signals more obvious (or less) and alter the timing and relationship with the far-field
signals. Elimination of the LAVA potentials was associated with successful ablation and free-
dom from recurrence of VT:n
Limitations of a maximal substrate ablation approach, aptly termed homogenization,42 include

the longer procedure and greater extent of ablation posing thromboembolic or other risk. It has
become clear that ablating every abnormal signal may be unnecessary, because not all of these
potentials are related to a critical isthmus for VT.
Advancing this concept further, scar dechanneling (Figure 18-15) seeks to eliminate channels
through infarcts by ablating the entrance and exit points rather than every strand of viable
tissue in between. After marking LAVA-type signals on an electroanatomic map and using the
location and timing of the near-field signal component, the scar channel's entrance and exit are
identified, mainly at the scar border. Success at eliminating the conducting channel was defined
by exit block from pacing within the scar and elimination of (local, near-field) potentials within
the interior of the conducting channels. After that step, it is advisable to ensure VT noninduc-
ibility because this further ablation to achieve it may improve the prognosis for recurrence-free
survival.'° Core isolation is a related technique,44 which involves selective ablation of the scar
border to render the area of dense scar electrically isolated by finding the earliest {first) and
any/all exit points from the scar region and ablating those exits. Thereafter, dissociated poten-
tials with entrance and exit block can be demonstrated, as for PVI.
Outcomes and Complications

The success of catheter ablation for post-MI VT is lower than that for normal heart VT due to
the progressive nature of the condition, multiple VT circuits, scar tissue, and patient instability.
A meta-analysis identified 4 RCTs comparing VT ablation with antiarrhythmic drugs in 521
patients. All-cause and cardiovascular mortality were unaffected, but cardiovascular hospital-
ization was reduced by 28% (p=0.02), and VT storm by 29% {p=0.03). ICD shocks were numer-
ically 41 % lower (significant or not depending on methodology used). In this meta-analysis,
30-day mortality was 0%, and the total complication rate due to catheter ablation was 5.7%.45 In
a multicenter cohort of over 2000 patients undergoing VT catheter ablation for structural heart
disease, 5% experienced mortality within 30 days. Mortality stemmed from VT in 22%, cardiac
decompensation in 39%, and noncardiac or unknown causes in the remainder.46
BUNDLE BRANCH REENTRANTVT AND INTERFASCICULARVT

Bundle Branch Reentrant VT
Bundle branch reentrant VT (BBRVT) may go undiagnosed if the His signal is not recorded
during VT or one is not mindful of the entity. (See Chapter 8 and Figures 8-30 and 8-31.)47-49
It is important to recognize BBRVT because it can be cured with RBB ablation. Ablation of
the RBB can be guided by recording the RBB potential. However, ablation of the LBB may
be preferable if antegrade LBBB is present in NSR, unless a functioning pacing (ideally CRT)
device is present. 50 LBB ablation in the setting of antegrade LBBB in NSR will need to be guided
by identifying retrograde LBB potentials during BBRVT. An alternative in this situation is
empiric ablation in the basal LV septum distal to the His potential. A recent single-center
study demonstrated an absence of long-term recurrence. Interestingly, patients with baseline
normal HV intervals and/or normal LV function were fairly common (22% and 31 %, respec-
tively) and these patients had excellent long-term, arrhythmia-free survival.51
lnterfascicular VT
Interfascicular VT, a very rare entity, displays RBBB and right axis deviation. The circuit involves
antegrade conduction over the LAF, myocardial exit and breakout, and then retrograde conduc-
tion over the LPF. The reverse circuit is possible and shows left axis deviation. As opposed to
ILVT (intrafascicular VT) pre-QRS His potentials are found though the HV is shorter than that
seen with BBRVT. Ablation of either LB fascicle is the treatment. 52 lnterfascicular VT has been
reported after RBB ablation for BBRVT. 53
-~-~.1.~~-~-~~~-~.A~.~-~-~-~'--~.~~-~.1. ~~L~~-~ -~~-~AT.1.9~....................................................................

Pioneered to treat the common epicardial foci in Chagas disease, pericardia! access, in the
absence of an effusion, uses a spinal needle (Tuohy) with a stylet to access the pericardia!
space underneath the cardiac apex. A guide wire is then inserted and confirmed to be in the
pericardia! space (as opposed to the RV and then possibly PA) by visualizing it overlapping
multiple chambers.54 In general, the mapping catheter can move relatively unimpeded around
the epicardial surface aside from pericardia! reflections forming the oblique and transverse
sinuses.ss Limitations include epicardialfat (especially at the AV grooves) and coronary arteries
that may overlie arrhythmia substrate preventing safe ablation. Irrigated RF ablation is used on
the epicardium. Monitoring fluid accumulation usually via intracardiac echo is important. Due
to the overlying fat, electrograms may be of lower voltage seemingly suggesting scar ( <1.0 mv
bipolar), but scarred myocardium additionally exhibits prolonged, fractionated signals. 56 Prior
pericarditis, pericardia! adhesions, and/or prior median sternotomy can make access unsafe
and/or impossible, in which case a surgical pericardia! window may be an option.
A multicenter series compiled 156 epicardial mapping procedures (out of a total of 913 abla-
tions) for the following conditions: post-MI (n"'51), NICM (n"'39), ARVC (n"'14), and other
(n"'30 ), respectively.s7.s8 Major complications occurred in 11 (7%) patients, including pericardial
bleeding >80 cc (n"'7), coronary stenosis (n"'l), RCA occlusion in a patient with ARVC (n"'l),
and delayed tamponade (n"'l). Another series found a 13% incidence (46 of 355 patients) of
significant pericardia! bleeding (>80 cc).s9 Other complications have included: intra-abdominal
bleeding; injury to the diaphragm, liver, or spleen; and left phrenic nerve injury. A newer alter-
native, the anterior approach, takes advantage of a higher likelihood of trace pericardia! fluid
anteriorly, and may be safer (Figure 18-16).i;o Access with a micropuncture 21-gauge needle
inside an 18-gauge needle (needle-in-needle approach) has been reported too and may lessen
bleeding though this is not yet confrrmed.61
NONISCHEMIC CARDIOMYOPATHY
Approaches and Outcomes
Catheter ablation tends to be less effective in nonischemic cardiomyopathy (NICM) than
in ischemic cardiomyopathy (ICM). Most monomorphic VTs are due to reentry, as in ICM
(Figure 18-16). A recent single-center series found a 67% vs 77% acute success rate that by
1 year regressed to 40% freedom from VT for the NICM group compared with 57% for ICM.62
In another comparative series from a leading center, freedom from VT at 6 years was also lower
with NICM than ICM (38% vs 54%).63 A large single-center study reported on 282 patients with
NICM undergoing VT ablation. The results featured a 69% 5-year freedom from VT (after last
procedure) or death; 32% of patients needed epicardial ablation, and 36% required multiple
ablation procedures. Complications occurred in 4% including the need for 2 open-chest surgi-
cal repairs. An international registry reported on VT ablation in 780 NICM patients (of 2075
total) and found a 69% freedom from VT at 1 year and 62% freedom from VT, transplanta-
tion, or death.64 The outcomes varied significantly by NICM subtype, being better in ARVC
and worse in HCM, sarcoidosis, and valvular cardiomyopathy.
Compared with ischemic cardiomyopathy, patients coming to VT ablation exhibit less endocardial-
based scar and the location is often basal.6s The general approach is location of substrate (low-
voltage, either endocardially or epicardially), activation and/or entrainment mapping, or pace
mapping and ablation through isthmuses. Elimination of potential channels and connection of
low-voltage zones to the valve annulus may be useful. For NICM with scar (voltage <0.5 mv, or
delayed hyperenhancement on CMR), 1 study demonstrated lower recurrence with attempted
homogenization of the entire scar on the endocardial and epicardial surface.42
ii ii ii Ji i i I ii II I j I II ii i i Ii j I II
4$.ti() 47 47.60
/ .__,
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Pa.MIB
FIGURE 11-16 • Patient with RHntmnt VT Due to NICM. The patient has arrhythrnogenic blventrlcular cardlomyopathy due to a
pathogenic desmoplakln muttltion. Several morphologies of monomorphlc VTwere refractDry tD antlarrhythmlc drugs and required
multiple ICD interventions. Pinet A (left) shows entrainment of MMVT from the lamt-al trialspid annulus region with concealed fusion.
The right image shows late diastolic potentials on the map catheter, and during ablation the VT tenninates. Additional ablation of the
basal RV scar region (Panel 8) targeting abnormal potentfals was petfonned. Panel Bdlsplays 3 ek!cU'oanrtomle maps of the Rv. On
the left Is the activation map during 1heVT In Panel A. Asmall clockwlse reentry drcult near the lateral TA ls suggested, situated In the
low-voltage (l'ft.f, sr.an region shown In the mlddle Image. The right Image (same scale) shows that aside from the RVOT most of the
rest of the RV had preserved voltage. Panel C (left) shows Induction of a second morphology of VT from the lateral LV. llkely epk:Brdlel
given QS in lead I and avL Indeed, CMR (right panel} demonstrated midrnyocardial scar in the basal lamt'al LV wall {whitestripe in
nonnal dark myocardium). In the middle is the epicardial voltage map (using same scale as hnel A). Mapping found LAVA potentials
In the region and pace mapping mil'tChed the VT. Ablatlon was performed though limited by phrenlc capture In nearby regions. {If
desired, a balloon can be placed to displace the pericardium and phrenlc nenie.) Panel Dshows eplc.ardlal ac:ce.ss wtth shallow LAO
(on left) and lateral view (on right). Note the needle with contrast In the perlardlal space along with the guldewlre spanning across
multiple cardiac c:flembl!fs from left tD right and entefforto posterior conflrmlng that the wire Is In the perlardlal space.
PanelC
PanelD
Zeppenfeld nicely highlighted the diversity of NICM VT ablation driven by genetic and other
distinct etiologies.66 The incidence of monomorphic VT in ICD recipients varies dramatically
by NICM diagnosis, being muc:h higher in lamin cardiomyopathy. other arrhyth.mogenic: car-
diomyopathies, cardiac sarcoidosis, and Chagasic: cardiomyopathy, among others. The substrate
location for ablation varies too with lamin and sarc:oid affecting the septum most often (but
other areas as well) and Chagas and cardiomyopathy due to phospholamban mutations the infe-
rior and/or lateral walls. Identification of epicardial scar is usually defined by an (endoc:ardial)
unipolar voltage of <8.3 mv.67 Septal scar in the midmyocardial zone, confirmed by MRI, may be
correlated with a unipolar voltage of <4.8 mv. Abnormal epicardial voltage was found in both the
septum and free wall in 82% and infrequently in only the septum or free wall.68
Several NICM processes deserve some specific attention. First, cardiac sarcoidosis (see
Chapter 15) represents less than 5% ofNICM VT ablations but is challenging, often requiring
an epicardial approach. Long-term success is low with 80% having recurrence due to the
multiple foci, intramural and/or epicardial scar, and the progressive nature. It is important
to keep in mind the potential need for immunosuppression to help manage VT flare-ups.
Advanced options in refractory cases include transcoronary ethanol ablation and/or sympa-
thetic denervation.69-71
Next, regarding ARVC (Chapters 11 and 15), ablation outcomes have improved in recent years
due to frequent epicardial mapping and a goal of eliminating all potential endo- or epicardial
channels. In fact, current outcomes for ARVC exceed the average for NICM with only about
15%-20% recurrence at 1 year.M-72•73 As for other structural heart VT, ablation is still considered
palliative. However, a small (n=32) multicenter, international series reported no mortality and
low VT recurrence (19% at 4 years) in patients either unable to afford or who declined an
ICD.74 Another recent series raised the strategy of deferring epicardial mapping if endocardial
substrate is targeted and leads to clinical VT noninducibility. Adhesions from an initial (discre-
tionary) epicardial ablation could limit the ablative options after disease progression.75
HCM is a third challenging subgroup, accounting for about 4% of VT ablations within the
NICM realm.64 Within this small group, there are several unique subtypes including patients
with apical aneurysms and "burned-out" HCM with reduced LVEF as well as those with neither
feature. The apical aneurysmal patients' VT exhibits an RBBB, northwest axis, and QS in V4-6.
Most can be ablated via the endocardium, especially from the anterior rim of the aneurysm.76 In
other HCM patients, epicardial ablation is needed in about two-thirds.77 Some deep intramural
septal circuits prove refractory to standard approaches prompting use of transcoronary ethanol
or bipolar ablation. Overall, the recurrence rate is higher than the average for nonischemic
cardiomyopathy with about 40% suffering recurrence within 1 year.64
VENTRICULAR FIBRILLATION AND POLYMORPHIC VT: MAPPING AND ABLATION

Several approaches to VF mapping and ablation have been attempted. The most commonly
reported technique seeks to identify reproducible PVC triggers most often originating from
the Purkinje system, including those in the RV near the moderator band, and those associated
with either the LAF or LPF.78 Purkinje sources of PVCs triggering VF are temporally variable in
frequency becoming less frequent after VF storms resolve, for reasons unknown.79 The reason
that Purkinje fibers are common sources may include their electrical isolation from myocar-
dium, susceptibility to ischemia or electrolyte disturbance in provoking ectopy, reduced cou-
pling with myocardial interface during ischemia, and the geometric connections between fibers
providing pathways for reentry. In sinus rhythm these sites have sharp potentials immediately
preceding the QRS (10-15 ms) but the Purkinje spikes emerge up to 100 ms or more before
ectopic impulses (Figure 18-17). Fascicular, bundle branch, or complete AV block (which may
be preexisting or induced by mapping or ablation) is an impediment. Ablation may trigger VF,
and even VF storm, either immediately or in the early post-procedural state. Infrequent ectopy
is a challenge. but pace mapping can be attempted; preprocedural body surface mapping of
ambient ectopy may be a solution too.79
Several reports have identified RVOT triggers in patients with PMVT or VF. Of patients under-
going ablatio.n for RVOT arrhythmia, 16of101 had PMVT; some had prior syncope while others
had exhibited only palpitations. The mechanism appeared to be triggered activity. not reentry,
based on an absence offractionated potentials. Most foci were in the posterior (or septal) RVOT
with 20% being free wall in origin.80
VF in the setting of prior MI, including VF storm, may be mediated by Purkinje fiber PVCs.
A recent series reported on 110 patients with VF storm due to prior Ml.81 The VF storm
occurred in the first 48 hours of infarction in -40%, subacutely (> 1 week after MI) in 4096,
and remote from infarction in the remainder (-2096). These Purkinje tissue PVCs, with
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Panel A
FIGURE 18-17 • Incessant, PVC-induced ventricular fibrillation. The patient presented with SCA and had recurrent VF requiring
multtple deflbrtllattons. hnet A shows frequent recurrent runs of rapid pclymorphlc VT often continuing Into VF. Note that the flrst
2 beats are ldentlail for each run of VT. He was treated with beta blockefs, general anesthesla, and multlple antlarrhythmlc drugs.
A resting 12-lead ECG and MRI were normal. The arrhytflmla subsided, foiling an EP study seeking to ablate the triggering PVCs;
he had no lndudble anhythmias and no spontllneaus PVCs occurred. He was discharged with an ICD and therapy with flealnlde
and bet! blocker. Panel B shows the ICD record of 24 episodes ofsustained and nons1ntalned VT/VF- within a 2-hour period, with
zero episodes over the previous 2 months. Various antiarrhythmics have been unsuccessful at preventing the intermittent flur-
ries of arrhythmia whose timing has defied Invasive Intervention so far. Biiaterai cervlcal sympathettc denervatlon seems to have
helped. Panel C: Twelve-lead ECG with associated endoardlal electrograms of a PVC arising from the left posterforfasclcular region
Purklnje system {from a different patient). The PurklnJe fasdcular potenttals precede QRS onset by 18 ms during sinus rhythm (bluf!
a"ow}. During the PVC. Purklnje potentials precede QRS onset by 108 ms (b/Uf! arrows}. Notice the presence of a retrograde Purklnje
potential (fed arrow} too. (Reproduced with pe1mlsslon from Chenltl G, et al. Mapping and ablatlon of idiopathic ventricular flbrill~
tion. Front Cardiovasc Med. 2018;5:123.)
ATP Time Duration Avg bpm Max bpm Activity at
Type Shocks Success ID# Date
Seq hh:mm hh:mm:ss AN AN Onset
VF 0 35J Yes 94 11-Jan-2017 01:21 :01 :14 97/194 -1240 Rest
Last Programmer Session 11-Jan-2017 -------
VT-NS 93 11.Jan-2017 01 :02 :01 831293 Rest
VF 0 92 11.Jan-2017 00:55 :04:24 911176 --1261 Rest
VT-NS 91 11.Jan-2017 00:35 <:01 821286 Rest
VT-NS 90 11.Jan-2017 00:35 :01 851279 Rest
VT-NS 89 11.Jan-2017 00:35 :01 83/300 Rest
VT-NS 88 11.Jan-2017 00:34 <:01 811273 Rest
VT-NS 87 11.Jan-2017 00:21 <:01 951273 Active
VF 0 35J Yes 86 11.Jan-2017 00:17 :15:46 94/188 -I- Rest
High Rate-NS 85 11-Jan-2017 00:16 :03 871279 Rest
High Rate-NS 84 11.Jan-2017 00:16 :01 821290 Rest
VT-NS 83 11-Jan-2017 00:16 :01 811300 Rest
VT-NS 82 11-Jan-2017 00:16 :01 871207 Rest
VT-NS 81 11-Jan-2017 00·16 :01 901250 Rest
VT-NS 80 11-Jan-2017 00:16 :01 821324 Rest
VT-NS 79 11-Jan-2017 00·16 <:01 821240 Rest
VT-NS 75 11.Jan-2017 00:15 :01 791286 Rest
VT-NS 74 11.Jan-2017 00:14 :01 791273 Rest
VT-NS 73 11-Jan-2017 00:14 :01 86/300 Rest
VT-NS 71 11-Jan-2017 00:13 :01 921300 Rest
VF 0 35J Yes 63 10.Jan-2017 23:33 :07:32 97/194 113/261 Rest
VF 0 18-0ct-2016 08:20 :15 1151400 -I- Rest
Panel B
I 200ma
FIGURE 1•'17 • (Continued)

472
preceding Purkinje spikes, were often in the septum or either PM and mapped to the border
zone in 80% and the dense scar in 14%.81 In the absence of PVCs, substrate-based ablation tar-
geting the scar may be effective. 81•82 This ablation strategy often (-80%) helps resolve VF storm,
but hospital mortality is high. Complications included LBBB (7%}, complete AVB (1 %), stroke
(1 %), worsening HF (4%), and intraprocedural death due to PEA (1 %). Delay in time from VF
storm to ablation predicted mortality.81 Although elimination of the trigger may be the goal,
Nogarni has noted that creation of exit block from the Purkinje network may be an operative
mechanism for ablation.u Due to the superficial nature of the Purkinje network, ablation
at 30 W with an irrigated catheter usually suffices because transmural lesions are not needed
unless adjunctive substrate ablation is pursued.
Another approach to VF ablation seeks to identify sites of reentry and target these for ablation.
In a canine model, VF (CL 121 ± 13 milliseconds) was initiated with very rapid burst pacing
(150 ms for 5 seconds} and mapped using basket catheters in both ventricles. The 64 unipolar
recordings were analyzed with a proprietary phase mapping algorithm. The RV rarely had sta-
ble rotors, but 56% of VF "beats" exhibited an LV rotor that persisted for an average of 10 rota-
tions. Sham ablation at distant sites did not affect VF inducibility but ablation at the location of
the rotors rendered 6 of 9 canines noninducible into VF with the other 3 requiring more rapid
burst pacing to induce VF. Purkinje potentials were not found more to be present at the rotor
sites. In one patient with drug-refractory, recurrent VF, rotors were identified at infarct border
zones in the RV and LV, distant from PMs and without Purkinje potentials, and ablation led to
freedom from VF.84 Other animal mapping studies of VF have identified phases during ongoing
VF with different activation patterns, some exhibiting dominant rotors.85
HEMODYNAMIC SUPPORT
Patients undergoing VT (or VF) ablation often exhibit tenuous baseline hemodynamics, which is
compounded by the hemodynarnic insult from spontaneous or induced VT/VF. This has spurred
interest in providing temporary hemodynamic support for these procedures (Figure 18-18).
Options include intra-aortic balloon pump, partial ventricular assist devices (PVAD; either
Impella or TandemHeart), and extracorporeal membrane oxygenation (ECMO). Decompensa-
tion during scar-related VT/VF ablation occurs in 10% or more of procedures and incurs a high
mortality rate. Predictors have been identified and include: ischemic cardiomyopathy, advanced
age, diabetes, general anesthesia, advanced HF, lower EF, and VT/VF storm.86,87 Knowing the
adverse prognosis for an intraprocedural decompensation and equipped with some ability to pre-
dict it, an interest in prophylactic hemodynamic support has grown.87-•9•91-94 Randomized trials are
lacking, but a propensity-matched study showed that the prophylactic PVAD group exhibited a
lower incidence ofhemodynamic collapse and I-year mortality. Studies have not demonstrated a
reduced VT recurrence rate, however. PVAD-related complications, especially vascular ones, are
frequent and these may be life-threatening.
The different support options vary considerably. Only ECMO supports the patient with RV as
well as LY dysfunction, and only ECMO is usable in patients with significant aortic regurgita-
tion. Impella can interfere with mapping by generating EMI. The Tandem Heart cannula occu-
pies transseptal access, whereas Impella generally precludes retrograde access for mapping. In
addition, spontaneous aortic valve opening may be limited during circulatory support, making
retrograde access problematic. Detailed reviews have been published.87•90
PanelD
Panel A PanelB
PanelC
PanelE
FIGURE 11-11 • Hemodynllmlc support systems used for VT abl11fon. Panel A:. Intra-aortic balloon pump (IABP) provides reduced
afterload for LV ejection. Panel B: Schematic drawing of lmpella system (left ventricular Inflow, ascending aorta outflow). Pantll C
Schematic drawing of Tandem Heart systl!m (left atrial Inflow, right lilac artery outflow). Panel D: Schematic drawing of extraa>fporeal
membrane oxygenation (ECMO) from RA to pe1ipheral artery. {Panefs A-C. reproduced with petmission from Desai NR. Bhatt DL Eval-
uatlng percutaneous support for earcllogenlc shock: data shock and S'tlcket' shock. Eur HeortJ. 2009',30'.2073-2075. Panel Dreproduced
with pennl$$1on from Guglln M, et al Venoarterfal ECMO for adults: JACC scientific expert panef.JAm Coll C/Jrdfol. 2019;73:698-716.)
REFERENCES
1. YOUBUf OK. et at 'lrend.s and. outi::omes of catheter ablation for V1:IltricWar tac.:hyc:aniia in a. c.:ommunity c.ohort.
JACC: Cliniail Bl~logy. 2018.
2. Okada. DR, et al. Ventricular arrhythmias in cardiac sarcoid.osis. CircultztUm. 2018;138:1253-1264.
3. Saremi F, Ho SY, Cabrera JA, Sanc.het-Quintana. D. Right ventricular outflow tract imaging with CT and MRI:
part 1, morphology. AJR Am JRomtgmoL 2013;200:W39-WSO.
4. Sa.uc.he.i-Qulntuia. D, Doblado-Calatraw. M. Cabrera JA, Macias Y, Saremi F. Anatomical bas.ls for the c:arcll.ac
intervenlional elec:trophysiologist. Biomed Ru Int. 2015;2015:547364.
5. Asirvatb.am SJ. Conela.tive anatomy for the inv.uive electrophysiologist: outflow tract and supravalvv anhJthmia.
l Omliowuc BlectrophysioL 2009;20:955-968.
6. Andmcn RH. Clinical anatomy of the aortic.: root. Hlart. 2000;84:670-673.
7. Stamm C. Allde.rson RH, Ho SY. Clinical anatomy of the normal pulmo.nary root compared with that ID. Isolated
pulmonary valwlar stenos.ls. JAm CcU Omllot l 998;31:1420-1425.
8. Sutton JP, Ho SY, Anderson RH. The forgotten interleaftet triang.tes: a review ofthe surgical mammy of the aortic.:
wlve. Ami Tlumu:. Surg. 1995;59:419-427.
9. Gami AS, et at Anatomical conela.tet relewnt to ablation above the smillunar wlve.! for the cardiac elec:trophpi-
ologist: a lltudy of 603 hearts. l Ittterv Qmi Blatroph}'$1oL 2010;30:5-15.
10. Cheung Jw. Andenon RH, Markowitz SM, Lerman BB. Catheter ablation of arrhythmias orlgin.atlng from the
left ventrlctilar outflow tract. JACC Clln BkctrophyrioL 2019;5:1-12.
11. Beten&ky BP. et al. The V(2) transition ratio: a new electroc:a.rdlographic: criterion for distinguishing left &om right
ventrictilar oudlowtract tachycardia. origin. I Am CcU QmlioL 2011;57:2255-2262.
12. Daniels DV. et al. Idiopathic.: epi.cardial left ventric:ular tac.:hycardia originating Rm.ate from the sinus of Vahalva:
electrophys:iological dwa.cteristics, catheter ablation, and identification from the 12-lead elec:troc:ardiogram.
Cfrl:ulatlon. 2006;113:1659-1666.
13. Haqqani HM, Morton JB, Kalman JM. Using the 12-lead ECG to localize the origin of atrial and ventricular tachy-
cardias: part 2-ventricular tachycardia. J Cardiowisc Electrophysiol. 2009;20:825-832.
14. Mountantonakis SE, et al. Ventricular arrhythmias from the coronary venous system: prevalence, mapping, and
ablation. Heart Rhythm. 2015;12:1145-1153.
15. Hoffmayer KS, et al. Safety of radiofrequency catheter ablation without coronary angiography in aortic cusp ven-
tricular arrhythmias. Heart Rhythm. 2014;11:1117-1121.
16. Latchamsetty R, et al. Multicenter outcomes for catheter ablation of idiopathic premature ventricular complexes.
JACC Clin ElectrophysioL 2015;1:116-123.
17. Zipes DP, Foster PR, 'Iioup PJ, Pedersen DH. Atrial induction of ventricular tachycardia: reentry versus triggered
automaticity. Am J Cardiol. 1979;44:1-8.
18. Klein GJ, Millman PJ, Yee R. Recurrent ventricular tachycardia responsive to verapamil. Pacing Clin ElectrophysioL
1984;7:938-948.
19. German LD, Packer DL, Bardy GH, Gallagher JJ. Ventricular tachycardia induced by atrial stimulation in patients
without symptomatic cardiac disease. Am/ Cardial. 1983;52:1202-1207.
20. Belhassen B, Rotmensch HH, Laniado S. Response of recurrent sustained ventricular tachycardia to verapamil. Br
Heart/. 1981;46:679-682.
21. Liu Y, et al. Catheter ablation of fascicular ventricular tachycardia: long-term clinical outcomes and mechanisms
of recurrence. Circ Arrhythm Electrophysiol. 2015;8: 1443-1451.
22. Nogami A, et al. Verapamil-sensitive left anterior fascicular ventricular tachycardia: results of radiofrequency
ablation in six patients. J Cardiowisc Electrophysiol. 1998;9: 1269-1278.
23. Nakagawa H, et al. Radiofrequency catheter ablation ofidiopathic left ventricular tachycardia guided by a Purkinje
potential. Circulation. 1993;88:2607-2617.
24. Nogami A, et al. Demonstration of diastolic and presystolic Purkinje potentials as critical potentials in a macrore-
entry circuit of verapamil-sensitive idiopathic left ventricular tachycardia. J Am Coll Cardiol. 2000;36:811-823.
25. Nogami A. Purkinje-related arrhythmias part I: monomorphic ventricular tachycardias. Pacing Clin Electrophysial.
2011;34:624-650.
26. Kapa S, Gaba P, DeSimone CV, Asirvatham SJ. Fascicular ventricular arrhythmias: pathophysiologic mechanisms,
anatomical constructs, and advances in approaches to management. Circ Arrhythm Electrophysiol. 2017;10.
27. Lin D, et al. Idiopathic fascicular left ventricular tachycardia: linear ablation lesion strategy for noninducible or
nonsustained tachycardia. Heart Rhythm. 2005;2:934-939.
28. Talib AK. et al. Verapamil-sensitive upper septal idiopathic left ventricular tachycardia: prevalence, mechanism,
and electrophysiological characteristics. /ACC Clin Electrophysiol. 2015;1:369-380.
29. Doppalapudi H, et al. Ventricular tachycardia originating from the posterior papillary muscle in the left ventricle:
a distinct clinical syndrome. Circ Arrhythm Electrophysial. 2008;1:23-29.
30. Yamada T, et al. Idiopathic focal ventricular arrhythmias originating from the anterior papillary muscle in the left
ventricle. J Cardiovasc Electrophysiol. 2009;20:866-872.
31. Santoro F, et al. Ventricular tachycardia originating from the septal papillary muscle of the right ventricle: electro-
cardiographic and electrophysiological characteristics. J Cardiovasc Electrophysiol. 2015;26: 145-150.
32. Rivera S, et al. Cryoablation for ventricular arrhythmias arising from the papillary muscles of the left ventricle
guided by intracardiac echocardiography and image integration. JACC: Clin Electrophysiol. 2015;1:509-516.
33. Enriquez A, Supple GE, Marchlinski FE, Garcia FC. How to map and ablate papillary muscle ventricular arrhyth-
mias. Heart Rhythm. 2017;14:1721-1728.
34. Gordon JP, et al. Percutaneous cryoablation for papillary muscle ventricular arrhythmias after failed radiofre-
quency catheter ablation. J Cardiowisc Electrophysiol. 2018;29:1654-1663.
35. Hourdain J, et al. Common phenotype in patients with mitral valve prolapse who experienced audden cardiac
death. Circulation. 2018;138:1067-1069.
36. Syed FF, et al. Sites of successful ventricular fibrillation ablation in bileaflet mitral valve prolapse syndrome.
Gire Arrhythm Electrophysiol. 2016;9.
37. Reimer KA, Lowe JE, Rasmussen MM, Jennings RB. The wavefront phenomenon of ischemic cell death. 1.
Myocardial infarct size vs duration of coronary occlusion in dogs. Circulation. 1977;56:786-794.
38. Bolick DR, Hackel DB, Reimer KA, Idekt:r RE. Quantitative analysis of myocardial infarct structure in patients
with ventricular tachycardia. Circulation. 1986;74:1266-1279.
39. Stevenson WG, Friedman PL, Sager PL, et al. Exploring postinfarction reentrant ventricular tachycardia with
entrainment mapping. J Am Coll Cardiol. 1997;29:1180-1189.
40. Di Biase L, et al. Ablation ofstable VTs versus substrate ablation in ischemic cardiomyopathy: the VISTA random-
ized multicenter trial. J Am Coll Cardiol 2015;66:2872-2882.
41. Jais P, et al. Elimination oflocal abnormal ventricular activities: a new end point for substrate modification in
patients with scar-related ventricular tachycardia. Circulation. 2012;125:2184-2196.
42. Gokoglan Y, et al. Scar homogenization versus limited-substrate ablation in patients with nonischemic cardiomy-
opathy and ventricular tachycardia. J Am Coll Cardiol. 2016;68:1990-1998.
43. Berruezo A, et al. Scar dechanneling: new method for scar-related left ventricular tachycardia substrate ablation.
Circ: Arrhythm Electrophysiol. 2015;8:326-336.
44. Thou WS, et al Core isolation of critical arrhythmia elements for treatment of multiple scar-based ventricular
tachycardias. Circ: Arrhythm Electrophysiol. 2015;8:353-361.
45. Maskoun W, Saad M, Abualsuod A, Nairooz R, Miller JM. Outcome of catheter ablation for ventricular tachycar-
dia in patients with ischemic cardiomyopathy: a systematic review and meta-analysis of randomized clinical trials.
Int I Canliol. 2018;267:107-113.
46. Santangeli P, et al. Early mortality after catheter ablation ofventricular tachycardia in patients with structural heart
disease. J Am Coll CardioL 2017;69:2105-2115.
47. Tchou P, et al. Tra.nscatheter electrical ablation of right bundle branch. A method of treating macroreentrant ven-
tricular tachycardia attributed to bundle branch reentry. Circulation. 1988;78:246-257.
48. Akhtar M, et al. Demonstration ofre-entrywithin the His-Purkinje system in man. Circulation. 1974;50:1150-1162.
49. Chen H, et al Electrophysiological characteristics of bundle branch re entry ventricular tachycardia in patients
without structural heart disease. Circ: Arrhythm ElectrophysioL 2018;1 l:e006049.
50. Blanck Z. Deshpande S, Jazayeri MR, Akhtar M. Catheter ablation of the left bundle branch for the treatment of
sustained bundle branch reentrant ventricular tachycardia. J Cardiovasc ElectrophysioL 1995;6:40-43.
51. Pathak RK, et al. Long-term outcome of catheter ablation for treatment of bundle branch re-entrant tachycardia.
JACC Clin Electrophysiol. 2018;4:331-338.
52. Crijns HJ, Smeets JL, Rodriguez LM, Meijer A, Wellens HJ. Cure of interfascicular reentrant ventricular tachycar-
dia by ablation of the anterior fascicle of the left bundle branch./ Cardiovasc ElectrophysioL 1995;6:486-492.
53. Blanck Z, Sra J, Akhtar M. Incessant interfascicular reentrant ventricular tachycardia as a result of catheter ablation
of the right bundle branch: case report and review of the literature. J Cardiovasc Electrophysiol. 2009;20: 1279-1283.
54. Sosa E, Scanavacca M, d'.Avila A, Pilleggi F. A new technique to perform epicardial mapping in the electrophysiol-
ogy laboratory. I Cardiovasc ElectrophysioL 1996;7:531-536.
55. Lach.man N, et al. Correlative anatomy for the electrophy•iologist, part I: the pericardia] space, oblique sinU5,
transverse sinus. J Cardiovasc E/ectrophysioL 2010;21:1421-1426.
56. Cano 0, et al Electroanatomic substrate and ablation outcome for suspected epicardial ventricular tachycardia in
left ventricular nonischemic cardiomyopathy. I Am Coll CardioL 2009;54:799-808.
57. Sarkozy A, et al. Epicardial ablation of ventricular tachycardia in ischemic heart disease. Circ Arrhythm Electro-
physiol. 2013;6:1115-1122.
58. Sacher F, et al. Epicardial ventricular tachycardia ablation: a multicenter safety study. J Am Coll Cardiol.
2010;55:2366-2372.
59. Nakamura T, et al. Complications and anticoagulation strategies for percutaneous epicardial ablation procedures.
Circ: Arrhythm Electrophysiol. 2018;11:e006714.
60. Keramati AR, et al. Anterior pericardia] access to facilitate electrophysiology study and catheter ablation of ven-
tricular arrhythmias: a single tertiary center experience. J Cardiovasc E/ectTOphysioL 2017;28:1189-1195.
61. Kumar S, et al. "Needle-in-needle• epicardial access: preliminary observations with a modified technique for facil-
itating epicardial interventional procedures. Heart Rhythm. 2015;12:1691-1697.
62. Dinov B, et al. Outcomes in catheter ablation of ventricular tachycardia in dilated nonischemic cardiomyopathy
compared with ischemic cardiomyopathy: results from the Prospective Heart Centre of Leipzig VT (HELP-VT)
Study. Circulation. 2014;129:728-736.
63. Kumar S, et al. Long-term outcomes after catheter ablation ofventricular tachycardia in patients with and without
structural heart disease. Heart Rhythm. 2016;13:1957-1963.
64. Vaseghi M, et al Outcomes ofcatheter ablation ofventricular tachycardia based on etiologyin nonischemic heart disease:
an international ventricular tachycardia ablation center collaborative study. JACC Clin Electrophysiol. 2018;4: 1141-1150.
65. Hsia H, Marchlinski FE. Characterization ofthe electroanatomic substrate for monomorphic ventricular tachycar-
dia in patients with nonischemic cardiomyopathy. Pacing Clin E/ectrophysioL 2002;25: 1114-1127.
66. Zeppenfeld K. Ventricular tachycardia ablation in nonischemic cardiomyopathy. ]ACC Clin Electrophysiol.
2018;4:1123-1140.
67. Hutchinson MD, et al. Endocardial unipolar voltage mapping to detect epicardial ventricular tachycardia substrate
in patients with nonischemic left ventricular cardiomyopathy. Gire Arrhythm E/ectrophysioL 2011;4:49-55.
68. Liang JJ, et al Importance of the interventricular septum as part of the ventricular tachycardia substrate in noni5-
chemic cardiomyopathy. JACC Clin ElectrophysioL 2018;4:1155-1162.
69. Markowitz SM, et al. Treatment of intramural ventricular tachycardia in cardiac sarcoidosis with transcoronary
ethanol ablation. Europace. 2017; 19: 1921.
70. Okada DR, et al. Cardiac sympathectomy for refractory ventricular arrhythmias in cardiac sarcoidosis. Heart
Rhythm. 2019.
71. Papageorgiou N, et al. Catheter ablation for ventricular tachycardia in patients with cardiac sarcoidosis: a system-
atic review. Europace. 2018;20:682-691.
72. Corrado D, et al. Treatment of arrhythmogenic right ventricular cardiomyopathy/dysplasia: an International Task
Force Consensus Statement Circulation. 2015;132:441-453.
73. Berruezo A, et al. Combined endocardial and epicardial catheter ablation in arrhythmogenic right ventricular
dysplasia incorporating scar dechanneling technique. Circ A"hythm Electrophysiol. 2012;5:111-121.
74. Santangeli P, et al. Outcomes of catheter ablation in arrhythmogenic right ventricular cardiomyopathy without
background implantable cardioverter defibrillator therapy: A Multicenter International Ventricular Tachycardia
Registry. JACC Clin Electrophysiol 2019;5:55-65.
75. Mathew S, et al Catheter ablation of ventricular tachycardia in patients with arrhythmogenic right ventricular
cardiomyopathy/dysplasia: a sequential approach. J Am Hearl Assoc. 2019;8:e010365.
76. lgarashi M, et al Radiofrequency catheter ablation ofventricular tachycardia in patients with hypertrophic cardio-
myopathy and apical aneurysm. JACC Clin Elutrophysiol 2018;4:339-350.
77. Santangeli P, et al. Radiofrequency catheter ablation of ventricular arrhythmias in patients with hypertrophic car-
diomyopathy: safety and feasibility. Heart Rhythm. 2010;7:1036-1042.
78. Anderson RD, et al. Catheter ablation ofventricular fibrillation. Heart Lung Circ. 2019;28: 110-122.
79. Cheniti G, et al. Mapping and ablation of idiopathic ventricular fibrillation. Front Cardiowuc Med. 2018;5:123.
80. Noda T, et al. Malignant entity of idiopathic ventricular fibrillation and polymorphic ventricular tachycardia initiated
by premature extrasystoles originating from the right ventricular outflow tract JAm Coll Cardiol. 2005;46:1288-1294.
81. Komatsu Y, et al. Catheter ablation of refractory ventricular fibrillation storm after myocardial infarction: a mul-
ticenter study. Circulation. 2019.
82. Nakamura T, et al. Catheter ablation of polymorphic ventricular tachycardia I fibrillation in patients with and
without structural heart disease. Heart Rhythm. 2019.
83. Nogami A, Sugiyasu A, Kubota S, Kato, K. Mapping and ablation of idiopathic ventricular fibrillation from the
Purkinje system. Heart Rhythm. 2005;2:646-649.
84. Krummen DE, et al. Modifying ventricular fibrillation by targeted rotor substrate ablation: proof-of-concept from
experimental studies to clinical VF. J Cardiovasc Electrophysiol. 2015;26:1117-1126.
85. Panitchob N, et al. Endocardial activation drives activation patterns during long-duration ventricular fibrillation
and defibrillation. Circ Arrhythm ElectrophysioL 2017; 10.
86. Santangeli P, et al. Acute hemodynamic decompensation during catheter ablation of scar-related ventricular tachy-
cardia: incidence, predictors, and impact on mortality. Circ Arrhythm Electrophysiol 2015;8:68-75.
87. Virk SA, et al Mechanical circulatory support during catheter ablation of ventricular tachycardia: indications and
options. Heart Lung Circ. 2019;28:134-145.
88. Enriquez A, et al. Outcomes of rescue cardiopulmonary support for periprocedural acute hemodynamic decom-
pensation in patients undergoing catheter ablation of electrical storm. Heart Rhythm. 2018;15:75-80.
89. Turagam MK, et al. Percutaneous ventricular assist device in ventricular tachycardia ablation: a systematic review
and meta-analysis. J Interv Card ElectrophysioL 2018.
90. Keebler ME, et al. Venoarterial extracorporeal membrane oxygenation in cardiogenic shock. JACC Heart Pail
2018;6:503-516.
91. Desai NR, Bhatt DL. Evaluating percutaneous support for cardiogenic shock: data shock and sticker shock. Eur
Heart J. 2009;30:2073-2075.
92. Guglin M, et al. Venoarterial BCMO for adults: JACC scientific expert panel. J Am Coll CardioL 2019;73:698-716.
93. Monaco F, Belletti A, Bove T, Landoni G, Zangrillo A. Extracorporealmembrane oxygenation: beyond cardiac surgery
and intensive care unit unconventional uses and future perspectives. J Cardiothorac Vase Anesth. 2018;32:1955-1970.
94. Al-Khatib SM, et al. 2017 AHA/ACCffiRS Guideline for Management of Patients With Ventricular Arrhythmias
and the Prevention of Sudden Cardiac Death: Executive Summary: A Report of the American College of Cardiology/
American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. I Am Coll
CardioL 2017.
95. Li A, et al. Endocardial ablation ofventricular ectopic beats arising from the basal inferoseptal process of the left
ventricle. Heart Rhythm. 2018;15:1356-1362.
96. Kawamura M, et al. Clinical and electrocardiographic characteristics of idiopathic ventricular arrhythmias with
right bundle branch block and superior uis: comparison of apical crlJl[ area and posterior septa! left ventricle.
Heart Rhythm. 2015;12:1137-1144.
Cardiac Implantable
Electronic Devices
INTRODUCTION
The very first cardiac implantable electronic devices (CIED) were single-chamber, ventricular
pacemakers with epicardial leads that offered only asyncluonous pacing. Essentially only
fixed or intermittent complete AV block was treatable. Patients had Stohs-Adams attacks and
life-threatening asystolic episodes. Transvenous leads led to less invasive implantation, and then
dual-chamber pacing allowed restoration ofAV synchrony for AV block patients and treatment
of sinus bradycardia with AV pacing. In the 1980s, implantable defibrillators were inserted,
initially for patients with recurrent sudden cardiac arrest (SCA, see Chapter 15). These followed
a similar evolution from epic.ardial to transvenous leads and from single to dual chamber as
technology developed. Indications expanded due to such progress and to clinical trials. More
recently, biventricular pacing in select patients with LBBB has been used for cardiac resynchro-
nization therapy (CRT). His bundle pacing has reemerged with the focus on more physiologic
pacing. While transvenous leads offered easier implantation than epicardial ones, long-tenu
risks include intravascular infection. and their removal in the event of either intravascular or
pocket infection or failure, poses significant risks. Thus, miniaturized, lead.less pacemakers and
subcutaneous defibrillators have been developed.
The indications for pacing have recently been updated,1 and the reader is referred to a discus-
sion of the causes ofbradycardia in Chapter 10 and indications for ICD in Chapter 15. In brief,
pacing to treat symptomatic bradycardia is needed either for a failure of impulse generation in
the sinus node or failure of AV conduction. Sinus node dysfunction is defined, in part, as a rest-
ing rate less than 50 bpm, diurnal pauses exceeding 3 seconds. and/or failure to augment heart
rate sufficiently with exercise (chronotropic incompetence). Recognition of reversible causes for
bradycardia, or normal variants (such as bradycardia or pauses due to high vagal tone in ath-
letes) and avoiding pacing in these cases constitutes l of the main c:hallenges.1 The other main
task is associating symptoms to the bradycardia. especially for sinus node dysfunction, because
it is rarely a life-threatening condition. AV block. on the other hand, requires a consideration of
pacing in some potentially asymptomatic scenarios, such as alternating bundle branch block.
Mobitz II block. or for prolonged HV interval (detectable at EP study; see Chapters 10 and 16).
Several types of patients present challenges from an indication perspective. With sinus
node dysfunction, it can be difficult firmly to link symptoms with significant bradycardia.
One should be wary of being asked to implant the patient before clarifying the time of day of
a tracing and/or any attendant symptoms. Prolonged monitoring, exercise testing, and a thor-
ough history sometimes resolve the uncertainty. If the situation remains unclear, these patients
can be followed closely before deciding on device implantation. With regard to the chrono-
tropic incompetence (Cl) subtype of sinus node dysfunction, it is again important to elicit
symptoms, although they can be subtle due to the patient's adjustment to their limitations.
Appropriate age and sex references are required too. Anecdotally, patients with severe Cl man-
ifest significant improvement with pacing. In less dramatic examples, Cl has been associated
with adverse survival, both in general2 and in HF patients, but controversy exists on whether it
is the cause of reduced exercise capacity, and the associated adverse survival.3•4 Moreover, while
beta blockers reduce mortality, they may exacerbate Cl.
In terms of AV block, first-degree AV block very rarely warrants pacing. Nevertheless, with
extreme PR interval prolongation, atrial contraction may occur while the AV valve remains
closed from the prior systolic event. Likewise, asymptomatic Wenckebach (Mobitz I) AV block
patients should not receive a pacemaker, but if the nonconducted beats are very frequent, and
lead to symptomatic bradycardia, then pacing is appropriate. With Mobitz II block, or with
infranodal AV block, pacing is warranted. (See Chapters 10 and 16.) Chapter 14 discusses the
role of pacing in vasovagal syncope also. 5.6 It is important to distinguish vagally mediated AV
block from "paroxysmal AV block." The latter lacks P-P prolongation and generally begins and
ends with a premature complex, often ventricular.7 Idiopathic AV block resembles paroxysmal
AV block in lacking vagal-like P-P slowing during episodes of AV block, but it is not punctuated
by extrasystoles. These patients have a normal ECG and lack overt heart disease. The proposed
mechanism of AV block is enhanced sensitivity to adenosine-mediated via Al receptors in the
AV node. The cohort described thus far has not exhibited progressive permanent AV block, and
has been effectively treated by pacing.8 Syncope in the setting of BBB is another vexing problem
as it may be due to intermittent complete AV block with risk of recurrent, abrupt syncope and
potentially dangerous falls in an often elderly population. Its evaluation and the role ofthe invasive
assessment of the conduction intervals are addressed elsewhere. (See Chapters 10, 14, and 16.)
Selected BBB patients with syncope may warrant empiric pacing; however, this scenario quali-
fies as a Class IIB indication. 9
SINGLE-AND DUAL-CHAMBER PACEMAKERS

Single-chamber right ventricular pacemaker systems are used for symptomatic bradycardia in
the setting of permanent atrial fibrillation. They can be used in infrequent AV block. Random-
ized trials have shown slightly superior outcomes with dual-chamber pacing compared with
ventricular only pacing, especially with regard to atrial fibrillation in follow-up. The occurrence
of heart failure had a near significant reduction, and various symptomatic outcomes have been
better with dual-chamber pacing. 10 Thus, patients with either sinus node dysfunction or AV
block who are indicated for pacing generally receive a dual-chamber system. An exception
could be the elderly, frail patient who is relatively immobile in whom a simpler single-chamber
ventricular device is reasonable. Single-chamber atrial pacemakers can treat sinus bradycar-
dia with intact AV conduction, but are rarely used because AV block can develop and 1 trial
showed lack of efficacy compared with dual-chamber systems. 11 In young patients with isolated
sinus node dysfunction and low risk for AV nodal disease, an AAI device warrants consider-
ation, and indeed they are used with greater frequency outside the United States.
CHAPTER 19 • Cardiac Implantable Electronic Devices 481
Content Chamber paced Chamber sensed Response to sensing Rate modulatlon

o,rtlons O=None O=None O=None O=None
A=Atrfum A= Atrium T =Triggered R=Rate modulation
V =Ventricle V=Ventricle I= Inhibited
D =Dual (A+V) D =Dual (A+V) D =Dual (T+I)
The function of mod.em pacing systems has become fairly complex with multiple algorithms,
but the basic behavior is relatively straightforward. A 3-letter (or more) naming convention
describes the pacing mode (Table 19-1). Single-chamber ventricular pacing can be either asyn-
chronous (VOO) or synchronous (VVI). In VOO, the pacemaker emits a pacing pulse at the
expiration ofa timing cycle based on the programmed pacing rate, for instance. An intervening
native beat will not reset the clock in VOO but will for VVI (Figure 19-1). A magnet applied to
a pacemaker will temporarily change the operating mode from synchronous (e.g., VVI) to asyn-
chronous (e.g., VOO) (Figure 19-1). VOO in this situation helps confirm capture and is used in
the operating room to prevent inhibition of pacing by electrocautery. The magnet also elicits a
characteristic pacing rate that lessens as battery depletion occurs. Thus, the maneuver can eval-
uate battery status too. The other common single-chamber mode is VVIR with the fourth letter
I I I
PanelB
FIGURE , .,, • Ventricular pacing mode1. Panel A shows pacemaker operation in VOO mode. Note pacing at
the programmed rate continues despite a native beat occurring. Panel BIllustrates pacemaker oper;11tton In WI
mode. Note that the native beat reset$ the lower rate •crock."
Ventri- Ventri- Ventri- Ventri- Ventri-

cular cular cular cular cular
pace pace sense pace Unsensed
I
I
I
I
I I
I I I I I
~ l:~;,;;;;~::::::::=:J:~:=:- ~:::::=:·:::_ rii:~:=:·:::::::__ .;·

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0
L-------1
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! !;I
I
i I !;I Fil
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Resat Reset
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AEI
Fundamental intervals Derived intervals

0 LRI = Lower rate interval TARP = Total atrial refractory period
=AVI + PVARP
© VRP = Ventricular refractory period = Upper rate interval
=URI
© AVI = Atrioventricular interval
AEI =Atrial escape interval
© PVARP = Postventricular atrial refractory period = LRl-AVI
FIG URE 19-2 • Dual-chamber pacing modes. The schematic ii lustrates the function of a pacemaker in DDD mode, illustrating
pacing as well as sensing in both the atrium and ventricle. Several intervals are critical to understanding function as shown!'
(Modified with permission from Baroid SS, Stroobandt R, Sinnaeve AF. Cardiac Pacemakers and Resynchronization Step by Step: An
Illustrated Gulde. 2nd ed. West Sussex, UK: Wiiey-Biackweii; 2010. e 201 Oby S. Serge Baroid, Roland X. Stroobandt, and Alfons F.
Sinnaeve.)
indicating rate response modulation, wherein the pacing rate is increased in proportion to the
sensed activity of the patient, thus supporting a higher cardiac output and workload.
The most common dual-chamber mode(s) had until recently been DDD (or DDDR) in which
the device may sense or pace in the atrium, then similarly either sense or pace in the ventri-
cle, (Figure 19-2) either at a base rate (or with rate response). While these modes restore AV
synchrony, they also exhibit 2 problems: (I) tracking an atrial tachyarrhythmia such as atrial
fibrillation, leading to rapid ventricular pacing up to the upper programmed rate and (2) a high
degree of (right) ventricular pacing even in non-pacemaker-dependent patients, especially those
with sinus node dysfunction but some degree of PR prolongation. Addressing the first issue, the
device can use the atrial channel to detect a nonphysiologic atrial rate and then switch modes
to a single-chamber-like ventricular mode while still watching for the possible restoration of
normal atrial rhythm, prompting a return to dual-chamber function (Figure 19-3). Prior to this
development, DDD programming was problematic in patients with episodes of atrial fibrilla-
tion, although another mode, DDI, was an option.
CHAPTER 19 • Cardiac Implantable Electronic Devices
Dual-chamber timing considerations are much more complex than those for single-chamber
devices and include atrial and ventricular blanking and refractory periods, AV intervals (that
can be variable), post-ventricular atrial refractory period, and others. The device may pace or
sense in each chamber depending upon the native rhythm and the programming.
In the early2000s. numerous studies1:w pointed out the adverse effects ofRV pacing, which causes
dyssynchro.nous ventricular activation potentially leading to left (and right) ventricular dysfunc-
tion and congestive heart failure. Several algorithms have been developed that basically function
in an atrial pacing mode (e.g., AAI), but revert to a DDD-based mode ifmore advanced AV block
develops.14'1 5 Disadvantages include fostering long PR intervals, occasional nonconducted beats
U
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Panel A
FIGURE 19-3 • Switch from DDD to VVl-llb mode with atri1I flbrlllltlon. Pan1I A: The device Is tracking atriaI events untll atrial
flbrlllatlon occurs and then switches to WI (or WIR) operation; the padng rate Is gradually decreased to avoid an abrupt drop.
Panel 8 illustrates tamination of atrial fibrillation and resumption of atrial pacing in DOD mode. Abbreviation: F8, fallback.
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PanelB
(F.lgure 19-4). and the potential for short-long-short sequence-induced ve.ntricular arrhythmia.
The mode can be generically described as ADI because the device paces the atrium only, but
senses the atrium and ventricle, and a native atrial impulse inhibits atrial pacing.
DEVICE IMPLANTATION
Detailed descriptions of transvenous implantation technique are available elsewhere,11s but a
high-level overview follows. Following informed consent, the fasting patient is placed on the
operative table and the right or left pectoral region carefully prepared with antiseptics and
draped. As most device implants are done in an EP lab, or a catheterization lab, and fewer now-
adays in the operating room, it is important to invoke the rigor for sterility more typical of the
operating room in minimizing device infections because they carry a high fatality rate. Preop-
erative antibiotics reduce infection and are mandatory. Although postoperative antibiotics have
·- L
p
FIGURE 1H • ADI mode operation. The pacemaker functions In AAJ (or AAIR) as long as AV conduction pefSlsts.
not shown benefit, absorbable, antibiotic-impregnated pouches did demonstrate a reduction in

infection for more complex implants.17
Most operators create a pocket and then gain vascular access, but the reverse can be done too. The
incision site, length, and orientation should be chosen based on the device size and intended vas-
cular access site. Access site approaches and options include: (1) surgic:al cutdown on the cephalic
vein, with direct introduction of a lead or a guidewire; (2) ex.trathoracic, fluoroscopic-guided
axillary vein access on top of the first rib18; or (3) intrathoracic, subc:lavian vein puncture.
Although traditional, the latter approach likely exhibits higher rates for pneumothorax rate and
for lead failure due to subclavian crush. The cephalic vein method avoids both pneum.ot-
horu: and subclavian crush, but expertise is less widespread, and even with training it is slightly
more time-consuming. Thus, the e:ttrathoracic approach has gained adherents. A subclavian
venogram is often helpful in pinpointing the appropriate puncture site. Recent modifications
gaining some traction are micropuncture access kits and ultrasound guidance.
After the lead(s) are introduced, they are carefully advanced under fluoroscopic guidance,
optimally with more than 1 angulation, keeping in mind the normal vascular anatomy and its
variations. Right ventricular leads historically were implanted in the apex to facilitate fixation
with passive tines, but active fixation leads are now commonly used and can be implanted in
other loci. Placement of the lead in the outflow tract or septum has been suggested to afford
better hemody:namic results, but the benefits have been modest,19 and the exact location often
at odds with that intended.20 Similarly, the appendage was the traditional location for passive
fixation RA leads. Active fixation leads allow placement elsewhere. Compared with intrinsic
sinus rhythm, pacing the appendage or lateral RA prolongs the time required to complete atrial
depolarization. This may worsen left atrial and mitral valve hemodynamics, thus fostering
atrial fibrillation. Pacing the atrial septa! area has been proposed, but definitive benefits are
unproven.21 Regardless of the site chosen, goals include good sensing and pacing numbers,
careful fixation to avoid dislodgement, and avoidance ofexcessive force to lower the risk of per-
foration. Minimum goals for sensed signals are 2 mV in the RA and 5 mV in the RV. Measured
at a pulse width of0.5 ms, the desired capture threshold is 1V or less in the RV and 1.SV or less
for the RA. With active fixation leads, the threshold often improves after several minutes. Thus,
temporizing can avoid unnecessary repositioning. After an acceptable position is confirmed,
the lead is carefully secured to the pectoral fascia. Operator failure in connecting the leads to
the header is an easily avoided reason for pacing failure and reoperation. Before pocket closure,
meticulous attention to hemostasis is vital because pocket hematoma occurrence dramatically
increases the risk ofinfection. Operating under uninterrupted anticoagulation with warfarin or
novel anticoagulants yields superior outcomes to use of heparin bridging.22.23
Implant complications include: pocket hematoma,24 pocket or intravascular infection,17•25

pneumothorax,26.27 hemothorax, central venous perforation or dissection, cardiac perforation,
tamponade,28 pericarditis, lead dislodgement, venous occlusion, and thromboembolism.29
Complications prolong hospitalizations and increase the risk of death. 27.3°
In addition to surveillance for complications, pacemaker follow-up entails observation of

thresholds, sensing, lead failure (insulation or fracture), premature battery failure, elective bat-
tery depletion, and arrhythmias. Most follow-up has shifted toward being remote, wireless, and
automatic.31
LEADLESS CARDIAC PACEMAKERS

Seeking to avoid complications of transvenous leads, their implantation, and the associated
pockets, leadless pacing capsules have been developed. Devices developed thus far are about
3 to 4 cm in length and are secured to the RV endocardium via large-bore (18-23F inner
diameter), deflectable femoral sheaths. The device encompasses pacing electrode, battery,
circuitry, and fixation mechanism. Initial models are single-chamber, ventricular only (VVI,
VVIR), but the capability to sense the atrium and thus allow tracking of sinus rhythm in
patients with AV block has just received FDA approval. Atrial pacing to treat sinus node
dysfunction is so far not available.
Complications differ somewhat from transvenous implants, but include femoral vascular ones,
potentially serious given the sheath size, cardiac perforation, and device embolization. It has
been posited that leadless pacemakers may be less prone to seeding with intravascular infection
due to small size and possible encapsulation over time; in 7 cases of staphylococcal bactere-
mia the patients were successfully treated without device removal.32 Leadless units have been
retrieved in the short term, and in a few instances after more than a year.33 The ease of or need
for long-term removal is so far unclear.
Their exact role is in evolution as capabilities increase and comparative complications and
costs are considered. At present, those with contraindications to transvenous systems such as
SVC syndrome, hemodialysis access, and patients at very high risk for infection, such as prior
extraction patients, are optimum candidates for a leadless device. Whether the presently higher
costs are offset by lower complications for other VVI device candidates (permanent atrial fibril-
lation with severe bradycardia) is unclear.
CARDIAC RESYNCHRONIZATION THERAPY

Cardiac resynchronization therapy (CRT), usually via biventricular pacing, has become a criti-
cal treatment for systolic heart failure with LBBB. The pivotal trials have included patients with
QRS prolongation of 120 or 130 ms or longer. Specifically, most have had LBBB, where the ben-
efit is clear-cut, and a Class I indication exists. In these patients CRT reduces HF hospitalization
and reduces mortality.34-38 Some trials have suggested a lack of benefit for the non-LBBB subset,
namely those with RBBB or IVCD (intraventricular conduction delay). Some data support a
benefit for CRT with non-LBBB for QRS duration exceeding 150 ms,3H 1 and Class II indica-
tions for CRT remain present. Importantly, harm was present in patients randomized to CRT
with QRS <130 ms!2 CRT trials were conducted in patients already receiving optimal medical
therapy (e.g., ACE inhibitors and beta blockers) and consequently indications specify use of
such therapy before implantation.43•44 As noted above, while biventricular pacing can treat heart
failure with a LBBB, RV pacing can cause LV dysfunction. When this happens, an upgrade to
CRT usually is beneficial.
LBBB causes delayed electrical, and thus mechanical, activation of the lateral LV wall. Abnor-
mal passive stretch, delayed contraction, and dyssynchronous LV activation result in abnormal-
ities in systolic and diastolic function, perfusion abnormalities, neurohumoral activation, gene
expression and protein synthesis, localized hypertrophy and structural remodeling, left atrial
enlargement, and mitral valve dysfunction45-53 CRT can partially to even fully reverse LV dys-
function in many patients with salient benefit with respect to MR and other abnormalities.54- 57
Seeking to correct the delayed lateral LV wall activation, LV leads have usually been placed via a
posterior-lateral or lateral branch (Figure 19-5). Evidence has emerged that avoiding the apical
region and probably also the anterior or septal regions yields better outcomes.5s,s9 Other mod-
ifications include sequential biventricular pacing, left ventricular only pacing (with or without
timing the impulse to fuse with the native RBB wavefront),60.61 and multipoint pacing with more
than 1 left ventricular stimulation site.61 In addition to the transvenous, coronary sinus route,
LV pacing has been accomplished with epicardial leads (via thoracotomy or by thoracoscopic
insertion), and rarely with a transseptal, endocardial approach. A leadless, endocardial-based
electrode system is under investigation.
The evidence base for CRT is now fairly robust, but some questions remain, including non-
LBBB patients as discussed. Other areas of uncertainty include whether CRT should be used
when the EF is only mildly reduced (above 35% or 40%), and for atrial fibrillation patients (in
whom AV junction ablation may be needed to ensure CRT). Predictors of response include
LBBB morphology, wider QRS (>150 ms), nonischemic cardiomyopathy, absence of scar, sinus
rhythm as compared with atrial fibrillation, and female sex.
IMPLANTABLE CARDIOVERTER-DEFIBRILLATORS (ICDs)

External cardioversion or defibrillation is lifesaving in SCA due to VT /VF, but the success
rate for conversion is highly time-sensitive. Consequently, in patients at high risk of SCA
or those with prior SCA who remain at risk, the ICD may be indicated (Table 15-5). The
ICD system includes 1 or more leads, and a device that includes sensing amplifiers, logic
circuitry, a battery, and a capacitor for converting the battery's low voltage to approximately
1OOO V for defibrillation. Implantation resembles the procedure for a transvenous pace-
maker, discussed earlier in this chapter. Single (RV lead only), dual, and CRT options exist
(Figure 19-5). Pacing and sensing thresholds are confirmed as for pacemakers. With respect
to sensing, ICDs have a more difficult task than pacemakers, in that they must highly reli-
ably detect the usually small signals in VF, yet avoid oversensing non-QRS events including
atrial events, pacing stimuli, diaphragmatic myopotentials, or the intracardiac equivalent of
T waves. In order to accomplish this, ICDs increase sensitivity after a sensed event seeking
to avoid the T wave but sense a potential VF signal.63 Because occasional signals may fall
below even the adjusted threshold, sensing algorithms typically detect X out of Y signals
faster than the detection rate, especially for the VF zone (Figure 19-6). In addition to shocks
(with programmable energy), ICDs often are programmed to deliver antitachycardia pacing
to convert VT (Figure 19-6).
PanelA
PanelB
FIGURE 19-5 • Blventrlcular padng or cardiac resynchronlZllltlon 1herapy (CRT}. Panel Adfsplays a coronary sinus balloon-
occlusion venogram. ltdemonstrate.s a large, high lateral vein into which the LV lead was implanted. (See Panel5 B-C.) Panel 8 is
a posterior-anterior chest x-ray showing a CRT system combined wtth an ICD, and Panel C Is a lateral chest x-ray. No A lead was
Implanted due to pe1manent atTlal flbrlllatlon. An AVN ablation was performed as well. Panel D Is a 12-lead ECG with ongoing
blventrlcular pacing, with underlying atrfal flbrlllatlon.
488
PanelC
Panel D
FIGURE 1..S • (Continlll!d)
Until recently, defibrillation capability was confirmed by inducing VF at the time of implan-
tation, and performing a defibrillation threshold procedure, or more often with 1 or 2 shocks
substantially below the maximum energy. Risks of VF induction included rare prolonged car-
diac arrest or frank failwe to convert the induced rhythm, as well as hemodynamic insult, and
thromboembolism.64 Moreover, defibrillation is probabilistic, and described by a sigmoidal suc-
cess curve, such that for shocks over a broad range, success may or may not occur. On the other
hand, a pacing threshold is essentially a single value above which capture is virtually assured.
An alternative or complementary method has been to measure the upper limit of vulnerability
(ULV) to induction of VF, with a shock timed on the T wave. The ULV has been found to be
correlated with the DFT experhnentally and theoretically.6M 6 With implementation ofbiphasic
shocks, the success of deflbrillation is now >95% at maximum energy. A randomized trial. as
well as corroborative data, has shown no benefit to routine defibrlllation testing compared with
implantation without such testing.67.68 A corollary to the improved sue<:ess rates for shocks is
the reduced need for additional shock coils, such as an SVC coil. other than the required RV
coil. Such SVC coils increase the challenge and risk associated with lead removal ifneeded.
Like pacemakers, ICD technology has undergone remarkable advancement The importance of
ICD programming had until recently been relatively neglected. After devices developed elec-
trogram storage capability, it was appreciated that some events leading to ICD therapy (ATP
or shock) were supravent.ricular arrhythmias or noise. Deemed "'inappropriate" therapy. these
events reduced quality oflife, caused hospitalization and psychological distress, and were found
to be associated with mortality.69•70 Several randomized, controlled trials explored novel pro-
gramming. basically consisting of either longer delays before intervention, or only treating
arrhythmias faster than a certain threshold such as 188 or 200 bpm (higher than that con-
ventionally used).71·"' In addition to reducing inappropriate shocks, there was evidence for a
possible reduction in mortality with the new programming.71•7• Although untreated VT. such
as below the cutoff rate, can certainly have serious clinical consequences, these studies did not
exhibit an increase in adverse events such as syncope (due to being untreated or delays in treat-
ment of VT). Subsequently, programming guidelines were recently issued.7>·76
•v
Shock
'
VS VF VF VF VF VF VF VF VF [VS] - VT VT VS VP
3S5 283 290 280 258 275 273 275 288 333 318 970 1000
Chrg 41.0 J Shk

Panel A
FIGURE 19-6 • ICD Detection and Therapy. Panel A shows an episode detected as VF, and a shock with comlefsion to nonnal
rhythm. Panel 8 shows an episode detected a5 VT. and then anti-tachycardia pacing that successfully converts it.
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FIGURE 1H • (Continued)
SUBCUTANEOUS IMPLANTABLE CARDIOVERTER·DEFIBRILLATOR (SICD)

..................................................................................................................................................
Analogous to the concerns about transvenous pacemaker leads are those for tran.svenous ICD
leads. An implantable defibrillator has been developed that uses only subcutaneous leads for sens-
ing ventricular activation, and for delivering shocks (Figure 19-7). A higher energy is needed,
namely. up to 80 Jas compared with up to 35-40 Jfor transvenous systems. Consequently. the gen-
erator is larger than the current transvenous type, and the implant site is in the mid to posterior
lateral chest to optimize the defibrillation shock vector. The currently approved device does not
offer pacing, either fur treatment of bradycardia, antitachycardia. or cardiac resynchronization
therapy, and patients needing such therapy are not candidates. The sensing algorithm is even more
challenging than that fur transvenous ICDs, but the inappropriate shock rate is now almost as low
Panel A
Panel B
FIGURE 19·7 • Subcutaneoua ICD {SICD). Panel A Is a postt!rior-an11!rfor c:hestx-ray showing an SICD system. Panel B
is a lateral chestx-ray; note the lead lying immediatl!fy adjaamtto1tte stem um, rather1ttan in the subartaneo~ fat.
as that for transvenous devices with state-of-the-art programming. Unlike for transve.nous ICDs,
present guidelines support defibr:illati.on testing. although some ce.nters evaluate the impedance of
a synchronized shock. A low impedance implies that the shock coil and device are appropriately
deep, and 1y:iDg on the musculature or bony chest cavity rather than in subcutaneous fat. Shocks
with a low impedance (<100 ohms) are more likely to successfully defibrillate.
TRANSVENOUS LEAD EXTRACTION

Pacemaker and ICD leads require removal (Class I indication) in the event of a pocket or intra-
vascular infection (FJgure 19-8). Such removal is termed lead extraction. Leads may be consicl-
ered for extraction in the event of an upgrade (e.g., from pacemaker to defibrillator}, or upon
their failure or being subject to a re<:all or advisory action (Class 11).77 Transvenous leads exhibit
a variable, largely time-dependent, but partly idiosyncratic, degree of adhesion with the veins
through which they travel and the atrial and ventricular walls. ICD leads, especially the shock
coils, including the SVC coil, are particularly prone to developing extensive adhesions. In lead
extraction, the leads are separated from the adhesions by navigating a sheath over the lead,
beginning at the point of insertion in the subclavian area. until it is free and can be easily with-
drawn. The sheaths use either a laser or a cutting mechanism. An alternative, or backup method-
ology, is snaring the leads via the femoral vein and IVC approach and retracting them downward
(after freeing the subclavian end). Owing to the thin walls of the veins and cardiac chambers,
PanelA
FIGURE 1H • Leid extraction and device Infection. Panel A Is an Image of a pacemaker pocket with 1
scaly lesion; the patient experienced Intermittent purulent drainage from this area. Panel B demonstrates
a much more obvious pocket lnf'l!ctlon with frank erosion. Pan1I C Is a large vegetation on a pacing lead.
Panel D Is a fluoroscopic Image during lead extraction using a laser sheath from the left pectoral approach.
Panel E Is a portion of an extracted ICD lead with extensive flbrlnous adhesions and externalized shock con-
ductor cables.
Panel B
PanelC
FIGURE 1H • (Continued)
Panel D
Panel E
there is risk of laceration or perforation. Even for expert operators, these major complication
occur in about I% of procedures. An especially high-risk area is the superior vena cava, owing
to the angulation with the innominate vein, and if relevant the proximal (SVC) coil of (some)
ICD leads. A tear above the pericardia! reflection will result in hemothorax and mediastinal
hemorrhage, whereas one below the reflection can result in tamponade. Thus, a pericardiocen-
tesis usually is insufficient, owing to the mechanism and extent of bleeding. Instead, emergent
median sternotomy, cardiopulmonary bypass, and direct repair are usually required, and must
be implemented within a few minutes to avert a fatality. A new technological advance that in
some cases affords some more time is a long balloon that can be expanded in the SVC area to
tamponade the bleeding. Nevertheless, access to near-immediate surgical backup is required.
The logistics and staffing issues for this backup process remain challenging, however. Attempts
have been made to risk-stratify the procedures in terms of their likelihood of such major com-
plications, though these are not fully vetted.
REFERENCES
1. Kusumoto FM, et al. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With
Bradycardia and Cardiac Conduction Delay. JAm Coll Cardiol. 2018.
2. Savonen KP, et al Chronotropic incompetence and mortality in middle-aged men with known or suspected coro-
nary heart disease. Eur Heart J. 2008;29:1896-1902.
3. Jamil HA, et al. Chronotropic incompetence does not limit exercise capacity in chronic heart failure. J Am Coll
Cardiol. 2016;67:1885-1896.
4. Zweerink A, van der Llngen ACJ, Handoko ML, van Rossum AC, Allaart CP. Chronotropic incompetence in
chronic heart failure. Circ Heart Fail. 2018;1 l:e004969.
5. Sheldon RS, et al. 2015 heart rhythm society expert consensus statement on the diagnosis and treatment of pos-
tural tachycardia syndrome, inappropriate sinus tachycardia, and vasovagal syncope. Heart Rhythm. 2015;12:
e41-e63.
6. Brignole M, et al. Benefit of pacemmr therapy in patients with presumed neurally mediated syncope and docu-
mented asystole is greater when tilt test is negative: an analysis from the Third International Study on Syncope of
Uncertain Etiology (ISSUE-3). Circ Arrhythm E/ectrophysiol. 2014;7:10-16.
7. Lee S, Wellens HJ, Josephson ME. Paroxysmal atrioventricular block. Heart Rhythm. 2009;6:1229-1234.
8. Brignole M, et al. Syncope due to idiopathic paroxysmal atrioventricular block: long-term follow-up of a distinct
form of atrioventricular block. JAm Coll Cardiol. 2011;58:167-173.
9. Brignole M, et al. 2018 ESC Guidelines for the diagnosis and management of syncope. Eur Heart/. 2018.
10. Dretzkc J, et al. Dual chamber versus single chamber ventricular pacemmrs for sick sinus syndrome and atrio-
ventricular block. Cochrane Database Syst Rev. 2004;CD003710.
11. Nielsen JC, et al. A comparison of single-lead atrial pacing with dual-chamber pacing in sick sinus syndrome. Bur
Heart/. 2011;32:686-696.
12. Steinberg JS, et al The clinical implications of cumulative right ventricular pacing in the multi.center automatic
defibrillator trial II. J Cardiovasc Electrophysiol. 2005; 16:359-365.
13. Wilkoff BI., et al Dual-chamber pacing or ventricular backup pacing in patients with an implantable defibrillator:
the Dual Chamber and VVI Implantable Defibrillator (DAVID) Trial. JAMA. 2002;288:3115-3123.
14. Sweeney MO, et al. The Managed Ventricular pacing versus VVI 40 Pacing (MVP) Trial: clinical background,
rationale, design, and implementation. J Cardiovasc ElectrophysioL 2006;17:1295-1298.
15. FrOhlig G, et al Use of a new cardiac pacing mode designed to eliminate unnecessary ventricular pacing. Europace.
2006;8:96-101.
16. Belott P,Reynolds D. (eds EllenbogenK.A., Wilkoff B. L., KayG. N., Lau C.-P., &: Auricchio A.,) 631-691 (Elsevier,
2017).
17. Tarakji KG, et al. Antibacterial envelope to prevent cardiac implantable device infection. N Engl J Med.
2019;380(20):1895-1905.
18. Byrd CL. Safe introducer technique for pacemaker lead implantation. Pacing Clin Electrophysiol. 1992;15:262-267.
19. Shimony A, Eisenberg MJ, Filion KB, Amit G. Beneficial effects of right ventricular non-apical vs. apical pacing: a
systematic review and meta-analysis of randomized-controlled trials. Europace. 2012;14:81-91.
20. Jackson LR 2nd, Piccini JP Sr, Daubert JP, Hurwitz Koweek LM, Atwater BD. Localization of pacing and defibril-
lator leads using standard x-ray views is frequently inaccurate and is not reproducible. / Interv Card Electrophysiol.
2015;43:5-12.
21. Lau CP, et al. Prospective randomized study to assess the efficacy of site and rate of atrial pacing on long-term pro-
gression of atrial fibrillation in side. sinus syndrome: Septa! Pacing for Atrial Fibrillation Suppression Evaluation
(SAFE) Study. Circulation. 2013;128:687-693.
22. Birnie DH, et al. Pacemaker or defibrillator surgery without interruption of anticoagulation. N Engl I Med.
2013;368:2084-2093.
23. Birnie DH, et al. Continued vs. interrupted direct oral anticoagulants at the time ofdevice surgery, in patients with
moderate to high risk of arterial thrombo-embolic events (BRUISE CONTROL-2). Bur HMrt /. 2018;ehy413.
24. Essebag V, et al. Clinically significant podc.et hematoma increases long-term risk of device infection: BRUISE
CONTROL INFECTION Study. I Am Coll Cardiol. 2016;67:1300-1308.
25. Olsen T, et al. Incidence of device-related infection in 97 750 patients: clinical data from the complete Danish
device-cohort (1982-2018). Bur Heart J. 2019;40:1862-1869.
26. Gupta N, et al. Multi-center, community-based cardiac implantable electronic devices registry: population, device
utilization, and outcomes./ Am HMrt Assoc. 2016;5:e002798.
27. Palmisano P, Guerra F, Dell'Era G, et al, Impact on all-cause and cardiovascular mortality of cardiac implantable
electronic device complications: results from the POINTED registry. JACC EP. 2020 In-Press.
28. Rajkumar CA, et al. Diagnosis and management of iatrogenic cardiac perforation caused by pacemaker and defi-
brillator leads. Europace. 2017;19:1031-1037.
29. Manda! S, et al. Permanent pacemaker-related upper extremity deep vein thrombosis: a series of 20 cases. PACE.
2012;35:1194-1198.
30. Rav Acha M, et al. The management of cardiac implantable electronic device lead perforations: a multicentre
study. Europace. 2019;21:937-943.
31. Slotwiner D, et al HRS expert consensus statement on remote interrogation and monitoring for cardiovascular
implantable electronic devices. Heart Rhythm. 2015;12:e69-el00.
32. El-Chami MF, et al. Incidence and outcomes of systemic infections in patients with leadless pacemakers: data from
the Miera IDE study. Pacing Clin Electrophysiol. 2019;42:1105-1110.
33. Tjong FVY, Reddy VY. Permanent leadless cardiac pacemaker therapy. Circulation. 20 l 7;135:1458-1470.
34. Bristow MR, et al. Cardiac-resynchronization therapy with or without an implantable defibrillator in advanced
chronic heart failure. N Engl JMed. 2004;350:2140-2150.
35. Cleland JGF, et al. The effect of cardiac resynchronization on morbidity and mortality in heart failure. N Engl J
Med. 2005;352:1539-1549.
36. Moss AJ, et al Cardiac-resynchronization therapy for the prevention of heart-failure lM:llts. N Engl/ Med.
2009;361:1329-1338.
37. Tang AS, et al Cardiac-resynchronization therapy for mild-to-moderate heart failure. N Engl J Med.
2010;363:2385-2395.
38. Linde C, et al Randomized trial of cardiac resynchronization in mildly symptomatic heart failure patients and in
asymptomatic patients with left ventricular dysfunction and previous heart failure symptoms. /Am Coll Cardiol.
2008;52:1834-1843.
39. Cleland JG, et al. An individual patient meta-analysis of five randomi?.ed trials assessing the effects of cardiac
resynchronization therapy on morbidity and mortality in patients with symptomatic heart failure. Bur Hearl /.
2013;34:3547-3556.
40. Singh JP, et al. Rationale and design for ENHANCE CRT: QLV implant strategy for non-left bundle branch block
patients. ESC Hearl Fail 2018;0.
41. Kutyifa V, et al. PR interval identifies clinical response in patients with non-left bundle branch block: a Multicenter
Automatic Defibrillator Implantation Trial-Cardiac Resynchronization Therapy substudy. Gire Arrhythm Blectro-
physiol. 2014;7:645-651.
42. Ruschitzka F, et al. Cardiac-resynchronization therapy in heart failure with a narrow QRS complex. N Engl JMed.
2013;369:1395-1405.
43. Ponikowski P, et al 2016 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure: The
task force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology
(ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Bur / HMrt
Fail 2016.
44. Epstein AE, et al. 2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guide-
lines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology
Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. JAm
Coll Cardiol. 2013;6l:e6-e75.
45. Grines CL, et al Functional abnormalities in isolated left bundle branch block. The effect ofinterventricular asyn-
chrony. Circulation. 1989;79:845-853.
46. Hayat SA, et al. Effects of left bundle-branch block on cardiac structure, function, perfusion, and perfusion
reserve: implications for myocardial contrast echocardiography versus radionuclide perfusion imaging for the
detection of coronary artery disease. Circulation. 2008;117:1832-1841.
47. Sze E, et al. Impaired recovery ofleft ventricular function in patients with cardiomyopathy and left bundle branch
block. l Am CoU Canliol. 2018;71:306-317.
48. Wang NC, et al. New-onset left bundle branch block-associated idiopathic nonischemic cardiomyopathy and
time from diagnosis to cardiac resynchronization therapy: the NEOLITH II study. Pacing Clin Electrophysiol.
2018;41:143-154.
49. Sze E. et al Compariaon of incidence of left ventricular systolic dysfunction among patients with left bundle
branch block versus those with normal QRS duration. Am J Cardiol. 2017;120:1990-1997.
50. Alelcsova A, et al New-onset left bundle branch bloclc. independently predicts long-term mortality in patients
with idiopathic dilated cardiomyopathy: data from the Trieste Heart Muscle Disease Registry. Europace.
2014;16:1450-1459.
51. Vernooy K, et al. Left bundle branch block induces ventricular remodelling and functional septal hypoperfu.ion.
Eur Heart J. 2005;26:91-98.
52. Smiseth OA, Aalen JM. Mechanism of harm from left bundle branch block. Trends Canliovasc Med.
2019;29:335-342.
53. Mihoa CG, et al. The effects of cardiac resynchronization therapy on left ventricular and mitral valve geometry and
secondary mitral regurgitation in patients with left bundle branch block. Echocardiography. 2019;36:1450-1458.
54. Vaillant C, et al. Resolution ofleft bundle branch bloclc.-induced cardiomyopathy by cardiac resynchronization
therapy. JAm CoU Cardiol. 2013;61:1089-1095.
55. Goldenberg I, et al. Predictors of response to cardiac resynchronization therapy in the Multicenter Auto-
matic Defibrillator Implantation Trial with Cardiac Resynchronization Therapy (MADIT-CRT). Circulation.
2011;124:1527-1536.
56. Ghio S, et al Long-term left ventricular reverse remodelling with cardiac resynchronization therapy: results from
the CARE-HF trial. Bur JHeart Fail. 2009;11:480-488.
57. Hsu JC, et al Predictors of super-response to cardiac resynchronization therapy and associated improvement in
clinical outcome: the MADIT-CRT (multicenter automatic defibrillator implantation trial with cardiac resynchro-
nization therapy) study. JAm Coll Canliol. 2012;59:2366-2373.
58. Singh JP, et al Left ventricular lead position and clinical outcome in the multicenter automatic defibrillator
implantation trial-cardiac resynchronization therapy (MADIT-CRT) trial Circulation. 2011;123: 1159-1166.
59. Kutyifa V, et al Left ventricular lead location and the risk of ventricular arrhythmias in the MADIT-CRT trial. Bur
Heart J. 2013;34:184-190.
60. Thibault B, et al. Left ventricular versus simultaneous biventricular pacing in patients with heart failure and a QRS
complex ~120 milliseconds. Circulation. 2011;124:2874-2881.
61. Birnie D, et al. Clinical outcomes with synchronized left ventricular pacing: analysis of the adaptive CRT trial.
Heart Rhythm. 2013;10:1368-1374.
62. Bodin A, Bisson A, Andre C, et al. Multisite pacing via a quadripolar lead for cardiac resynchronization therapy.
l Interv Card Electrophysiol. 2019;56(1):117-125.
63. Swerdlow CD, Brown ML, Bordachar P. (eds Ellenbogen K.A., Wilkoff B. L.. Kay G. N .. Lau C.P., & Auricchio A.)
Clinical cardiac pacing, defibrillation and resynchronization therapy. 114-167 (Elsevier, 2017).
64. Birnie D, et al Complications associated with defibrillation threshold testing: the Canadian experience. Heart
Rhythm. 2008;5:387-390.
65. Chen PS, Shibata N, Dixon EG, Martin RO, Ideker RE. Comparison of the defibrillation threshold and the upper
limit of ventricular vulnerability. Circulation. 1986;73: 1022-1028.
66. Swerdlow CD, et al. Using the upper limit of vulnerability to assess defibrillation efficacy at implantation ofICDs.
Pacing Clin ElectTOphysiol. 2007;30:258-270.
67. Healey JS, et al. Cardioverter defibrillator implantation without induction ofventricular :fibrillation: a single-blind,
non-inferiority, randomised controlled trial (SIMPLE). Lancet. 2015;385:785-791.
68. Blatt JA, et al No benefit from defibrillation threshold testing in the SCD-HeFT (Sudden Cardiac Death in Heart
Failure Trial). I Am Coll Cardiol. 2008;52:551-556.
69. Daubert JP, et al. Inappropriate implantable cardioverter-defibrillator shocks in MADIT II: frequency, mecha-
nisms, predictors, and survival impact JAm Coll Cardiol. 2008;51:1357-1365.
70. Poole JE, et al Prognostic importance of defibrillator shocks in patients with heart failure. N Engl J Med.
2008;359:1009-1017.
71. Mosg AJ, et al Reduction in inappropriate therapy and mortality through ICD programming. N Engl J Med.
2012;367:2275-2283.
72. Gasparlni M, et al Effect of long-detection interval vs standard-detection interval for implantable cardioverter-
defibrillators on antitac:hycardia pacing and shock delivery: the ADVANCE III randomized clinical trial. JAMA.
2013;309:1903-1911.
73. Saeed M, et al Programming implantable cardioverter-defibrillators in patients with primary prevention indica-
tion to prolong time to first shock: results from the PROVIDE study./ Canliovasc Electrophysial. 2014;25:52-59.
74. Tan VH, Wilton SB, Kuriachan V, Sumner GL, Exner DV. Impact of programming strategies aimed at reducing
nonessential implantable cardioverter defibrillator therapies on mortality: a systematic review and meta-analysis.
Circ Arrhythm Electrophysiol. 2014;7:164-170.
75. WilkofJBL, et al 2015 HRS/EHRA/APHRS/SOLAECE expert congensus statement on optimal implantable car-
dioverter-defibrillator programming and testing. Heart Rhythm. 2016;13:e50-e86.
76. Stiles MK, Fauchier L, Morillo CA, WilkoffBL. 2019 HRS/EHRA/APHRS/LAHRS focused update to 2015 expert
consensus statement on optimal implantable cardioverter-defibrillator programming and testing. Heart Rhythm.
2019.
77. Kusumoto FM, et al. 2017 HRS expert consensus statement on cardiovascular implantable electronic device lead
management and extraction. Heart Rhythm. 2017.
78. Baroid SS, Stroobandt R, Sinnaeve AF. Cardiac Pacemakers and Resynchronization Step by Step: An nlustrated
Guide. West Sussex, UK: Wiley; 2010.
Index
Note: Page numbers followed byf and t indicate figuree and table..
A pp phenomenon and. 85
AA interval. 387, 390/ HH interval and, 387
Ablation catheter. See Catheter ablation ltoproterenol and, 26/
Accelerated !dloventric:\llv rhythm (AIVR), 171-172, 172.f.173/ LOCmd,334
Acmsorypathway effec;tive refractory period (AP-E.RP), Pwa.veand, 14
168.169 PAC.and,41
A«atory pcthways (APs) premature junctional oomplexea and. 44.f. 4Sf
AFand, 120 PVC. md, 46, 47.f. 49, SO, 52, 52.f. 53, 54
atrioventricular reciprocating ~ardia and, 148, 149, SVTand,292
lS0, 151-152, 155, 155t, 156.f. 157, 157f.1S8, 160-163, in Wenckeba.ch block, 17, 25
162f-163/ ~ iaterval, 87
AV ree.ntzy and.149 AIVR. See Accele.rated idlovmtric:\lla.r rhythm
catheter ablation ot 404-410, 406/-409/ Alcohol
prec:xcitation syndromes and, 142, 143, 14:4, 144/ atrial tlutrer and, 122
preeuited tachycardia and. 163, 163/-1~ 164.-165, sinus tachycardia and, 113
166.f.168/ Alpha blockers
PVC.and,54 forSVT,296
refractorineaa ot 160, 261 forWQT,320
retrograde conduct:lo.n and, 18, 19.f. 20, 21, 21/ ALPM. See Anterior lateral papillary muscle
supernormal conduction and, 90, 91/ ALVC. See Arrhythmogenic left ventric:\lla.r cardlomyopadxy
SVT and. 290/, 295/ AMC. See Aorromitnl continuity
vmlricular preeumtion and. 260, 261, 261/, 262/, 263/ Amiodarone
WPWand.141 for AP. 224, 225, 225t, 226
AcidDSU for AT, 117-118
CADand.344 for a1rial flutter. 123
multifocal atrial ta.c.bycard.ia. and, 118 for atrioventricular reciprocatingtll:hycardia. 159t
Aconlline, 98 for AVNR'.t 133
Actlon potentlal for RMVT, 175
BBBand.68 for SCA, 347, 351
cardiac conduction synem and. 3 forSVT,296
electrolytes and. 95 for T-CM, 177
QRS complex and. 73 forWQ't320
SCAmd,357t Andmon-Tawil syndrome, 190
supernormal conduction and, 89 Anemia
Aciivation 1equence mapping.109 LOCand,325
Adenoslne sinus tachycardia and, 113
AT md, 116, 117 ANS. See Autonomic: nervous system
for atrio'f'CD.tricular reciprocating ta.chycardia. 160 Anterior lateral papillary mu.cle (ALPM), 458-459,
for AVNR.T, 132, 133 459f,'8'f
for exerdae-indw:ed VT, 182 Ante.rograde conduction
for SVT, 113, 295, 297/ atriove.atricular reciprocating tachycvdia and. 129, 149
for WQT, 314, 316.f. 317-320 BB:Band,77
AED. See Automated. extemal. defibrillaior BBRVT and, 201-202
M. See Atrial fibrillation PJRT and, 140
AH iDte.rvaJ. 6 PRinte.rvalmd, 10-12
ANS and. 27, 27/ preocited tachy<:ardia and. 163, 164. 165, 166/. 168/
atrial pacing and, 13, 13/, 15-17 PVC! and, 46/, 385
atrioveD.tricular reciprocating tachycardia md. 154/ QRS romplei and, 44f
AVNR.T and, 131.f. 13lt, 132f ventric:\llar preadlatlon and. 263/
502 INDEX
Anticoagulants sick sinus syndrome and, 241

for AF, 220-222, 222/, 232, 257 sinus node dysfunction and, 255
forSVT,296 sleep apnea and, 259
Antidromic reentry (ART), 394/, 395/ substrate of, 216
Antidromic tachycardia, 147 SVT and, 287, 290/. 291, 296
APs and, 164, 167/ tachycardia classical reentry and, 103
PACs in, 394, 394/ T-CM and, 175
Anxiety treatment fur, 220-222, 22 lf. 222t
with sarcoidosis, 358 triggers of, 215-216, 216/
sinus tachycardia and, 113 ventricular preexcitation and, 168, 169, 259, 260, 261
Aortomitral continuity (AMC), 452 WPW and, 142, 142/
AP-ERP. See Accessory pathway effective refractory period WQTand,307
Apixaban, 222, 222t Atrial flutter, 120-122, 121/, 122/, 125/
APs. See Accessory pathways AT and, 117
Arrhythmogenic left ventricular cardiomyopathy (ALVC), 360 cardioversion fur, 123, 231-232
Arrhythmogenic right ventricular cardiomyopathy (ARVC), 262, catheter ablation for, 123, 402/, 422-433, 423/-432/
275-280, 277/-280/. 448 classification of, 417t
NICM and, 467, 470 CTI, 422-433, 423/-432/
SCA and, 35lt, 354t, 360-361 entrainment in, 124/
ART. See Antidromic reentry preexdted tachycardia and, 165
ARVC. See Arrhythmogenic right ventricular cardiomyopathy SVT and, 287, 290/. 291-292, 296
Ashman phenomenon tachycardia classical reentry and, 104/
AV reentry and, 336 WQT and, 303-304
RBBBand,64 Atrial myocardium, 3
AT. See Atrial tachycardia Atrial pacing
Atenolol, 226t AH interval and, 15-17
Atria. See also Left atrium; Right atrium AT and, 117
activation of, 3, 4/ atrial flutter and, 123
ANSand,30 atrioventrlcular reciprocating tachycardia and, 156
ectopic complexes of, 35-45, 36/-45/, 257 AV block and, 13, 13/, 247, 247/, 256, 377
refractoriness of, 30 AV node and, 15-16
tachycardia classical reentry and, 100, 101 bradycardia and, 237
Atrial fibrillation (AF), 119-120, 119f.120f. 214/, 257 gap phenomenon and, 85
AT and, 116, 117 His bundle and
atrial flutter and, 122 deflection of, 379/
atrioventricular reciprocating tachycardia and, 154-155, 215/ depolarization of, 378
BTS and, 229-230, 229/, 230/, 241, 242/ JTand, 136
cardioversion fur, 231-232 PACs and, 41, 41/
catheter ablation for, 215, 218, 224, 402/. 433-442, 434/. sick sinus syndrome and, 243
436/-439/ Wenckebach block and, 378
classification of, 213 Atrial septa] defect, 290/
clinical presentation of, 217-218 Atrial tachycardia (AT), 29/, 115-119, 116/-119/, 385
CPVT and, 274 atrial flutter and, 120
cryoablation fur, 439, 440 catheter ablation for, 402/, 417-422, 418/-421/
epidemiology of, 214 classification of, 417t
etiology of, 214-215 SVT and, 287, 288/, 296
HBE and, 38, 4lf WQT and, 303, 313/
LBBB and, 68/ Atrioesophageal fistula, 441-442
long-standing persistent, 213 Atrio-His interval. See AH interval
nonpulmonary triggers of, 435t Atrioventricular. See AV Conduction
NSVT and, 178, 179/ Atrioventricular node reentrytachycardia (AVNRT), 123-135,
paroxysmal, 213 127/-132/, 13 lt, 134/, 135/
patient evaluation for, 218-219, 218/-220/ AFand, 119/
permanent, 213 catheter ablation for, 130/, 402/, 410-416, 411/
persistent, 213 classical reentry and, 100
postoperative, 232 cryoablation fur, 404, 415-417, 416/
preexdtation syndromes and, 142 diagnostic maneuvers fur, 383-394, 386/. 387/.
preexdted tachycardia and, 163, 165, 166-167 389/-391/
PV and, 216, 216/, 217/ PACs and, 391/
PVI fur, 433-435, 434/, 440 radiofrequency ablation for, 133, 412-415, 413/-415/
rate control fur, 226-229, 226t, 227/. 228/ RP interval and, 127, 389/
rhythm control fur, 224-226, 225/ ventricular pacing in, 387/
SCA and, 357t Atrioventricular (AV) pacing, 249
INDEX 503
Atrioventricular reciprocating tachycardia (AVRT), 154-163, paroxysmal, 248, 248/

155t, 156/, 157/, 159/-162/, 159t QRS complex and, 15
AFand,215/ sarcoidosis and, 358
catheter ablation for, 158-159, 161, 395, 398, 4-02/ SCAand,347
OT arrhythmias and, 452 second-degree, 244/, 245
ventricular pacing in, 386/ in sleep apnea, 18f, 28
WQT and, 313/ spurious bradycardia and, 238
Atrioventricular reentrant tachycardia (AVRT), 147-152, 148f, SVT and, 287-289, 292, 295
150/-154/ tachycardia programmed electrical stimulation and, 381
Atrioventricular (AV) reentry, 18/ third-degree, 246
anterograde conduction and, 129 ventricular preexcitation and, 260
APsand, 149 VTand,470
Ashman phenomenon and, 336 Wenckebach, 13-18, 13/, 14/-15/, 249/
diagnostic maneuvers for, 383-398, 384f, 385t, 386/ AH and,25
endocardial catheter mapping for, 381-383, 383/ atrial flutter and, 120
WCand,336 atrial pacing for, 378
programmed electrical stimulation for, 107-108 bradycardia and, 235
RBBBand, 72 in HPS, 15, 17/
SVTand,292 P wave and, 27/
tachycardia classical reentry and, 101, 103/ PACs and, 40/
Atropine sleep and, 27, 27f, 258
atrioventricular reciprocating tachycardia and, 152, 153/ tachycardia and, 26
for bradycardia, 237 vagal tone and, 27
for carotid sinus hypersensitivity, 249 WQT and, 313f, 317-320
Mobitz type II AV block and, 29, 31/ AV conduction
programmed electrical stimulation for, 108 atrial flutter and, 123
sinus tachycardia and, 113 LBBB and, 9-10, lOf, 11/
Automated external defibrillator (AED), 346 PACs and, 37-42, 40/-42/
Automaticity programmed electrical stimulation and, 375, 377-381,
ATand, 117 377/-381/
overdrive suppression of, 96 supernormal conduction and, 91/
in subsidiary pacemakers, 31 WQTand,310
tachycardia and, 95-98, 96f, 96t, 97/ AV dissociation
Autonomic nervous system (ANS) AVNRT and, 13lt, 410
AH interval and, 27, 27/ VT and, 291, 303, 305, 306/, 314
atria and, 30 AV node, 3, 4, 4/
AV node and, 25-28, 26/-30/ ANS and, 25-28, 26/-30/, 31/
cardiac conduction system and, 22-32, 23/-32/ AT and, 116
HPS and, 28-30, 29/-31/ atrial flutter and, 123
PR interval and, 27, 27/ atrial pacing for, 15-16
sinus node and, 22-25, 22f-25f electrophysiologic study of, 12-13, 12/
vasovagal phenomenon and, 30-31, 32/ gap phenomenon and, 84-85, 86, 89/
ventricles and, 30, 32/ preexcitation syndromes and, 142, 143, 144
AV block, 256 premature junctional complexes and, 43
ATand,422 PVCs and, 45-46, 46f, 49f, 50-51, 51/, 52, 52f, 53/, 54
atrial pacing and, 13, 13/ RBBBand,62
AVNRT and, 13lt reentry, 123-135
bradycardia and, 235, 243-248, 244/-248/ bisoprolol for, 327/
Brugada syndrome and, 270 )Tand, 114/
CIED and, 479, 480 paroxysmal tachycardia and, 101
congenital, 246-247 refractoriness and, 42, 47/, 117-118, 181
DDDand,483 RF for, 379
first-degree, 10-11, llf, 244 SVT and, 113, 114/, 115/, 287-289, 288/, 289/, 293/, 294/
leadless cardiac pacemakers for, 486 tachycardia classical reentry and, 101
WCand,326 WQT and, 303, 304/, 305-306, 306/, 307/
Mobitz type I, 13, 245, 256 AVNRT. See Atrioventricular node reentry tachycardia
CIED and, 480 AVRT. See Atrioventricular reciprocating tachycardia;
Mobitz type II, 244f, 245 Atrioventricular reentrant tachycardia
atropine and, 29, 31f
beta-adrenergic blockers and, 29 B
CIED and, 479, 480 Baroreflex, sinus node and, 25/
premature junctional complexes and, 43-45, 44f, 45/ Baroreflex sensitivity (BRS), SCA and, 357t
sinus node exit block and, 241 BBB. Su Bundle branch block
504 INDEX
BBRVT. Su Bundle branch reentrant ventricular tachycardia AFand,68f

Beta blockers, 18 atrioventricular reciprocating tachycardia and, 150
for AF, 224, 225, 226t, 232 AV block and, 247f
for AT, 117 AV conduction delay and, 9-10, 10/, 11/
for atrial flutter, 123 AVRC and, 276, 277, 278/, 280/
for atrioventricular reciprocating tachycardia, 155, 159t BBRVT and, 466
for AVNRT, 133 Brugada syndrome and, 270
carotid sinus hypersensitivity and, 249 ILVT and, 455, 457, 457t
for exercise-induced VT, 182, 183 LOC and, 334/
forIST, 115 OT arrhythmias and, 452, 454t
forJT, 136 PACs and, 64-66, 65/, 66f
for LQTS, 269, 362 repetition of, 71-72
Mobitz type II block and, 29 RMVT and, 174
for multifucal atrial tachycardia, 118-119 sarcoidosis and, 358
forMVP, 183 SCA and, 357t
for NSVT, 181 sustained monomorphic VT and, 193, 195/,
for preexcited tachycardia, 167-168 207-208
forRMVT, 175 SVTand,287
for SCA, 351-352 tachycardia and, 66-69, 67f-70f
sick sinus syndrome and, 243 WQT and, 305/, 306, 309-310, 311/, 312/
for sinus tachycardia, 113 preexdted tachycardia and, 163
for sustained monomorphic VT, 207 RBBB, 5, 7f, 57-59, 58/, 58t
for SVT, 295, 296, 298 atrioventricular reciprocating tachycardia and, 149
forWQT,320 AV block and, 247f
Bidirectional tachycardia, 190 AVRC and, 277
CPVT and, 273/ fascicular block and, 40/
Bifascicular block, 247, 257 interfascicular VT and, 466
Bipolar electrograms, 373-374, 374/ NICM VT and, 470
Bisoprolol OT arrhythmias and, 454t
for AF, 226t PACs and, 62-66, 63/-65/
for AV node reentry, 327/ repetition of, 70-75, 71/, 73/, 74f
Bradycardia sarcoidosis and, 358
AV block and, 235, 243-248, 244f-248/ sustained monomorphic VT and, 199, 204, 207,
CIED and, 480 207/-209f
classification of causes of, 238-250, 239/-249/ SVTand,287
diagnosis of, 235-238 tachycardia and, 66-69, 67f-70f
EADsand,98 Wenckebach block and, 15
programmed electrical stimulation for, 108 WQT and, 305/, 306, 307, 309-310, 311/, 319/
neurally-mediated, vagal, 248-250, 249f SVTand,292
sinus node and, 237, 240-243, 240f-243/ VTand,470
dysfunction of, 255 WQT and, 305, 305/, 307
in sleep, 258, 258/ Bundle branch reentrant ventricular tachycardia {BBRVT), 199,
sleep apnea and, 259 200-203,201/-206/
spurious,238-240,239/ catheter ablation for, 466
Bradycardia-tachycardia syndrome {BTS), 229-230,
229/, 230/ c
sick sinus syndrome and, 241, 242/ CAD. Su Coronary artery disease
SNRT and, 237 Calcium,4
BRS. Su Baroreflex sensitivity DADsand,98
Brugada syndrome, 262, 270, 271f-273/ Calcium channel antagonists/blockers
ERand,363 for AF, 226t
LOCand,325 for AVNRT, 133
SCA and, 35lt, 354t, 361 for multifocal atrial tachycardia, 119
BTS. Su Bradycardia-tachycardia syndrome sick sinus syndrome and, 243
Bundle branch block {BBB), 256-257 forSVT,298
action potential and, 68 Cannon A waves
anterograde conduction and, 77 AV dissociation and, 291, 303
atrioventricular reciprocating tachycardia and, 147, 153/, AVNRT and, 126
155, 158 SVTand, 192
bradycardia and, 235 Cardiac arrest Su also Sudden cardiac arrest {SCA)
CIED and, 479, 480 atrioventrlcular reciprocating tachycardia and, 155
JT and, 136 ERand,275/
LBBB, 5, 7f, 58t, 59-62, 60/-62/ exercise-induced VT and, 183
INDEX 505
Cardiac catheterization. See Electrophysiologic testing for preexcited tachycardia, 167, 168
Cardiac conduction system, 3-31. See also specific types of forSVT,296
conduction for WQT, 317, 320
ECG electrophysiologic studies and, 5-18, 6/-18/ Cardizem, 123
retrograde conduction, 18-21, 18/-21/ Carotid sinus hypersensitivity, 249-250
Cardiac implantable electronic devices (CIED) WCand,325
CRT, 486-487, 488/-489/ Carotid sinus massage, 115
for BBRVT, 466 for AVNRT, 133
forLBBB,69 for bradycardia, 235, 238
forSCA,352 for LBBB, 67/
DDD, 480-484, 482/-485/ for SVT, 289, 294-295, 296/
for sick sinus syndrome, 243 Carvedilol, 226t
implantation of, 484-486 Catecholaminergic polymorphic ventricular
leadless cardiac pacemakers, 479, 486 tachycardia (CPVT), 190, 262, 270-274, 273/,
SICD,491-493,492/ 274,274/
single-chamber pacemakers, 480-483 SCA and, 35lt, 354t, 362
transvenous lead extraction for, 493-496, 493/-495/ Catecholamines
Cardiac magnetic resonance (CMR) DADsand,98
for AF,218 EADsand,98
forMVP, 184 papillary muscles and, 458
for NICM, 467 Catheter ablation, 168. See also Cryoablation; Radiofrequency
for T-CM, 177 ablation
Cardiac resynchronization therapy (CRT), 486-487, for AF, 215, 218, 224, 402/, 433-442, 434/, 436/-439/
488/-489/ of APs, 404--410, 406/-409/
for BBRVT, 466 for AT, 402/, 417-422, 418/-421/
forLBBB,69 for atrial flutter, 123, 402/
forSCA,352 CTI, 422-433, 423/-432/
Cardiac tamponade, 486 for atrioventricular reciprocating tachycardia, 158-159, 161,
AF catheter ablation and, 441 395, 398, 402/
ventricular preexcitation and, 260 for AVNRT, 130/, 402/, 410-416, 411/
Cardiomyopathy BBRVT,466
AFand,217 ECMO and, 473, 474/
ALVC, 360 forJT,136,442-443
ARVC, 262, 275-280, 277/-280/, 448 for NICM, 467-470, 468/-469/
NICM and, 467, 470 for NSVT, 181
SCA and, 35lt, 354t, 360-361 for preexcited tachycardia, 163/-164/, 167
dilated for RMVT, 174, 175
VT and, 199, 258 for sustained monomorphic VT, 199, 208
VT-NS and, 177 for SVT, 298, 401-443, 402/
HCM,467 for ventricular preexcitation, 260
NICM VT and, 470 for VF, 470-473, 471/-472/
SCA and, 35lt, 353t-354t, 358-360, 359/-360/ hemodynamic support for, 473, 474/
ICM, 168,467 for VT
SCA and, 342t hemodynamic support for, 473, 474/
idiopathic dilated after MI, 461-466, 461/-465/
sustained monomorphic VT and, 197 forWPW, 169
VT-NS and, 178 Cavotricuspid isthmus (CTI), atrial flutter, 422-433,
NICM 423/-432/
catheter ablation for, 467-470, 468/-469/ Cesium,98
SCAin,345 Chagas disease, 467
PIC,448 CHF. S~ Congestive heart failure
SCA and, 350-357, 35lt, 353t Chronotropic incompetence (Cl), 240
sustained monomorphic VT and, 199 CIBDand,480
SVTand,257 CIED. See Cardiac implantable electronic devices
T-CM, 175-177 Cimetidine, 243
Cardiopulmonary resuscitation (CPR) CL. See Cycle length
ECPR,347 Classical reentry
for SCA, 345-347, 346/ atrial flutter and, 104/
Cardioversion. See also Implantable cardioverter-defibrillator tachycardia and, 98-104, 100/, 101/, 103/-105/
for AF, 231-232 CMR. See Cardiac magnetic resonance
for atrial flutter, 123, 231-232 Concealed conduction
for atrioventricular reciprocating tachycardia, 160 PVCs and, 46, 49, 49/, 50/
for AVNRT, 132 RBBB and, 70-71, 72
506 INDEX
Concealed conduction (Cont.): forAT,420

retrograde for AVNRT, 133, 415-417, 416/
AVRTand, 149, 150, 161 CS. See Coronary sinus
PVCs and, 50, 53-54, 53/ CSNRT. See Corrected sinus node recovery time
refractoriness and, 50 CT. See Crista terrninalis
spurious bradycardia and, 238 CTI. See Cavotricuspid isthmus
Conduction velocity (CV) CV. See Conduction velocity
gap phenomenon and, 84 Cycle length (CL), 385
tachycardia clanical reentry and, 100
Congenital AV block, 246-247 D
Congenital heart disease Dabigatran, 222, 222t
SCA and, 342t DADs. See Delayed after-depolarizations
SVT and, 290/ DCS. See Distal coronary sinus
Congestive heart failure ( CHF) DDD. See Dual-chamber pacing
atrial flutter and, 123 Defibrillation. See also Implantable
BBRVT and, 201 cardioverter-defibrillator
NSVT and, 178 for SCA, 341, 346
SVTand,257 forVF,471/
Cor pulmonale, 259 Delayed after-depolarizations (DADs), 97,
Coronary artery disease (CAD) 98,99/
carotid sinus hypersensitivity and, 249 programmed electrical stimulation for, 108
LBBBand,60 Delta waves, 156
SCA and, 344-345, 345/ Depolarization
sustained monomorphic VT and, 190, 197-199 AIVR and, 172
Coronary occlusion DADs, 97, 98, 99f
MI and, 461 programmed electrical stimulation for, 108
SCA and, 342t EADs, 97-98, 97f
SCDand, 344 bradycardia and, programmed electrical
tachycardia classical reentry and, 101 stimulation for, 108
Coronary sinus (CS) of His bundle
AF and, 216 in atrial pacing, 378
ATand,422 AVRT and, 150
atrial flutter and, 122, 122/ BBRVT and, 202
atrioventricular reciprocating tachycardia and, PVCs and, 46, 53
148 JTand, 136
AVNRT and, 129, 130, 13lt, 135/ overdrive suppression of, 375
DCS, 18/ preexdtation syndromes and, 142
AVRTand, 149, 150 forSVT,291
HPSand,30f tachycardia classical reentry and, 102
preexcitation syndromes and, 145/ of ventricles
endocardial catheter placement and, 8f AVNRT and, 131t
PCS WQT and, 310, 313/
HPSand,30f Diabetes mellitus
preexcitation syndromes and, 145/ atrial flutter and, 122
preexcitation syndromes and, 144 multifucal atrial tachycardia and, 118
preexcited tachycardia and, 163f-164f Digitalis
PVCsand,49 for AT, 117
Corrected QT interval. See QTc for atrioventricular reciprocating tachycardia, 159t
Corrected sinus node recovery time (CSNRT), bidirectional tachycardia and, 190
375,376/ DADsand,98
Coupling interval JTand, 136
AVNRT and, 131/ for preexcited tachycardia, 167
SACT and, 376 sick sinus syndrome and, 243
CPR. See Cardiopulmonary resuscitation forSVT,298
CPVT. See Catecholaminergic polymorphic ventricular for tachycardia, 95
tachycardia Digoxin
Crista terminalls (CT) for AF, 226t
AF and, 435t for AVNRT, 132, 133
AT and, 417, 419-420 CPVT and, 271
atrial flutter and, 122, 122/ Dilated cardiomyopathy
CRT. See Cardiac resynchronization therapy idiopathic
Cryoablatlon, 404, 405/ sustained monomorphic VT and, 197
forAF,439,440,442 VT-NS and, 178
INDEX 507
NSVT and, 177 Effective refractory period (ERP)

VT and, 199, 258 AP-ERP, 168, 169
Diltiazem AVNRT and, 13lf
fur AF, 225, 226t ventricular preexdtation and, 261
fur atrioventricular reciprocating tachycardia, 160 Ejection fraction
fur AVNRT, 133 EP testing and, 334
fur multifocal atrial tachycardia, 119 HFwith,228
furSVT,295 LVEF
Direct current cardioversion, for AF, 231-232 AFand,218
Direct-acting oral anticoagulants (DOAC), NICM VT and, 470
222,222t sarcoidosis and, 358
Disopyramide SCA and, 351, 352
furAF,225 sustained monomorphic ventricular tachycardia and,
fur atrioventricular reciprocating tachycardia, 191-192, 19lf
159t T-CM and, 176, 177
fur AVNRT, 132 VT-NS and, 188/
furSVT,298 PVCs and, 184
Distal coronary sinus (DCS), 18/ PVI and, 434/
atrioventricular reciprocating tachycardia and, RVEF
149,150 ARVC and, 361
HPSand, 30/ ICDs and, 353f
preexcitation syndromes and, 145/ SCA and, 344, 350
Diuretics, LQTS and, 187, 269 Electrocardiogram (ECG), 3, 4/. See also $pecific arrhythmias and
Dizzy spells, 338 ECG parameters
DOAC. Su Direct-acting oral anticoagulants Electrolytes
Dofetilide,224,225,225t action potential and, 95
Dronedarone, 224, 225t, 226 AF and, 219
Dual pathway, AVNRT and, 123, 131-132, 131/, LQTS and, 189
133,410 multifocal atrial tachycardia and, 118
Dual-chamber (DDD) pacing, 480-484, QT interval and, 362
482f-485f VT and, 199
fur sick sinus syndrome, 243 Electrophysiologic testing (EP testing), 373-398, 376/-384/.
Dyspnea See also Endocardial catheter mapping; Programmed
AFand,217 electrical stimulation
AT and, 117 for Brugada syndrome, 270
atrial flutter and, 123 diagnostic maneuvers of, 383-398, 384/, 384t, 385t,
AVNRT and, 126 386f-398f
bradycardia and, 235 for LOC, 334-336, 337/
LBBBand,69 forSCA,350
pulmonary vein stenosis and, 441 forSVT,292
Encainide
E for SCA, 351
Early after-depolarizations (EADs), 97-98, 97f for ventricular ectopy, 258
bradycardia and, programmed electrical stimulation Endocardial catheter mapping, 381-383, 384/
for, 108 placement of, 8f
Early repolarization (ER), 274-275, 275/, 277/ for RBBB, 57-58
SCA and, 35lt, 362-363, 364f Entrainment
Ebstein's anomaly activationsequencemapping,109
preexcited tachycardia and, 164 in atrial flutter, 124/
SVTand,291 AVNRT and, 131t
ECG. Su Electrocardiogram ILVT and, 457
Echo zone, AVNRT and, 131t tachycardia classical reentry and, 102
ECMO. Su Extracorporeal circulation and oxygenation of VT, 105f
ECPR. See Extracorporeal CPR after MI, 462-463, 462f
Ectopic complexes EP testing. See Electrophysiologic testing
of atria, 35-45, 36/-45/, 257 Epicardial access, mapping, and ablation,
ECG of, 35-54, 36f-53f 466-467
of ventricles, 45-54, 46/-53/, 257-258 Epinephrine, programmed electrical stimulation
WQTand,307 for, 108
Edoxaban,222,222t Epsilon waves, AVRC and, 277, 279/, 280
Edrophonium (Tensilon) ER. See Early repolarization
fur AVNRT, 132 ERP. See Effective refractory period
fur narrow QRS tachycardia, 295 Esmolol, 226t
508 INDEX
Excitable gap HBE. See His bundle electrogram

AF and, 121-122 HBED. See His bundle electrogram distal
tachycardia clanical reentry and, 99-100, 102, 105/ HBEP. See His bundle electrogram proximal
Exercise stress test HCM. See Hypertrophic cardiomyopathy
for CPVT, 362 Heart block, 22
graded treadmill exercise test, fur LOC, 326, 327/-330/ Heart failure (HF)
for LQTS, 265-267 AF and, 218
Extracorporeal circulation and oxygenation (ECMO), 347 AT and, 117
catheter ablation and, 473, 474/ CHF
Extracorporeal CPR (ECPR), 347 atrial flutter and, 123
Extrastlmuli BBRVT and, 201
activation sequence mapping, 109 NSVT and, 178
AT and, 117 SVTand,257
AVNRT and, 124, 131, 131t CIED and, 480
DADs and, 98, 99/ with ejection fraction, 228
SACT and, 376 sinus tachycardia and, 113
sinus node reentry and, 114 sleep apnea and, 259
sustained monomorphic VT and, 197 T-CM and, 177
tachycardia and Hemiblocks, LBBB and, 60
classical reentry and, 101, 102, 106t Hemothorax, 486
programmed electrical stimulation and, 381 HF. See Heart failure
VF and, 186 HH interval, 387, 390/
H 1H 2 interval, 87
F High right atrium (HRA), 6, 9f, 18/
Fascicular block bipolar and unipolar electrograms and, 374/
AV block and, 247 PACs and, 40/
LBBB and, 60-62, 61/ preexcltation syndromes and, 144/
RBBB and, 40/ His bundle, 4, 4f. See also AH interval
Fasclcular foci, 135 atrial flutter and, 122/
Fast conducting pathway atrioventricular reciprocating tachycardia and,
atrioventricular reciprocating tachycardia and, 149,157
154/ AVNRT and, 130, 131t
AV node and, 13 BBRVT and, 201
AVNRT and, 411 congenital AV block and, 247
Filled squares, AVNRT and, 131/ deflection of, 9
First-degree AV block, 10-11, llf, 244 atrial pacing and, 379/
Flecainide bipolar electrogram and, 3 74
for AF, 224, 225, 225t bradycardia and, 237
for atrial flutter, 123 HBEand, 13
for atrioventricular reciprocating tachycardia, preexcitation syndromes and, 143
159t PVCsand,49
for AVNRT, 132, 133 QRS complex and, 28
forRMVT, 175 depolari7.ation of
for SCA, 351 in atrial pacing, 378
forSVT,298 AVRT and, 150
for ventricular ectopy, 258 BBRVT and, 202
Foramen ovale (FO) PVCs and, 46, 53
antidromic tachycardia and, 167/ endocardial catheter placement and, 8/
atrial flutter and, 122/ EP testing and, 373
first-degree AV block and, 244
G gap phenomenon and, 89/
Gap phenomenon, 83-88, 84/-89/ LBBBand,59
Gastric reflux, AF catheter ablation and, 442 LOCand,336
Glycosides premature junctional complexes and,
for bidirectional tachycardia, 190 43
sick sinus syndrome and, 243 PVCs and, 47/, 49/
Graded treadmill exercise test, fur LOC, 326, 327/-330/, QRS complex and, 15
329/ RBBBand, 72
RV and, 394-395
H spurious bradycardia and, 238
HA interval, 390/ sustained VT and, 184
AVNRT and, 412 SVT and, 287, 289, 290/
retrograde conduction and, 19, 20, 21 tachycardia classical reentry and, 100
INDEX 509
His bundle electrogram (HBE), 6, 9f Hypothermia, ER and, 274

AF and, 38, 41/ Hypoventilation, in sleep apnea, 259
atrioventricular reciprocating tachycardia and, 154/ Hypovolemia, sinus tachycardia and, 113
AVNRT and, 132/ Hypoxia
bipolar and unipolar electrograms and, 374/ EADsand,98
His bundle deflection and, 13 multifocal atrial tachycardia and, 118
PACs and, 37, 40/, 41/ sinus tachycardia and, 113
preexcitation syndromes and, 144/
preexcited tachycardia and, 163/-164/ I
PVCs and, 51, 51/ IABP. See Intra-aortic balloon pump
retrograde conduction and, 20 Ibutilide
His bundle electrogram distal (HBED), 7, 9/, 16/ for atrial flutter, 123
His bundle electrogram proximal (HBEP), 7, 9f, 16/, 18/ for atrioventricular reciprocating tachycardia, 159t
His-Purkinje system (HPS), 3, 6 ICD. See Implantable cardioverter-defibrillator
ANS and, 28-30, 29/-31/ ICM. See Ischemic cardiomyopathy
atrial and ventricular pacing for, 377 Idiopathic dilated cardiomyopathy
atrioventricular reciprocating tachycardia and, 147, 148, 149, NSVT and, 178
151-152, 157/ sustained monomorphic VT and, 197
AV block and, 256 Idiopathic left ventricular tachycardia (ILVT), 203-204, 455-457,
AV conduction delay and, 10, 11/ 457t, 458/
BBRVT and, 201 Idiopathic ventricular fibrillation (IVF), 363-364
gap phenomenon and, 84-85, 85/, 86, 86/-87/ IHR. See Intrinsic heart rate
LBBB and, 66, 66/ ILVT. See Idiopathic left ventricular tachycardia
PACs and, 38, 40/, 41/ Implantable cardioverter-defibrillator (ICD), 487-490,
preexcited tachycardia and, 164-165, 166/ 490/-491/
PVCs and, 45, 46, 46/ for CPVT, 362
RBBB and, 62, 64 for exercise-induced VT, 182, 183
refractoriness of, 62, 3 79 for IVF, 364
sustained monomorphic VT and, 193 for LOC, 336
tachycardia automatidty and, 95 for LQTS, 267-269
Wenckebach block.in, 15, 17/ forMVP, 184
His-ventricle interval See HV interval NICM VT and, 469, 470
Holter monitoring for SCA, 348-350, 348t-349t, 352-357, 353t-354t,
forAF,226 356/, 487
for IST, ll5 SICD, 491-493, 492/
for we, 327-329, 330/-333/, 335/ for sustained monomorphic VT, 199, 200/
forRMVT, 174 transvenous lead extraction for, 493-496, 493/-495/
HPS. See His-Purkinje system Inappropriate sinus tachycardia (IST), ll5-116, 442
HRA. See High right atrium Incomplete interpolation, 36, 39/
HV interval, 6, 9 PVCs and, 49, 50/
atrioventricular reciprocating tachycardia and, Inferior pulmonary vein, 3
149,158 Inferior vena cava (IVC), 3
BBBand,257 atrial flutter and, 122, 122/
BBRVT and, 466 Interpolation
bradycardiaand,237 in PACs, 35-37, 36/, 39/
CIED for, 479 in PVCs, 46-48, 50/
LBBBand,65 lnterventricular septum, RBBB and, 58, 71
we and, 334, 336 Intra-aortic balloon pump (IABP), 474/
sustained monomorphic VT and, 191 Intrinsic heart rate (IHR), 238
Hypertension Ischemia
atrial flutter and, 122 EADsand,98
carotid sinus hypersensitivity and, 249 SCA and, 344, 345/
LBBBand,60 tachycardia classical reentry and, 100
SVT and, 290/ Ischemic cardiomyopathy (ICM), 168, 467
Hyperthyroidism, sinus tachycardia and, 113 SCA and, 342t
Hypertrophic cardiomyopathy (HCM), 467 Isoproterenol
NICM VT and, 470 forAF,434
SCA and, 35lt, 353t-354t, 358-360, AH interval and, 26/
359/-360/ AT and, 116
Hypokalemia, EADS and, 98 atrioventricular reciprocating tachycardia and,
Hypotension 152,153/
atrial flutter and, 123 programmed electrical stimulation for, 108
vasodepressor syncope and, 333/ for RMVT, 174
51 O INDEX
Isoproterenol (Cont.): ILVT and, 455, 457, 457t

for sustained monomorphic VT, 207 WCand,334f
tachycardiaand,28,30/ OT arrhythmias and, 452, 454t
IST. See Inappropriate sinus tachycardia PACs and, 64-66, 65/, 66/
Ivabradine, 115, 443 repetition of, 71-72
IVC. See Inferior vena caw. RMVT and, 174
IVF. See Idiopathic ventricular fibrillation sarcoidosis and, 358
SCA and, 357t
J sustained monomorphic VT and, 193, 195/.
J waves, 274-275, 275/, 276/ 207-208
ERand,362 SVTand,287
LOCand,325 tachycardia and, 66-69, 67f-70f
JT. See Junctional tachycardia WQT and, 305/. 306, 309-310, 311/, 312/
Junctional recovery time, for AV block, 256 Left coronary cusp (LCC), 449-452, 452/
congenital, 247 Left interventricular septum, 4
Junctional tachycardia (JT), 135-136 Left posterior fascicle (LPF), 455, 457
catheter ablation for, 442-443 Left ventricle (LV)
nonparoxysmal, 136 AF and, 218
SVT and, 288/ ALVC, 360
PJRT,140 ATand,419
SVTand,289 BBRVT and, 466
DDDand,483
K EP testing and, 373
Kent bundle, 259 ILVT, 203-204, 455-457, 457t, 458/
Koch's triangle, 133 OT of, 359
sarcoidosis and, 358
L SVTand,296
LA. See Left atrium Left ventricular ejection fraction (LVEF)
LAA. See Left atrial appendage AF and, 218
LAD. See Left anterior descending coronary artery NICM VT and, 470
LAF. See Left anterior fascicle sarcoidosis and, 358
LBB. See Left bundle branch SCA and, 351, 352
LBBB. See Left bundle branch block sustained monomorphic ventricular tachycardia and,
LCC. See Left coronary cusp 191-192, 19lf
Leading circle reentry, 99, 103-104 T-CM and, 176, 177
Leadless cardiac pacemakers, 479, 486 VT-NS and, 188/
Left anterior descending coronary artery (LAD), Left ventricular ejection time (LVET), 315/
6f.7f Left ventricular outflow tract (LVOT), 447-457, 449/-453/, 454t,
OT arrhythmias and, 448 455/-456/, 457t
Left anterior fascicle (LAF), 455 Lidocaine
Left atrial appendage (LAA), 435-436 for atrioventricular reciprocating tachycardia, 159t
Left atrium (LA), 3, 4/ forSCA,347
atrial flutter and, 122/ Ligament of Marshall, 216
atrioventricular reciprocating tachycardia and, AF and,435t
156 Lithium carbonate, 243
EP testing and, 373 WC. See Loss of consciousness
preexdtation syndromes and, 145/ Long QT syndrome (LQTS), 187-190, 262, 263-269,
Left bundle branch (LBB), 4f, 5, 5f 264/-269/
BBRVT and, 201, 202t-206f EADsand,98
gap phenomenon and, 86 we and, 325, 326/
refractoriness of, 64 SCA and, 35lt, 354t, 361-362
retrograde conduction and, 19 TdP and, 187
Left bundle branch block (LBBB), 5, 7f. 58t, 59-62, Long-standing persistent atrial fibrillation, 213
60f-62f Loss of consciousness (WC), 323-338, 324t, 326/-333/,
AFand,68/ 335/. 337/
atrioventricular reciprocating tachycardia and, Brugada syndrome and, 325
150 carotid sinus hypersensitivity and, 325
AV block and, 247/ His bundle and, 336
AV conduction delay and, 9-10, 10/, 11/ Holter monitoring for, 327-329, 330/-333/. 335/
AVRC and, 276, 277, 278/, 280/ HV interval and, 334, 336
BBRVT and, 466 ICDfor,336
Brugada syndrome and, 270 LBBB and, 334/
INDEX 511
LQTS and, 325, 326/ Narrow QRS tachycardia. See Supraventrlcular tachycardia
QT interval and, 326/ (SVT)
LPF. See Left posterior fascicle NCC. See Noncoronary cusp
LQTS. See Long QT syndrome Neck-collar suction, 23-25, 25/
LY. See Left ventricle Neurally-mediated, vagal bradycardia, 248-250, 249/
LVEF. See Left ventricular ejection fraction NICM. See Nonischemic cardiomyopathy
LVET. See Left ventricular ejection time Nicotine, sinus tachycardia and, 113
LVOT. See Left ventricular outflow tract Nodofasclcular fiber, PJRT and, 140
Nodofascicular pathways, junctional tachycardia and, 135
M Noncoronary cusp (NCC), 422
Mahaim fibers, 139 Nonischemic cardiomyopathy (NICM)
Malignant mitral valve prolapse (MVP) syndrome, 183-184 catheter ablation fur, 467-470, 468/-469/
Metoprolol, 226t, 227 SCAin,345
Mexiletine Nonparoxysmal junctional tachycardia, 136
fur atrioventricular reciprocating tachycardia, 159t SVT and, 288/
fur ventricular ectopy, 258 Non-ST elevation MI (NSTEMI), SCA and, 347
MI. See Myocardial infarction Nonsustained ventricular tachycardia (VT-NS, NSVT), 172-181,
Mitral valve, 4/ 173/-180f, 447
Mitral valve opening time (MVOT), 315/ NSTEMI. See Non-ST elevation MI
Mitral valve prolapse (MVP), 183-184 NSVT. See Nonsustained ventricular tachycardia
papillary muscles and, 458-461, 459f, 460/
SCA and, 342t, 35lt 0
Mobitz type I AV block, 13, 245, 256 Obesity, atrial flutter and, 122
CIED and, 480 Obstructive sleep apnea
Mobitz type II AV block, 244f, 245 AF and, 214, 218
atropine and, 29, 3lf SCA and, 343t
beta-adrenergic blockers and, 29 Ordered entry. See Classical reentry
CIED and, 479, 480 Orthodromic tachycardia, 147
premature junctional complexes and, 43-45, 44f, 45/ Orthodromic wave, tachycardia classical reentry and,
sinus node exit block and, 241 102, 103/
Morlcizine Outflow tract (OT)
fur SCA, 351 arrhythmias, 447-457, 449/-453f, 454t, 455/-456f,
fur ventricular ectopy, 258 457t
Multifucal atrial tachycardia, 118-119, 119/ ofLV, 359
MUSE system, LQTS and, 264 PVCs,280
MVOT. See Mitra] valve opening time RBBBand,57
MVP. See Mitral valve prolapse of RV, 174
Myocardial infarction (MI) VT,203-204
NSTEMI,347 Overdrive pacing
SCA and, 341, 344, 347 ATand,402t
sick sinus syndrome and, 243 of sinus node, 375
STEMI,347 tachycardia classical reentry and, 102, 106t
sustained monomorphic VT and, 199 Overdrive suppression
tachycardia and of automaticity, 96
automatidty and, 95 AV block and, 246
classical reentry and, 102 of sinus node, 96, 241
VF and, 186 of spontaneous depolarization, 375
VTand,258 of subsidiary pacemakers, 95, 96, 241
catheter ablation for, 461-466, 461/-465/ tachycardia automaticlty and, 95
WCTand,302
Myocarditis p
JT and, 136 Pwave,3,4/
SCA and, 351t AH interval and, 14
Myofibrils, AF and, 216 AT and, 116, 417-419, 422
Myotonic dystrophy, SCA and, 343t, 354t atrial flutter and, 120, 121/
atrioventricular reciprocating tachycardia and,
N 155
Nzone,3 AVNRT and, 127f, 128, 128f, 129f, 134f
N-acetyl procainamide, 98 bradycardia and, 235
Nadolol first-degree AV block and, 244
furAF,226t multifocal atrial tachycardia and, 118
fur LOC, 326/ neck-collar suction and, 25/
512 INDEX
P wave (Cont.): PR interval, 3, 6-18, 9f

PACs and, 37, 38 AIVR and, 172
PR interval and, 9, 13 ANS and, 27, 27/
premature junctional complexes and, 43, 45/ anterograde conduction and, 10-12
PVCsand,49 AV block and, 247/
RBBBand, 70 AVNRT and, 127, 129, 130f, 132
sick sinus syndrome and, 241, 243/ BBBand,257
sinus node reentry and, 114 DDDand,483
sinus tachycardia and, 113 first-degree AV block and, 244
forSVT,291 P wave and, 13
SVT and, 290f, 292-293, 293f, 294, 294f, 295/ preexdtation syndromes and, 144
ventriculophasic sinus arrhythmia and, 24 premature junctional complexes and, 43, 44f, 45/
Wenckebach block and, 27f, 249/ PVCs and, 46, 49, 50, 52f, 53
WQT and, 304f, 306, 306/ sick sinus syndrome and, 243
PA interval stability of, 12, 12/
bradycardia and, 237 SVT and, 289, 292, 294, 294f, 295, 295/
LOCand,334 ventricular preexcitation and, 259, 260
PACs. See Premature atrial complexes Wenckebach block and, 249/
Palpitations, 338 Preexcitation syndromes, 139-169, 140f, 141f, 143f, 144.f.
Papillary muscles, 458-461, 459f, 460/ See also Ventricular preexcitation; Wolff-Parkinson-White
Para-Hisian pacing, 394-395, 396/-398/ syndrome
Parasympathetic tone atrioventricular reciprocating tachycardia, 147-152, 148f,
phenylephrine and, 26, 26/ 150f-154f, 154-163, 155t, 156f, 157f, 159/-162.f. 159t
Wenckebach block and, 27 mechanisms of, 142-144, 145/
Paroxysmal atrial fibrillation, 213 Preexcited tachycardia, 163-168, 163/-167.f. See also Wide QRS
Paroxysmal AV block, 248, 248/ tachycardia
Paroxysmal tachycardia Pregnancy, AVRT and, 158
AT and, 116, 117 Premature atrial complexes (PACs), 35-42, 36/-42/
AV node reentry and, 101 in antidromic tachycardia, 394, 394/
AVNRT and, 124 atrioventricular conduction and, 37-42, 40/-42/
Partial ventricular assist devices (PVADs), 473 atrioventricular reciprocating tachycardia and, 147-149
PCS. See Proximal coronary sinus AVNRT and, 391/
PDA. See Posterior descending coronary artery gap phenomenon and, 83-88, 84/-89/
PEA. See Pulseless electrical activity interpolation in, 35-37, 36f, 39/
Pericarditis, 486 LBBB and, 64-66, 65f, 66/
AF catheter ablation and, 441, 442 preexdtation syndromes and, 142-143
epicardial access, mapping, and ablation and, 467 QRS complex and, 38, 71
Permanent atrial fibrillation, 213 RBBB and, 62-66, 63/-65/
Permanent furm ofjunctional reciprocating tachycardia (PJRT), 140 spurious bradycardia and, 238
Persistent atrial fibrillation, 213 supernormal conduction and, 90, 91/
Pharmacologic cardioversion, for AF, 232 tachycardia programmed electrical stimulation
Phenylephrine, 24/ and, 381
parasympathetic tone and, 26, 26/ Premature junctional complexes, 43-45, 43/-45/
PIC. See PVC-induced cardiomyopathy Premature ventricular complexes (PVCs), 45-54,
PJRT. See Permanent form of junctional reciprocating 46/-53/
tachycardia anterograde conduction and, 46f, 385
PMVT. See Polymorphic ventricular tachycardia ATand,419
Pneumothorax, 486 atrioventricular reciprocating tachycardia and, 147, 149-151,
Polymorphic ventricular tachycardia (PMVT), 98, 172, 177, 156-158, 157f, 159/
185f, 186/ AVNRT and, 134f, 151/-152/
CPVT, 190, 262, 270-274, 273f, 274/ AVRC and, 278f, 280, 280/
SCA and, 35lt, 354t, 362 Brugada syndrome and, 270
VTand,471 CPVT and, 270-274, 362
Post pacing interval. See PPI exercise-induced VT and, 181
Posterior descending coronary artery (PDA), 6f, 7f IVFand,364
Posterior septal papillary muscle (PSPM), 458-459, 459f, 460/ LVOT and, 453/
Postrepolarization refractoriness, 69 MVPand,184
Postural tachycardia syndrome (POTS), 115 NSVT and, 179-180
Potassium, DADs and, 98 OT,280
POTS. See Postural tachycardia syndrome arrhythmias and, 448, 452
PPI papillary muscles and, 458
sinus node exit block and, 241 RBBB and, 72, 73/
ventriculophasic sinus arrhythmia and, 23, 24 SCA and, 351, 355f, 357t
VT after MI and, 463/ SVT and, 290/
INDEX 513
tachycardia classical reentry and, 103/ AIVR and, 172

T-CM and, 175-176 anterograde conduction and, 44/
VT and, 447, 470, 471-472, 471/ AT and, 116, 117/
WCT and, 303/, 317 atrial flutter and, 121/, 125/
WQT and, 307/, 308/ atrioventricular reciprocating tachycardia and, 147, 149, 150,
Presyncope 152, 155
carotid sinus hypersensitivity and, 249 AV block and, 15, 256
sick sinus syndrome and, 242 AVNRT and, 127/, 128, 128/, 130/, 132/, 134f
Procainamide AVRC and, 276, 277, 278/, 279/, 280
furAF,225 BBRVT and, 202
fur atrioventricular reciprocating tachycardia, 159t, 160 Brugada syndrome and, 270
fur AVNRT, 132 conversion from wide to narrow, 75-77, 75t, 76/, 78f-79f
ERPand,261 ERand,362
fur preexcited tachycardia, 167 gap phenomenon and, 87
furSVT,298 His bundle and, 15
furWQT,320 deflection of, 9, 28
Programmed electrical stimulation, 107-109, 375/-382/ HPSand,30/
fur atrioventricular conduction, 377-381, 377/-381/ ILVT and, 457, 457t
fur RMVT, 174 rr
and, 135, 136
of sinus node, 375-376, 376/, 377/ LBBB and, 58t, 59, 60, 61, 65-66, 67, 67/
fur tachycardia, 381, 382/, 383/ LVOT and, 453/
fur ventriculoatrial conduction, 377-381, 377/-381/ neck-collar suction and, 25/
Propafenone NSVT and, 177/, 179
fur AF, 224, 225, 225t, 232 PACs and, 38, 71
fur atrial flutter, 123, 125/-126/ papillary muscles and, 458
fur atrioventricular reciprocating tachycardia, preexcitation syndromes and, 142, 143, 143/, 144/
159t preexcited tachycardia and, 163, 166
fur AVNRT, 132, 133 premature junctional complexes and, 43, 44/
fur RMVT, 175 PVCsand,45,50,51,53/
Propranolol RBBB and, 57, 58, set, 64, 70, 72-73, 73/
furAF,226t RMVT and, 173, 174, 175, 176/
fur exercise-induced VT, 182 RVOT and, 452/
Proximal coronary sinus (PCS) SCA and, 357t
HPSand, 30/ sick sinus syndrome and, 243
preexcitation syndromes and, 145/ supernormal conduction and, 90, 92/
PSPM. See Posterior septal papillary muscle sustained monomorphic VT and, 191, 193, 194/, 196/, 199
Pulmonary embolism, 402t sustained VT and, 184
atrial ectopy and, 257 SVT and, 287-298, 287/-29(}/, 291, 292, 293/-297/, 294, 294/, 297t
SCA and, 343t tachycardia classical reentry and, 102, 103/
Pulmonary vein (PY) TdPand, 186
AF and, 216, 216/, 217/ ventriculophasic sinus arrhythmia and, 23, 24
ATand,417 VF and, 186
stenosis, AF catheter ablation and, 441 VTand,470
Pulmonary vein isolation (PVI), 433-435, 434/, 440 after Ml, 462/
Pulmonic valve (PY), 448 QT interval. See also Long QT syndrome; Short QT syndrome
Pulseless electrical activity (PEA) AF and, 225, 226
SCA and, 342t, 343, 345 AV block and, 256
VFand,473 electrolytes and, 362
Purines, for AVRT, 159t WCand,326/
Purkinje fibers, 4, 4/ supernormal conduction and, 90-92
DADsand,98 TdP and, 186, 187
EADs and, 97/ QTc
tachycardia automaticity and, 95 LQTS and, 189-190, 263-267, 361
PV. See Pulmonary vein; Pulmonic valve SQTS and, 269, 362
PVADs. See Partial ventricular assist devices Quinidine
PVC-induced cardiomyopathy (PIC), 448 for AF, 224-225
PVCs. See Premature ventricular complexes for atrioventricular reciprocating tachycardia, 159t
PVI. See Pulmonary vein isolation for AVNRT, 132
EADsand,98
Q
Qwaves R
LBBBand,61 Rwave
VT after MI and, 462, 463/ AVNRT and, 205/
QRS complex, 5, 6f ERand,362
514 INDEX
R wave (Cont.): Right atrium (RA), 3, 4f

LBBB,58t AF and, 216
OT arrhythmias and, 452 atrial flutter and, 122
RBBBand,57 atrioventrlcular reciprocating tachycardia and,
VTand,308 147,156
RA. See Right atrium AVNRT and, 132f
Radiofrequencyablation,401-404,403/,404f endocardial catheter placement and, Bf
for AF,442 EP testing and, 373
for AVNRT, 133, 412-415, 413f-415f gap phenomenon and, 85
for exercise-induced VT, 182 HRA, 6, 9.f. lBf
for sustained monomorphic VT, 208, 209f bipolar and unipolar electrograms and, 374f
Random reentry, 99, 105f PACs and, 40f
RBB. See Right bundle branch preexcitation syndromes and, 144f
RBBB. See Right bundle branch block preexcltation syndromes and, 145f
RCC. See Right coronary cusp Right bundle branch (RBB), 4/, 6, 9f
Reflection, tachycardia classical reentry and, BBRVT and, 201, 202, 206.f. 466
101 gap phenomenon and, 89f
Refractoriness ILVT and, 455
of APs, 160, 261 preexcited tachycardia and, 165
AT and, 117 refractoriness of, 64, 71
of atria, 30 retrograde conduction and, 19, 21
AV node and, 42, 47/, 117-llB, 181 Right bundle branch block (RBBB), 5, 7/, 57-59, 5Bf, 58t
classical reentry and, 9B, 100 atrioventricular reciprocating tachycardia and, 149
ofHPS, 62, 379 AV block: and, 247/
ofLBB, 64 AVRC and, 277
PACsand,35 fascicular block and, 40f
postrepolarization, 69 interfascicular VT and, 466
programmed electrical stimulation and, 375 NICM VT and, 470
ofRBB, 64, 71 OT arrhythmias and, 454t
retrograde concealed conduction and, 50 PACs and, 62-66, 63f-65f
of sinus node, 115 repetition of, 70-75, 71/, 73/, 74f
SNRT and, 239 sarcoidosis and, 358
ofVAconduction,379-3Bl sustained monomorphic VT and, 199, 204, 207,
of ventricles, 30, 48f 207f-209f
Refractory period (RF) SVTand,287
for AT,420 tachycardia and, 66-69, 67/-70/
for AV node, 379 Wenck:ebach block and, 15
AVNRT and, 131 WQT and, 305/, 306, 307, 309-310, 311.f. 319/
SACT and, 376 Right coronary cusp (RCC), 449-452, 451/, 452f
tachycardia classical reentry and, 100 Right ventricle (RV), lBf
Repetitive monomorphic ventricular tachycardia (RMVT), ARVC, 262, 275-280, 277f-2B0f, 448
173-174,174f-176/ NICM and, 467, 470
Repolarization SCA and, 35lt, 354t, 360-361
ER, 274-275, 275/, 277/ ATand,419
SCA and, 35lt, 362-363, 364f bipolar and unipolar electrograms and, 374f
LOCand,325 DDDand,4B3
forSVT,291 endocardial catheter placement and, Bf
Respiratory failure EP testing and, 373
multifocal atrial tachycardia and, 118 His bundle and, 394-395
sinus tachycardia and, 113 OT of; 174
Retrograde conduction, 18-21, 1Bf-21f preexcitation syndromes and, 144f
atrioventricular reciprocating tachycardia and, 148, PVCs and, 47/, 54
149,156 RBBBand, 57
AVNRT and, 129, 131t retrograde conduction and, 19, 20
BBRVT and, 202 sarcoidosis and, 358
concealed VA conduction and, 395
AVRTand, 149, 150, 161 VA interval in, 392f
PVCs and, 50, 53-54, 53f ventricular pacing in, 3B8, 392.f. 394
refractoriness and, 50 Right ventricular ejection fraction (RVEF)
gap phenomenon and, B7, B9f ARVC and, 361
preexcited tachycardia and, 164 ICDs and, 353f
Return of spontaneous circulation (ROSC), 341, Right ventricular outflow tract (RVOT), 447-457, 449f-453f, 454t,
345-346 455f-456f, 457t
RF. See Refractory period VTand,471
INDEX 515
Rivaroxaban,222,222t refractorinea. of, 115

RMVT. See Repetitive monomorphic ventricular tachycardia sinus tachycardia and, 113
ROSC. See Return of spontaneous circulation tachycardia and, 95
RP interval Sinus node recovery time (SNRT), 237
AVNRT and, 127, 129, 389/ Sinus pause
PVCs and, 49-50 sinus node dysfunction and, 255
SVT and, 292, 294/ in sleep, 258, 258/
RR interval Sinus tachycardia, 113
atrioventricular reciprocating tachycardia and, 155 IST, 115-116, 442
LBBBand,67 Sleep
RBBBand, 70 arrhythmias in, 258-259, 258f
SRR,259 Wenckebach block and, 27, 27f
ventricular preexcitation and, 168, 169 Sleep apnea, 259
rScomplex AF and, 214, 218
ARVC and, 280 AV block in, 18/, 28
LBBBand,60 SCA and, 343t
RV. See Right ventricle Slow conduction zone (pathway)
RVEF. See Right ventricular ejection fraction activationsequencemapping,109
RVOT. See Right ventricular outflow tract atrial flutter and, 122
Ryanodine receptor (RyR2), 271 atrioventricular reciprocating tachycardia and,
148, 154f
s AVNRT and, 135f
Swave AVRC and, 276
AVRC and, 278/ tachycardia classical reentry and, 102
RBBBand,57 SNRT. See Sinus node recovery time
WQTand,307 Somnolence, in sleep apnea, 259
SA. See Sinoatrial node Sotalol
SACT. See Sinoatrial conduction time fur AF, 224, 225-226, 225t
Sarcoidosis fur AT, 117-118
NICM VT and, 470 fur atrial flutter, 123
SCA and, 342t, 35lt, 353t, 357-358, 358/ fur atrioventricular reciprocating tachycardia, 159t
SCA. See Sudden cardiac arrest fur AVNRT, 133
SCD. See Sudden cardiac death EADsand,98
Schizophrenia, SCA and, 343t fur RMVT, 175
Second-degree AV block, 244/, 245. See also Mobitz type I AV furSVT,298
block; Mobitz type II AV block fur T-CM, 177
S2 tt,. interval, 89/ Spurious bradycardia, 238-240, 239f
Short QT syndrome (SQTS), 269 SQTS. See Short QT syndrome
SCA and, 35lt, 354t, 362, 363/ SRR (shortest R-R interval), 259
Shortest R-R interval (SRR), 259 s,s. interval, 89/
SICD. See Subcutaneous implantable cardioverter-defibrillator ST elevation MI (STEM!), 347
Sick sinus syndrome, 240-243, 240/-243/ ST segment
sinus node dysfunction and, 255 atrioventricular reciprocating tachycardia and,
Single-chamber pacemakers, 480-483 154
Sinoatrial conduction time (SACT), 376, 377/ AVRC and, 276
bradycardia and, 237 Brugada syndrome and, 270, 272f
Sinoatrial (SA) node, 3 ER and, 275, 362
Sinotubular junction, 450 SQTS and, 362
Sinus arrest, 240-241, 240/ SVT and, 291, 295/
Sinus bradycardia, 240 WQT and, 304/
Sinus node, 3, 4/ STEMI. See ST elevation MI
ANS and, 22-25, 23/-25/ Stroke
baroreflex and, 25/ AFand
bradycardiaand,237,240-243,240/-243/ catheter ablation and, 441
dysfunction of, 255-256 prevention of, 220-222, 22 lf, 222t
exit block, 241, 241/, 242/ VTand,473
IST and, 115 Subcutaneous implantable cardioverter-defibrillator (SICD),
overdrive pacing of, 375 491-493,492/
overdrive suppression of, 96, 241 Subsidiary pacemakers
PACs and, 35-42, 36/-42/ automaticity in, 31
programmed electrical stimulation of, 375-376, 376/, overdrive suppression of, 95, 96, 241
377/ Substrate mapping and ablation, for VT, 464-466,
reentry, 114-115 465/
516 INDEX
Sudden cardiac arrest (SCA), 341-364, 345t, 348t, 349t, 352f, T

358f-360f, 363f, 364/ Twave
cardiomyopathy and, 350-357, 351t ATand,419
CPR for, 345-347, 346/ atrioventricular reciprocating tachycardia and, 154
etiology of, 343-345, 344/ AVRC and, 277, 278f, 279/
ICD for, 348-350, 348t-349t, 352-357, 353t-354t, LQTS and, 264-265, 267
356f, 487 MVP and, 183-184
risk stratification for, 350-357, 35lt, 355f, 356f, 357t NSVT and, 177
subsets of, 342t-343t PACs and, 37, 38
survivor evaluations for, 347-350, 349/ PVCsand,51
Sudden cardiac death (SCD), 341-342 SCA and, 357t
atrioventricular reciprocating tachycardia and, 159 Tachycardia. See also Ventricular tachycardia
Brugada syndrome and, 270 activation sequence mapping for, 109
ERand,274 AF and, 103
exercise-induced VT and, 183 antidromic, 147
MVP and, 183, 184 APs and, 164, 167/
NSVT and, 177-188 PACs in, 394, 394/
ventricular ectopy and, 257-258 AT, 29f, 115-119, 116f-119f, 385
ventricular preexcltation and, 168, 259, 261/ atrial flutter and, 120
VT and, 257-258 catheter ablation for, 402f, 417-422, 418/-421/
WPWand, 141 classification of, 417t
Superior vena cava (SVC), 3 SVT and, 287, 288f, 296
AF and, 216 WQT and, 303, 313/
atrial flutter and, 122/ atrioventricular reciprocating, 154-163, 155t, 156f, 157f,
Supernormal conduction, 89-92, 91f, 92/ 159/-162f, 159t
preexcitation syndromes and, 142, 144/ AFand,215/
Supraventricular tachycardia (SVT), 113-120, 114f, 114t, 115f, catheter ablation for, 158-159, 161, 395, 398, 402/
257, 287-298, 287f-290f, 293f-297f, 297t. See also Wide OT arrhythmias and, 452
QRS tachycardia ventricular pacing in, 386/
AF and, 119-120 WQT and, 313/
AT and, 116 automaticity and, 95-98, 96f, 96t, 97/
atrial flutter and, 120 AVNRT, 123-135, 127f-132f, 13lt, 134f, 135/
AVreentry and, 292 AFand, 119/
AVNRT and, 132 catheter ablation for, 130f, 402f, 410-416, 411/
catheter ablation for, 298, 401-443, 402/ cryoablation for, 404, 415-417, 416/
endocardial catheter mapping for, 381 diagnostic maneuvers for, 383-394, 386f, 387f, 389/-391/
preexcited and, 163 PACs and, 391/
programmed electrical stimulation and, 375, 381 radiofrequency ablation for, 133, 412-415, 413/-415/
RMVT and, 175 RP interval and, 127, 389/
sustained monomorphic VT and, 191 tachycardia classical reentry and, 100
ventricular pacing in, 386/ ventricular pacing in, 387/
verapamil for, 107 bidirectional, 190
Sustained monomorphic ventricular tachycardia, 190-197, 192f, CPVT and, 273/
194f-196f BTS, 229-230, 229f, 230/
CAD and, 190, 197-199 bradycardia and, 237
ICD for, 199, 200/ side sinus syndrome and, 241, 242/
SVC. See Superior vena cava classical reentry and, 98-104, lOOf, lOlf, 103/-105/
SVT. See Supraventricular tachycardia DADsand,98
Swan-Ganz catheters, 58 lsoproterenol and, 28, 30/
Syncope, 329/-330/ IST, 115-116, 442
AF and, 217 JT, 135-136
ARVC 5nd, 361 catheter ablation for, 442-443
atrial flutter and, 123 PJRT, 140
atrioventricular reciprocating tachycardia and, 158 SVTand,289
AV blode and, 256 LBBB and, 66-69, 67f-70f
AVNRT and, 126 we and, 324-325
Brugada syndrome and, 270 mechanisms of, 95-109, 96f, 96t, 97f, 99f-101f, 103/-105f, 106t,
carotid sinus hypersensitivity and, 249 107f, 108/
causes of, 329 multifocal atrial, 118-119, 119/
EP testing for, 336, 337/ orthodromic, 147
LOC and, 323, 324, 324t, 326 paroxysmal
LQTS and, 269 AT and, 116, 117
side sinus syndrome and, 242 AV node reentry and, 101
vasodepressor, 250, 325, 333/ AVNRT and, 124
INDEX 517
POTS, 115 Trifascicular system, LBBB and, 5, 60

preexcited, 163-168, 163/-167/ TT. See Tendon of Todaro
programmed electrical stimulation for, 107-108, 381,
382/, 383/ u
RBBB and, 64, 66-69, 67f-70f ULV. See Upper limit of vulnerability
sinus, 113 Unipolar electrograms, 373-374, 374f
sinus node dysfunction and, 255 Upper limit of vulnerability (ULV), 490
SVT, 113-120, 114/, 114t, 115/, 257, 287-298, Upright tilt testing, for LOC, 331-334
287/-290/, 293/-297/, 297t
AF and, 119-120 v
AT and, 116 VA,378-379,380/
atrial flutter and, 120 VA conduction, 18
AV reentry and, 292 atrioventricular reciprocating tachycardia and, 150-151
AVNRT and, 132 gap phenomenon and, 87
catheter ablation for, 298, 401-443, 402/ preexcited tachycardia and, 165-166
endocardial catheter mapping for, 381 programmed electrical stimulation for, 377-381, 377/-381/
preexclted tachycardia and, 163 refractoriness of, 379-381
programmed electrical stimulation and, RVand,395
375,381 WQTand,304
RMVT and, 175 VA interval, 378-379
sustained monomorphic VT and, 191 atrioventricular reciprocating tachycardia and, 155, 161
ventricular pacing in, 386/ PVCs and, 50, 51/, 52-53
verapamil for, 107 inRV,392/
VA-RT, 385, 386/ VACS. See Ventriculoatrial conduction system
VF and, 103 Vagal tone, 18, 18/
WCT, 301-320, 302/-313/, 315/-320/, 320t exercise-induced VT and, 182
LOCand,334f systolic blood pressure and, 24/
VT and, 383 Wenckebach block and, 27
Wenckebach block and, 26 Vagotonic maneuver. See also Carotid sinus massage
Tachycardia cycle length (TCL), 385, 389/, 390/ for sinus tachycardia, 113
Tachycardia-related cardiomyopathy (T-CM), forSVT,295
175-177 Valsalva maneuver
TAD. See Terminal activation duration for atrioventricular reciprocating tachycardia, 160
TCI. See Tricuspid caval isthmus for AVNRT, 132
TCL. See Tachycardia cycle length for SVT, 291, 295
T-CM. See Tachycardia-related cardiomyopathy VA-RT (ventriculoatrial interval during tachycardia),
TdP. See Torsade de pointes 385, 386/
TEE. See Transesophageal echocardiography Vasodepressorsyncope,250
Tendon of Todaro (TT), 122/ hypotension and, 333/
Tensilon. See Edrophonium LOCand,325
Terminal activation duration (TAD), 277, 278/ Vasovagal phenomenon, ANS and, 30-31, 32/
Third-degree AV block, 246 Ventricles, 3. See also Left ventricle; Right ventricle
Thromboembolism ANS and, 30, 32/
AF catheter ablation and, 441 depolarization of
anticoagulants for, 441 AVNRT and, 13lt
stroke from, 220 WQT and, 310, 313/
Thyrotoxicosis, 257 ectopic complexes of, 45-54, 46/-53/, 257-258
Torsade de pointes (TdP), 186-190, 188/, 189/ refractoriness of, 30, 48f
AFand,225 tachycardia classical reentry and, 101
DADsand,98 Ventricular epicardial activation, 5, 6f, 7f
IVFand, 364 Ventricular fibrillation (VF), 186
LOCand,325 atrioventricular reciprocating tachycardia and, 155, 160
LQTS and, 361 Brugada syndrome and, 270, 361
Transeptal conduction catheter ablation for, 470-473, 471/-472/
BBRVT and, 202 hemodynamic support for, 473, 474/
RBBB and, 72, 73/, 74f CPVT and, 271
Transesophageal echocardiography (TEE) ER and, 274, 275, 362, 363
for AF, 231, 231/ HCMand,360
catheter ablation for, 442 ICD for, 487-490, 490/-49 lf
Transvenousleadextraction,493-496,493/-495/ ILVT and, 455
Tricuspid annulus, 417 IVF, 363-364
Tricuspid caval isthmus (TCI), 122, 122/, 123 LBBBand,60
Tricuspid ring, 156 LOCand,325
Tricuspid valve, 4/ MVPand, 184
518 INDEX
Ventricular fibrillation (Cont.): preexcited and, 163

sarcoidosis and, 358 programmed electrical stimulation and, 375, 381
SCA and, 344, 347, 487 PVCs and, 447
SQTS and, 269, 362 RMVT, 173-174, 174f-176/
tachycardia clanical reentry and, 103 sarcoidosis and, 358
ventricular preexcitation and, 168, 169, 259, 260 SCA and, 344, 347, 357t, 487
WPWand, 141 SQTS and, 269, 362
Ventricular flutter, 186 substrate mapping and ablation for, 464--466, 465f
ventricular pacing for, 187/ sustained, 184, 185/, 186f
Ventricular pacing sustained monomorphic, 190-209, 191/, 192/, 193f-196f,
inAT,388f 194/-196/, 198/, 200/-209/, 203t
in atrioventricular reciprocating tachycardia, 386f CAD and, 190, 197-199
in AV block, 377 ICD for, 199, 200/
in AVNRT, 387/ SVT and, 287, 291
PVCs and, 49, 53/ T-CM,175-176
in RV, 388, 392/, 394 verapamil and, 107, 108/
in sick sinus syndrome, 243 WCTand,383
in single-chamber pacemaker, 481 Ventriculoatrial. See VA
in sustained monomorphic VT, 198/ Ventriculoatrial conduction system (VACS), 18-19, 19/, 20/, 21
inSVT,386/ Ventriculoatrial interval during tachycardia (VA-RT), 385, 386/
in VA block, 378-379, 380f Ventriculophasic sinus arrhythmia, 22-23, 23/
in ventricular flutter, 187/ Verapamil, 17
Ventricular preexcltation, 140, 259-262, 261/-263/ for AF, 225, 226t
risks fur, 168-169 for AT, 117
variable degrees of, 146f-147f for atrial flutter, 123
Ventricular repolarization, LOC and, 325 for atrioventricular reciprocating tachycardia, 160
Ventricular return cycle, AVNRT and, 131t for AVNRT, 132, 133
Ventricular tachycardia (VT), 171-208, 257-258. See also for exercise-induced VT, 182
Supraventricular tachycardia (SVT) for preexcited tachycardia, 167
AIVR, 171-172, 172/, 173f for RMVT, 175
AVRC and, 277, 279/, 280 for sustained monomorphic VT, 207, 208
BBRVT, 199, 200-203, 201f-206f for SVT, 107, 295
catheter ablation for, 466 VT and, 107, 108/
bidirectional, 190 forWQT, 314, 317
Brugada syndrome and, 270, 361 VF. See Ventricular fibrillation
catheter ablation for, 447-473 VT. See Ventricular tachycardia
hemodynamic support for, 473, 474f VT-NS. See Nonsustained ventricular tachycardia
classical reentry and, 100-101
CPVT, 190, 262, 270-274, 273/, 274, 274/ w
SCA and, 35lt, 354t, 362 Warfarin,222,222t
DADsand,98 WCT. See Wide QRS tachycardia
endocardial catheter mapping for, 381 Wenckebach block, 13-18, 13/, 14f-15f,249/
entrainment of, 105f AHand,25
ERand,274 atrial flutter and, 120
exercise-induced, 181-183, 182t, 183t atrial pacing for, 378
fasdcular, 455-457, 457t, 458/, 466 bradycardia and, 235
HCM and, 359, 360 in HPS, 15, 17f
ICD for, 487-490, 490/-491/ P wave and, 27f
ILVT, 203-204, 455-457, 457t, 458f PACs and, 40f
interfascicular, 455--457, 457t, 458/, 466 sleep and, 27, 27/, 258
JT and, 136 tachycardia and, 26
LOC and, 325, 326/, 335, 335/, 336 vagal tone and, 27
after MI, catheter ablation for, 461-466, 46lf-465f Wide QRS tachycardia (WCT), 301-320, 302f-313f, 315f-320f,
MVP, 183-184 320t
NICM and, 467--470, 468f-469f LOC and, 334f
NSVT, 172-181, 173f-180f, 447 VT and, 383
papillary muscles and, 458 Wolff-Parkinson-White syndrome (WPW), 5, 141, 141/, 142, 142f
paroxysmal nonsustained, 177-181, 177f-180f ABLfor, 169
PMVT, 98, 172, 177, 185/, 186f SVTand,291
CPVT, 190, 262, 270-274, 273/, 274/, 35lt, 354t, 362 ventricular preexcitation and, 259-260
SCA and, 35lt, 354t, 362 WQTand,310
VTand,471

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To my wife and best friend, Klara.

14 Undiagnosed Syncope, Dizzy Spells, Palpitations ............................................................................................ 323

=== i:::_ -_~ p R

FIGURE 1·7 • A cllnlal electrophyslologlst's view of the electroCllrdlogram.

111 11111 1111 111111 II 1 11 1111111 111 11 111 I 11 111 11 1111111111

11-......__, .__ _ _ ___,_ _, .__ _ ____,,_ _

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RV _.. . ._. r-----r-o----ir---------r- AH A

FIGURE 1-17 • (Conrfnued)

On occasion, a Wenckebach conduction pattern can occur in the His-Purkin.je system

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that is, depress conduction, on the AV node-such as verapamil or beta-adrenergic blockers-

Right atrium Septum Left atrium

Right ventricle Left ventricle

VA Interval During Incremental V Pacing

0 100 200 300 400 500 600 700 800

o~ 0 225 250 275 300 325 350

AUTONOMIC NERVOUS SYSTEM EFFECTS

Control 200 µg Phenylephrfne

Effect of lsoproterenol (1 tJg/min) on Paced AH Interval

Ef1'11cte of HR and ANS on AV Nodal Conduction

Indirect ANS eft'ect

Another manifestation ofdisturbed AV nodal conduction, at least in part related to autonomic

conduction-for example, Mobitz type II block-can be worsened with beta-adrenergic block-

lsoproterenol 3.0 1o11>'min

Atrium and Ventricle

11 - - - - - - ' " ' - - - - - - -- -------' ......___ _ _ __

PREMATURE ATRIAL COMPLEXES

III I II II II Ill II II II II II I II II II III II II II II III II II II II III II II II IIII I II I

690 600 790 700

Effects on Atrioventricular Conduction

1111111 11111111111111 I I I I I I I I I I I I I I I I 111111111111111111111111111111

A, 700 A, 440 Ai. 850 730

A, 690 A, 800 770

11111 l I l I I l I "1111 l I I l I l I I l I I l I I I I l I I l I I tl 1111111111111

I IIIIIII IIIIIIIIIIIIII IIIIIII IIIIIIIIIIIIII IIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIIII

Ill - - - - " l l l ' - - - - - - - 1 , 1 - - - - - - - - - " ' 1... -----'ll...___

PREMATURE JUNCTIONAL COMPLEXES

-~~' j ,. r•· n- 1•· ·m ... .. rn . ., c::

- IJ: ·~ j:: ~ : ; ,._, : ~

PREMATURE VENTRICULAR COMPLEXES

HRA -t--t--~--~- FIGURE 2-16 • Premature ventricular complex with

:: .,, ., < H ·: tii

... ++- t:1 tt+

A' VA 190 A' VA 190

11111 1 1111 11 11 11 111111 1 11111 1 11

V1 ----l r----------"' ,..___

RV--1r~------...-r-~-. . t. . . . .-t~_......,_..~ 1-200_,

PERMANENT BUNDLE BRANCH BLOCK

TABLE 3-1 Criteria for bundle branch block.2

Left Bundle Branch Block

Pathology studies in patients with complete LBBB demonstrate destruction of a substantial

FIGURE 3-:Z • Twelve-lead ECG of left bundle branch block.

FUNCTIONAL BUNDLE BRANCH BLOCK

p.p 920 420 940

11-......, . _ _ ___,_ _, .__ _ ____,,_ _

V1 - - - - . . . r----.. . r----.. ,_ ~-~ ,--.. ,...---...._