Supraventricular Tachyarrythmias

SUPRAVENTRICULAR
TACHYARRYTHMIAS
Abnet M,October30,2017
Harrison’s and UpToDate
SUPRAVENTRICULARY
TACHYARRYTHMIAS
1. Atrial Premature Complexes
 Junctional Premature Complexes
2. Sinus Tachycardia
3. SA Node Reenterant Tachycardia (SANRT)
4. Atrial Fibrillation
5. Atrial Tachycardias
i. Atrial Flutter and Macroreentrant Atrial Tachycardias
ii. Focal and Multifocal Atrial Tachycardia
iii. AV Nodal Tachycardias
iv. AV Junctional Tachycardias
6. Tachycardias Associated with Accessory AV
Pathways (separate ppt)
The key to this, as in any arrhythmia, is to determine the relationship of
the P wave to the QRS complex. In particular:
• How many P waves to each QRS complex?
• If there are more P waves than there are QRS complexes (and provided
the QRS rate is fast, i.e. this is not pathological heart block), then
the diagnosis is an atrial arrhythmia with a degree of ‘physiological
block’. What is this? Many atrial arrhythmias beat at rates of 200–300
per minute, and the normal AV node cannot repolarize fast enough to
allow this number of impulses to the ventricle. The AV node will then
often let every second or third beat through, resulting in the QRS rate
being half or one third of the atrial rate. This is physiological block, a
finding that does not imply any pathological damage to the conducting
tissue of the heart. Arrhythmias with organized atrial beats, and so
similar shaped P waves, include atrial flutter, and atrial tachycardia
If the ratio of P waves to QRS complexes is 1 to 1, next
ascertain whether the P wave precedes or follows the
QRS? If the P wave precedes the QRS complex (i.e. the PR
interval is short, and conversely the RP interval is long),
then the diagnosis is usually sinus tachycardia
. If the P wave closely follows the QRS complex (i.e. the RP
interval is short, and conversely the PR interval is long),
then the diagnosis is usually an arrhythmia (very rarely
sinus rhythm with a very long PR interval gives rise to this
pattern). If the P wave follows very close indeed to the
QRS complex , then the diagnosis is usually atrioventricular
nodal re-entrant tachycardia (AVNRT); if the P wave is
quite distinct, and occurs within the T wave, usually the
diagnosis is atrioventricular re-entrant tachycardia
(AVRT).
• If the P waves cannot clearly be seen, either the
rhythm is sinus, and the heart rate is so high that
the P waves of one beat are buried in the T
wave of the preceding beat, or, more likely, the P
wave occurs simultaneously with the QRS complex,
so hiding its appearance, as in most cases of
AVNRT.
ATRIAL PREMATURE COMPLEXES
 APCs are the most common arrhythmia identified
during extended ECG monitoring.
 The incidence of APCs frequently increases with

age and with the presence of structural heart
diseases.
 Atrial premature complexes typically are

asymptomatic, although some patients
experience palpitations or an irregularity of the
pulse.
ATRIAL PREMATURE COMPLEXES-
ECG
 The ECG diagnosis of APCs is based on the
identification of a P wave that occurs before the
anticipated sinus beat
 The source of the APC appears to parallel the
typical sites of origin for ATs.
 The P-wave contour typically differs from that
noted during sinus rhythm
 However, APCs from the right atrial appendage,
superior vena cava (SVC), and superior aspect of the
crista terminalis in the region of the sinus node may
mimic the sinus P-wave morphology.
ECG
 In response to an APC, the PR interval lengthens,
 However, APCs that originate near the
atrioventricular (AV) nodal region may actually have
a shorter PR interval because the atrial conduction
time to the junction is shortened.
 A very early APC may not conduct to the

ventricle and can create a pulse irregularity that
may be perceived as a pause or "dropped beat."
ECG
 If the APC conducts rapidly through the AV
node, a partially recovered His-Purkinje system
will be encountered and a QRS pattern
consistent with a right or left bundle branch
block may occur
 This wide QRS pattern and the failure to

recognize the preceding P wave may result in
misdiagnosis of VPCs. APCs characteristically
reset the sinus node. The resulting sum of the
pre- and post-APC RR interval is less than two
sinus PP intervals.
The APC resets the sinus node, and no compensatory pause is
present even when conducted aberrantly in the ventricles with
a bundle branch block-type QRS pattern
RX
 Atrial premature complexes generally do not
require intervention.
 For extremely symptomatic patients who do not

respond to explanation and reassurance, an
attempt can be made to suppress the APCs with
pharmacologic agents.
 The repetitive focus can even be targeted for
catheter ablation.
 Beta blockers may be tried
RX
 Note: Of note, these agents may uncommonly
exacerbate symptoms if AV block occurs with
the APC and irregularity of the pulse
consequently becomes more profound.
 The use of class IC antiarrhythmic agents may

eliminate the APCs but should be avoided if
structural heart disease is present.
JUNCTIONAL PREMATURE
COMPLEXES
 Junctional premature complexes are extremely
uncommon.
 The complexes originate from the AV node and

His bundle region and may produce retrograde
atrial activation with the P wave distorting the
initial or terminal portions of the QRS complex,
producing pseudo Q or S waves in leads II, III,
and aVF.
COMPLEXES
COMPLEXES
 Extrasystoles originating in the bundle of His
that do not conduct to the ventricle and also
block the atria can produce unexplained surface
ECG PR prolongation that does not follow a
typical Wenckebach periodicity
 I.e.,gradual PR prolongation culminating in atrial
activity that fails to conduct to the ventricles
 Intracardiac recordings frequently can identify
a His depolarization, thus identifying the origin
of the complex to the AV junction.
COMPLEXES
 Symptomatic patients typically may be treated
with beta blockers or, if there is no structural
heart disease, class IC antiarrhythmic agents.
SINUS TACHYCARDIA
 Physiologic sinus tachycardia represents a
normal or appropriate response to physiologic
stress, such as that which occurs with exercise,
anxiety, or fever.
 Pathologic conditions such as thyrotoxicosis,

anemia, and hypotension also may produce sinus
tachycardia
 It is important to distinguish sinus tachycardia

from other SVTs
SINUS TACHYCARDIA
The key features pointing to sinus tachycardia are:

• The P waves are usually clearly visible; their shape is the
same as normal rhythm.
• Usually there is an obvious illness (sepsis, hypovolaemia,
thyrotoxicosis, drugs, etc.). If not, and the P wave is
normally shaped, consider:
(a) inappropriate sinus tachycardia due to sick sinus
syndrome; (b) postural orthostatic tachycardia (PAT)
syndrome; or (c) sinus node reentrant tachycardia (very
rare).
• PR interval << RP interval, a ‘long RP’ tachycardia; most,
not all, long RP tachycardias are sinus . If the PR
interval > RP interval then the diagnosis is usually an
arrhythmia.
SINUS TACHYCARDIA
 Sinus tachycardia will produce a P-wave contour
consistent with its origin from the sinus node
located in the superior-lateral and posterior
aspect of the right atrium.
 The P wave is upright in leads II, III, and aVF and
negative in lead aVR
 The P-wave morphology in lead V1 characteristically
has a biphasic, positive/negative contour.
SINUS TACHYCARDIA
 Onset of sinus tachycardia is gradual, and in
response to carotid sinus pressure there may be
some modest and transient slowing but no abrupt
termination.
 Importantly, the diagnosis should not be based
on the PR interval or the presence of a P wave
before every QRS complex
 The PR interval and the presence of 1:1 AV
conduction properties are determined by AV nodal
and His-Purkinje conduction; therefore, the PR
interval can be dramatically prolonged while sinus
tachycardia remains the atrial mechanism.
SINUS TACHYCARDIA
 Inappropriate sinus tachycardia represents an
uncommon but important medical condition in which
the heart rate increases either spontaneously or out
of proportion to the degree of physiologic
stress/exercise
 Cause-autonomic neuropathy-eg
DM/dysautonomia,neurohormonal disturbances and altered
sensitivity of SA node
 Secondary to increased automaticity of the SAN or an
automatic atrial focus near the SAN(dx by EPS)
 Defect in either sympathetic or vagal nerve control of SA automaticity
or from an abnormality of the intrinsic HR
SINUS TACHYCARDIA
 Inappropriate sinus tachycardia ctd
 In many patients, the syndrome occurs after a viral
illness and may resolve spontaneously over the course
of 3–12 months, suggesting a postviral dysautonomia
 Excluding the diagnosis of an automatic AT that

originates in the region of the sinus node can be
difficult and may require invasive electrophysiologic
evaluation.
 Frequently, patients are misdiagnosed as having an

anxiety disorder with physiologic sinus tachycardia
PHYSIOLOGIC SINUS TACHYCARDIA:
RX
 Treatment of the underlying condition
 We suggest using ivabradine (5 mg twice daily) for patients
with symptomatic IST. Addition of a beta blocker may be
effective if the cause of IST is overactivity of the
sympathetic nervous system . However, control of the heart
rate (HR) is difficult if the sinus tachycardia results from
depressed vagal activity. Limited published data exist on the
use of non-dihydropyridine calcium channel blockers (eg,
verapamil) .
 Ivabradine is a drug that decreases the depolarizing
I f current in the sinoatrial node, thereby decreasing the
heart rate . A large randomized study of ivabradine versus
placebo in patients with coronary artery disease and left
ventricular dysfunction supports the safety and efficacy of
ivabradine for lowering heart rates (although these patients
did not have IST
 Uncommonly, beta blockers are used to minimize
the tachycardia response if it is determined to
be potentially harmful, as may occur in a patient
with ischemic heart disease and rate-related
anginal symptoms.
INAPPROPRIATE SINUS
TACHYCARDIA: RX
 For symptomatic patients, maintaining an
increased state of hydration, salt loading, and
careful titration of beta blockers to the
maximum tolerated dose, administered in divided
doses, frequently minimize symptoms.
 For severely symptomatic patients who are

intolerant of or unresponsive to beta blockers,
catheter ablation directed at modifying the
sinus node may be effective
INAPPROPRIATE SINUS
TACHYCARDIA: RX
 Because of the high recurrence rate after
ablation and the frequent need for atrial pacing
therapy, this intervention remains second-line
treatment.
SA NODE REENTERANT
TACHYCARDIA
 SANRT has an activation sequence similar to
that of normal sinus rhythm so that the P waves
on the surface ECG appear to be normal.
 In comparison, intraatrial reentry has a

different activation sequence of atrial
depolarization, leading to a P wave morphology
that differs from that of normal sinus rhythm
SA NODE REENTERANT
TACHYCARDIA
 The exact mechanism of SA nodal reentry is not
known; however, three possibilities have been
suggested
i. Reentry occurring entirely within the SA node.
ii. Reentry involving the SA node and perinodal tissue,
iii. Reentry using the SA node as the refractory
center around which reentry occurs
SA NODE REENTERANT
TACHYCARDIA
 The diagnosis of SANRT should be considered in
the presence of a regular but rapid pulse and
heartbeat on physical examination.
 ECG: P waves with a rate between 100 and 150

beats per minute.
 Given that the P waves are virtually identical to
those observed in sinus rhythm, patients may often
be thought to have inappropriate sinus tachycardia.
 In most cases, the diagnosis of SANRT cannot be
confirmed without invasive electrophysiologic
studies.
SA NODE REENTERANT
TACHYCARDIA
 So any clue to differentiate from sinus
tachycardia without invasive tests?
 The abrupt onset and termination of the arrhythmias
 The rate in SANRT is usually between 100 and 150
beats per minute.
 Episodes vary in length, lasting anywhere from seconds to
hours.
 The response to vagal maneuvers
 Gradual slowing in response to vagal stimulus for sinus
tachycardia vs
 Abrupt termination for SANRT
 Patients should undergo continuous ECG monitoring

during the vagal maneuvers.
 Postural orthostatic tachycardia
syndrome — Postural orthostatic tachycardia
syndrome (POTS) occurs predominantly in young
women with normal hearts, who have a normal
resting heart rate and an exaggerated postural
sinus tachycardia elicited by upright tilt table
testing in the absence of orthostatic
hypotension
ATRIAL FIBRILLATION
 Read the link
ATRIAL FLUTTER
Atrial flutter is the prototypic macroreentrant atrial
rhythm. The
typical atrial flutter is a reentrant rhythm in the right
atrium that is constrained anteriorly by the tricuspid
annulus and posteriorly by the crista terminalis and
eustachian ridge. The flutter can circulate in a
counterclockwise direction around the tricuspid annulus
in the frontal plane (typical flutter, counterclockwise
flutter) or in a clockwise direction (atypical, clockwise,
or reverse flutter). Rarely, intra-isthmus flutter can
occur when the reentrant circuit is isolated to the
cavotricuspid isthmus rather than rotating around the
entire tricuspid annulus; this typically occurs after
ablation in this region (usually done as treatment of
typical flutter).
 The traditional classification distinguishes two types of atrial flutter:
type I (typical, common, or counterclockwise isthmus-dependent) and
type II (atypical). These arrhythmias were differentiated by Wells
et al in 1979 . Type I was separated from type II on the basis of the
flutter rate (240 to 340 beats/min compared to 340 to
440 beats/min in type II), the existence of an excitable gap, the
ability to transiently entrain type I but not type II, and the
observation that type II can change in a "stepwise" manner to type I.
 In 2001, the European Society of Cardiology and the North American
Society of Pacing and Electrophysiology proposed a classification that
takes into consideration both anatomic features and
electrophysiologic mechanisms [. Type I atrial flutter was classified
as a macroreentrant atrial tachycardia, while type II atrial flutter
was considered unclassified because the mechanisms are not fully
understood.
 The Wells classification remains the most commonly used in the
clinical literature and by clinicians.
Other forms of atrial flutter are now recognized
as distinct types and include atrial macroreentry
caused by incisional scars from previous atrial
surgery, previous atrial ablation, mitral annular
flutter, idiopathic fibrosis in areas of the atrium,
or other anatomic or functional barriers to
conduction in the atria. Because the barriers that
constrain these atrial flutters are variable, the
electrocardiographic pattern of these so-called
atypical atrial flutters can be varied. Sometimes,
flutter wave morphology changes during the same
episode of flutter, which indicates multiple
circuits or nonfixed conduction barriers.
ATRIAL FLUTTER AND
MACROREENTRANT ATRIAL
TACHYCARDIAS
 Macroreentrant arrhythmias involving the atrial
myocardium are referred to collectively as AFL.
 The terms AFL and macroreentrant AT

frequently are used interchangeably, with both
denoting a nonfocal source of an atrial
arrhythmia
ATRIAL FLUTTER AND MACROREENTRANT
ATRIAL TACHYCARDIAS
 The posterior boundary of the right AFL circuit
is defined by the crista terminalis, the
eustachian ridge, and the inferior and superior
vena cavae.
 Counterclockwise right AFL represents ~80%

of all AFL with superiorly directed activation of
the interatrial septum, which produces the saw-
toothed appearance of the P waves in ECG leads
II, III, and aVF
ATRIAL TACHYCARDIAS
 Clockwise rotation of the same right atrial
circuit produces predominantly positive P waves
in leads II, III, and aVF.
 Macroreentrant left AFL also may develop,

albeit much less commonly.
 This type of arrhythmia may be the sequela of
surgical or catheter-based ablation procedures that
create large anatomic barriers or promote slowing of
conduction in the left atrium, especially around the
mitral valve annulus or partially disconnected
pulmonary veins.
ATRIAL TACHYCARDIAS
 Atypical AFL or macroreentrant AT can also
develop around incisions created during surgery
for valvular or congenital heart disease or in
and/or around large areas of atrial fibrosis
 Classic or typical right AFL has an atrial rate of

260–300 beats per minute with a ventricular
response that tends to be 2:1, or typically 130–
150 beats per minute
ATRIAL TACHYCARDIAS
 In the setting of severe atrial conduction
disease and or antiarrhythmic drug therapy, the
atrial rate can slow to <200 beats per minute.
 In this setting, a 1:1 rapid ventricular response

may occur, particularly with exertion, and
produce adverse hemodynamic effects
ATRIAL TACHYCARDIAS
 Atypical AFL or macroreentrant AT related to
prior surgical incisions and atrial fibrosis
demonstrates less predictability in terms of the
atrial rate and is more likely to demonstrate slower
rates that overlap with those identified with focal
atrial tachycardias
 Because lead V1 is frequently monitored in a

hospitalized patient, coarse AF may be
misdiagnosed as AFL. This occurs because in both
typical right AFL and coarse AF the crista
terminalis in the right atrium may serve as an
effective anatomic barrier.
ATRIAL TACHYCARDIAS
 The free wall of the right atrium, whose
electrical depolarization is best reflected on the
body surface by lead V1, may demonstrate a
uniform wavefront of atrial activation in both
conditions.
 The timing of atrial activation is much more

rapid in AF and always demonstrates variable
atrial intervals with some intervals between
defined P waves <200 ms
ATRIAL TACHYCARDIAS
 A review of the other ECG leads demonstrates
the disorganized atrial depolarization that is
characteristic of AF.
 Frequently, an individual patient may alternate

between AF and AFL or, less commonly, may
manifest AF in one atrium and AFL in the other,
making the distinction more difficult
B
In typical atrial flutter, the ECG reveals identically recurring,
regular, sawtooth flutter waves and evidence of continual electrical
activity (lack of an isoelectric interval between flutter waves), often
best visualized in leads II, III, aVF, or V1 . In some cases, transient
slowing of the ventricular response, via either carotid sinus massage
or adenosine, is necessary to visualize the flutter waves. The flutter
waves for the most common form of atrial flutter, counterclockwise
typical atrial flutter, are inverted (negative) in these leads because
of a counterclockwise reentrant pathway, and sometimes they are
upright (positive) when the reentrant loop is clockwise . When the
flutter waves are upright from clockwise rotation, they are often
notched. If the AV conduction ratio remains constant, the
ventricular rhythm will be regular; if the ratio of conducted beats
varies (generally the result of a Wenckebach AV block), the
ventricular rhythm will be irregular, although this is rare.
 The counterclockwise rotation involves the direction of the
activation wavefront within the right atrium with respect to
the tricuspid valve annulus in the left anterior oblique
projection (ie, activation proceeding up the intraatrial septum,
superiorly over the roof of the right atrium, down the lateral
wall and through the “isthmus” of atrial tissue between the
inferior vena cava and the tricuspid valve annulus). Another
form of typical flutter has the same isthmus-dependent
features, the same anatomic barriers, and the same cycle
length, but the reentrant circuit has a clockwise rotation
 Type II or atypical atrial flutter is not isthmus-dependent,
seems to lack an excitable gap, and cannot be entrained. It is
thought that these characteristics result from an intraatrial
reentrant circuit that is very short in contrast to the long
isthmus in type I atrial flutter
 GENERAL TREATMENT ISSUES — As is true
for atrial fibrillation, there are four major
issues that must be addressed in the treatment
of atrial flutter:
 Reversion to normal sinus rhythm (NSR)
 Maintenance of NSR
 Control of the ventricular rate in patients
 Prevention of systemic embolization, particularly

in the patient who also has atrial fibrillation
AFL TREATMENT
 Thromboembolic risk and Rx-similar to AF
 Prevention of recurrent atrial flutter
 Difficult to achieve medically.
 AV blocking is necessary before using class I/III AAD
 Cardioversion of 50–100 J
 Can ppt VAs in digitalis rx patient
 Catheter ablation--cavoisthmus /mapping for atypical
 considered in patients refractory to medical therapy
 a long-term success rate of 90% to 100
 Reversion to NSR — The standard approaches to converting
atrial flutter to sinus rhythm are synchronized internal or
external DC cardioversion or pharmacologic cardioversion
with class IA (eg, quinidine , procainamide , disopyramide ),
class IC (eg, flecainide , propafenone ), or class III
antiarrhythmic agents ( amiodarone , sotalol , ibutilide ,
dofetilide ). DC cardioversion is indicated in patients who are
hemodynamically unstable, while either medical or electrical
cardioversion can be performed in stable patients in whom
spontaneous reversion due to correction of an underlying
disease is not likely
 the usual precautions should be taken with regard to
preparatory anticoagulation or TEE, if the duration of atrial
flutter is beyond 48 hours or of unknown duration
 In the hemodynamically stable patient, watchful waiting may be sufficient since
atrial flutter is usually an unstable rhythm that generally reverts spontaneously
to normal sinus rhythm in days to weeks. As in atrial fibrillation, the best
candidate has a left atrial size less than 4.5 to 5 cm, atrial flutter of recent
onset, little or no heart failure, and an underlying reversible cause such as
hyperthyroidism, myocardial infarction, and pulmonary embolism
 If pharmacologic reversion is deemed necessary, ibutilide , which is approved by
the Food and Drug Administration only for intravenous use, is the drug of choice .
It can revert atrial flutter to a sinus mechanism in approximately 60 percent of
patients and is more effective than procainamide ,sotalol , or amiodarone .
Ibutilide therapy carries a risk of QT prolongation and torsades de pointes. One
report noted an 8.3 percent incidence of torsades de pointes . Although the
arrhythmia is usually not sustained because of the short-half life of ibutilide,
cardioversion was required for sustained arrhythmia in 1.7 percent. As a result,
the use of ibutilide requires continuous monitoring, resuscitative equipment
including a defibrillator, and personnel trained in the use of electrical
cardioversion and resuscitation.
Other medications, such as procainamide or
amiodarone, can be given to convert atrial flutter
chemically, but they are generally less effective
than ibutilide.
Rapid atrial pacing with a catheter in the
esophagus or the right atrium can effectively
terminate typical and some forms of atypical atrial
flutter in most
 Rate control with an AV nodal blocker with a
calcium channel blocker (particularly verapamil
and diltiazem ), beta blocker, or, if the patient
has heart failure or hypotension, digoxin should
be attained before instituting class IA and IC
drugs because of possible recurrence with atrial
flutter and a very rapid ventricular rate. Long-
term therapy with one of these drugs may be
required in the event of atrial fibrillation that
may appear, even after ablative cure of the
atrial flutter.
Cardioversion () is commonly
the initial treatment of choice for
atrial flutter because it promptly and
effectively restores sinus rhythm. Cardioversion
can be accomplished with synchronous
direct current (DC), which
often requires relatively low energy
(≈50 J). If the electrical shock results in
atrial fibrillation, a second shock at a
higher energy level is used to restore sinus
rhythm, or depending on clinical circumstances,
the atrial fibrillation can be left
untreated and can revert to atrial flutter or
sinus rhythm.
 The pharmacologic strategies, as with atrial fibrillation, are to
depress initiating atrial premature beats, which may require
the use of class IA and IC drugs, beta blockers, and
amiodarone , and to prolong the atrial refractory period with
class III drugs. Amiodarone is often used since, in addition to
helping maintain normal sinus rhythm, it also helps control the
ventricular response if atrial fibrillation or atrial flutter
occurs.
 However, because of the high rate of recurrence in patients
without a correctable cause, and because of the high success
rate with radiofrequency ablation, ablation is generally
preferable to long-term pharmacologic therapy in patients
with type I (typical) atrial flutter. The isthmus between the
inferior vena cava and the tricuspid annulus (IVC-TA isthmus)
is an obligatory route for type I flutter, and, as such, is the
preferred anatomic target for ablatio
 Successful outcomes with ablation can also be achieved in
patients with type II atrial flutter, although the experience is
more limited
 Rate control in chronic atrial flutter — Rate control in
chronic atrial flutter, as in atrial fibrillation, usually involves
the administration of a calcium channel blocker, particularly
verapamil or diltiazem or a beta blocker. Digoxin is used less
often because its major action is an enhancement of vagal tone,
which is offset during exertion. The main indication is
concurrent heart failure in which it is often given in
combination with another drug that decreases AV nodal
conduction.
 Ablative therapy of the AV node is rarely indicated unless the
atrial flutter is resistant to ablation or antiarrhythmic drugs
or is associated with atrial fibrillation in which the ventricular
response cannot be controlled.
Guidelines published in 2008 from the American College of Chest
Physicians on antithrombotic therapy in atrial fibrillation and in 2006
from the American College
of Cardiology/American Heart Association/European Society of
Cardiology (ACC/AHA/ESC) recommend that consideration be given
to managing anticoagulation during cardioversion of atrial flutter in a
manner similar to that for AF
OUR RECOMMENDATIONS FOR ANTICOAGULATION IN PATIENTS WITH ATRIAL
FLUTTER WHO ARE TO UNDERGO CARDIOVERSION ARE AS FOLLOWS UPTODATE
 Patients presenting with an initial episode of atrial flutter should have

a transthoracic echocardiogram to evaluate for possible rheumatic
mitral valve disease and to assess left ventricular systolic function.
 Patients with atrial flutter who have rheumatic heart disease,
depressed left ventricular systolic function, a history of
thromboembolism, atypical atrial flutter, or a prior history of atrial
fibrillation are at increased risk for atrial thrombus formation and are
best treated conservatively with three to four weeks of warfarin prior
to cardioversion . The goal INR is 2.0 to 3.0. It has been suggested
that it may be prudent to aim for a minimum INR of 2.5 before
cardioversion or documentation that the INR has consistently been
≥2.0 in the weeks before cardioversion .
 Another option, which has been evaluated in patients with atrial
fibrillation, is TEE-guided early cardioversion with the use of short-
term heparin orwarfarin at the time of TEE and continued for four
weeks after cardioversion. The safety of this approach has not been
formally studied in atrial flutter.
 As in patients with atrial fibrillation,
cardioversion can be safely performed if the
arrhythmia duration is less than 48
hours and the patient has no high-risk features
(eg, rheumatic heart disease, depressed left
ventricular function, or a history of
thromboembolism). Although long-term
anticoagulation is not recommended following a
defined episode of less than 48 hours, risk
factors for developing atrial flutter and atrial
fibrillation may increase the risk of recurrence,
and close clinical follow-up is recommended.
ATRIAL TACHYCARDIAS- TREATMENT
 Because of the anticipated rapid regular
ventricular rate associated with AFL and the
failure to respond to pharmacologic therapy
directed at slowing the ventricular rate, patients
frequently are treated with DC cardioversion
 The organized atrial flutter activity frequently

can be terminated with low-energy external
cardioversion of 50–100 J.
 The risk of thromboembolic events associated with
typical AFL is high, and anticoagulation must be
managed similarly to what was described for
patients with AF
 Asymptomatic patients with AFL may develop heart

failure symptoms with tachycardia-induced severe
LV dysfunction.
 In all patients, an effort should be made to control the
ventricular rate pharmacologically or restore sinus
rhythm.
 Rate control with calcium antagonists (diltiazem or
verapamil), beta blockers, and/or digoxin may be
difficult.
 Even higher-grade AV slowing, such as a 4:1 AV
response, may be only transient and is easily
overcome with activity or emotional stress.
 Owing to the typically faster ventricular rate,

AFL tends to be poorly tolerated in comparison
to AF.
 In patients with macroreentrant atrial
tachycardia or AFL involving prior surgical
incisions or catheter ablation or in areas of
atrial fibrosis, detailed mapping of the
arrhythmia circuit is required to design the best
ablation strategy to interrupt the circuit.
 In selected patient with AF and typical right

AFL, pharmacologic therapy may help prevent
the AF but not the AFL.
 In this type of patient, hybrid therapy with
antiarrhythmic agents coupled with a right atrial
isthmus ablation may produce AF and AFL
control.
MULTIFOCAL ATRIAL TACHYCARDIA
 arrhythmia that can be seen in a variety of clinical
disorders . In addition to a heart rate greater than
100 beats per minute, the characteristic
electrocardiographic feature is variability in P wave
morphology, with each unique P wave morphology felt
to indicate a different site of atrial origin. Although
this abnormality had been noted for many years
during some types of atrial tachycardia, the term
MAT became commonplace terminology in the late
1960s . Patients with multiple P wave morphologies
but a normal heart rate (60 to 100 beats per minute)
are considered to have a wandering atrial pacemaker,
since the heart rate does not meet criteria for a
tachycardia
 Multifocal AT (MAT) is the signature tachycardia of patients
with significant pulmonary disease
 The atrial rhythm is characterized by at least three distinct P-

wave morphologies and often at least three different PR
intervals, and the associated atrial and ventricular rates are
typically between 100 and 150 beats per minute
 Some patients have similar electrocardiographic (ECG) findings
with multiple P wave morphologies but do not meet criteria for
tachycardia. The arrhythmia is called a multifocal atrial rhythm
or wandering atrial pacemaker if the rate is between 60 and 100
beats per minute. A distinction has been made between the two
based on the clinical picture, with a wandering atrial pacemaker
usually occurring in the asymptomatic or less ill individual
MECHANISMS —
 The changing morphology of the P waves and the
variable PR interval suggests that the atrial
pacemaker activity arises from different atrial
locations. However, the variable PR interval is
probably more likely a result of the variable atrial
rate. Alternatively, a single focus with different
exit pathways or abnormalities in intraatrial
conduction could produce the identical
electrocardiographic findings. There have only been
a few invasive electrophysiologic investigations of
MAT, but one study did show abnormal intraatrial,
atrionodal, and atrioventricular nodal conduction in
many individuals with MAT
 It is thought that MAT results from right atrial hypertension and
distension, either from secondary pulmonary hypertension from
advanced COPD or left ventricular dysfunction caused by
comorbid processes such as coronary heart disease, systemic
hypertension, or aortic stenosis . However, although frequently
associated with exacerbations of pulmonary disease, MAT may
occur in other circumstances, so atrial distension may not be a
universal mechanism.
 Associated arrhythmias — MAT (and wandering atrial

pacemaker) is commonly accompanied by atrial premature beats
and can itself be considered a prolonged sequence of atrial
premature beats . The majority of episodes of MAT are self-
limited and non-sustained.
 MAT may be associated with or precede atrial fibrillation
 Pulmonary disease — MAT is associated with
significant lung disease in roughly 60 percent of
cases . Furthermore, this arrhythmia has been
identified in up to 20 percent of patients
hospitalized for acute respiratory failure . COPD
is the most common pulmonary disorder
associated with MAT, but this arrhythmia can
also occur with pneumonia and pulmonary
embolism. Hypoxia, hypercapnia, acidosis,
autonomic imbalance, right atrial enlargement, and
therapy with aminophylline , theophylline , or
isoproterenol all may contribute to the enhanced
ectopic atrial activity
A DIAGNOSIS OF MAT REQUIRES THE
FOLLOWING BE PRESENT ON THE ECG
 Discrete P waves with at least three different

morphologies (including the normal sinus P wave).
 An atrial rate greater than 100 beats per minute,
which is the classic definition of MAT . However,
based upon data from a series of patients with
chronic obstructive pulmonary disease (COPD), a
threshold of 90 bpm has been proposed.
 P waves which return to the baseline and thus are
separated by isoelectric intervals.
 P-P intervals, P-R duration, and R-R intervals
which vary.
 Electrocardiogram showing multifocal atrial tachycardia
in a woman with severe pulmonary disease. The
diagnostic criteria include an average atrial rate above
100 beats/min and at least three different non-sinus P
waves in the same lead. Note the multiple P wave
morphologies - inverted (I), upright (U), and biphasic
(B).
MULTIFOCAL ATRIAL TACHYCARDIA
 The presence of an isoelectric baseline
distinguishes this arrhythmia from AF
 The absence of any intervening sinus rhythm

distinguishes MAT from normal sinus rhythm
with frequent multifocal APCs, although this
distinction may be moot as these processes
define an electrophysiologic continuum.
MULTIFOCAL ATRIAL TACHYCARDIA-
TREATMENT
 Therapy for MAT should be directed at
improving the underlying medical condition, which
is typically, although not invariably, chronic
obstructive or restrictive lung disease.
 COPD- commonest
 Treatment with the calcium channel
blocker verapamil also may provide some benefit.
 The judicious use of flecainide or propafenone

may also decrease atrial arrhythmias.
 Magnesium and potassium repletion — Patients
with MAT and associated hypokalemia or
hypomagnesemia should undergo electrolyte
repletion prior to the initiation of additional
medical therapy for MAT.
 Hypomagnesemia appears to promote the
development of some atrial and ventricular
arrhythmias. The administration of magnesium
has been reported to suppress MAT in the
hypomagnesemic patient and, at times, in
patients with normal plasma magnesium level
 Pharmacologic therapy — The use of
antiarrhythmic drugs in the treatment of MAT has
generally been disappointing. There is, however,
evidence of benefit with agents to control the
ventricular heart rate, namely verapamil and beta
blockers.
 Medical therapy for MAT is indicated only if MAT
causes a sustained rapid ventricular response that
causes or worsens myocardial ischemia, heart
failure, peripheral perfusion, or oxygenation . For
patients with symptomatic MAT requiring
ventricular rate control, we recommend therapy
withverapamil or a beta blocke
 Antiarrhythmic drugs — For patients with symptomatic MAT that
remains inadequately rate-controlled following treatment of the
underlying disorder and initiation of rate controlling therapy, we
do not use an antiarrhythmic drug. This is based on extensive literature
showing a general lack of efficacy of standard antiarrhythmic drugs in
treating MAT. Ineffective drugs include quinidine , procainamide ,
lidocaine , and phenytoin , among others. Digitalis also appears to have
little benefit .
 Ibutilide has been used successfully to treat MAT in one elderly patient,
but more experience with this drug is need

 DC cardioversion — DC cardioversion has not proven effective in
converting MAT into a sinus rhythm . As such, we do not perform
cardioversion for patients with symptomatic MAT that remains
inadequately rate-controlled.
 Radiofrequency ablation — Ablation of the AV node and the use of a
permanent ventricular pacemaker is an option for patients with ongoing
symptomatic MAT who do not respond to, or cannot tolerate,
pharmacologic therap
MULTIFOCAL ATRIAL TACHYCARDIA-
TREATMENT
 Patients should be screened for the presence of
significant ventricular dysfunction or CAD
before these agents are started.
 Low-dose amiodarone therapy may also control

the arrhythmia and minimize the risk of
pulmonary toxicity noted with the drug
TREATMENT OF MAT
CONT…
FOCAL ATRIAL TACHYCARDIA
 The two general mechanisms for focal ATs can

be distinguished by observations made at AT
initiation and in response to adenosine.
 Automatic ATs
 Focal re-entrant ATs
IN 2001, THE JOINT EXPERT GROUP FROM THE WORKING GROUP OF
ARRHYTHMIAS OF THE EUROPEAN SOCIETY OF CARDIOLOGY AND THE NORTH
AMERICAN SOCIETY OF PACING AND ELECTROPHYSIOLOGY (NOW CALLED THE
HEART RHYTHM SOCIETY) CLASSIFIED REGULAR ATS ACCORDING TO
ELECTROPHYSIOLOGIC MECHANISMS AND ANATOMY
 The Joint Expert Group defined focal AT as

"being characterized by atrial activation starting
rhythmically at a small area (focus) from where it
spreads centrifugally." This definition indicates
that the arrhythmia arises from an area that is
smaller than would be required for classical
macroreentry, which conventionally is considered
to be a circuit greater than 2 cm in diameter.
 Incidence — Repetitive focal AT is relatively
rare, accounting for between 5 and 15 percent of
arrhythmias in adults undergoing study for
paroxysmal supraventricular tachycardia . Men
and women seem to be equally affected.
ELECTROPHYSIOLOGIC MECHANISMS — THE FOCAL ACTIVITY RESPONSIE FOR AT CAN BE PRODUCED BY THREE
DISTINCT ELECTROPHYSIOLOGIC MECHANISMS
 Enhanced automaticity — Enhanced automaticity refers to an acceleration

of a normal automatic pacemaker by an increase in the slope of phase four
depolarization , shortening of the refractory period, a decrease in the
threshold for excitation, or some combination of these mechanisms.
 Triggered activity — Triggered activity is the result of electrophysiologic
phenomena called afterdepolarizations. Afterdepolarizations are focal
electrical events that result in repeat depolarization of a single cell or
small area prior to full repolarization. Early afterdepolarizations occur
during the plateau phase of the action potential, while delayed
afterdepolarizations occur during phase four.
 Microreentry — Microreentry requires a small circuit in which conduction
is sufficiently slow that the tissue can recover its excitability and be re-
excited by the time the wave of depolarization returns. Such slow
conduction may be due to a variety of mechanisms, including a rise in the
maximum diastolic potential, changes in threshold, alterations in the
activation and inactivation of channels responsible for depolarization or
repolarization, and poor cell-cell coupling due to a decrease in
transmission through gap junctions.
 Incessant AT resulting in cardiomyopathy — The term
“incessant" is applied to an AT when the AT is present
for at least 90 percent of the time a patient is
monitored . Incessant AT is often found in otherwise
normal young individuals, including children, although it
may occur in patients with organic heart disease . The
rate tends to be faster during the day than at night, and
it may increase with exercise or pregnancy
 Incessant focal AT may be responsible for tachycardia-
mediated cardiomyopathy, which refers to left
ventricular (LV) chamber dilatation and systolic
dysfunction in a patient with persistent
tachyarrhythmias . Focal ATs originating in the atrial
appendages and pulmonary veins are more frequently
associated with cardiomyopathy
 Digitalis toxicity — In patients taking digitalis, toxicity
should be suspected if a new AT develops, particularly if
2:1 or higher grade AV block is present. Digitalis should
be discontinued in this case, and anti-digitalis antibodies
should be considered if hemodynamic compromise is
present or other dangerous arrhythmias accompany the
tachycardia
 Post-atrial fibrillation ablation — The incidence of
atrial tachycardia appears to be higher among patients
who have undergone catheter ablation for atrial
fibrillation (AF) . Catheter ablation of persistent AF
commonly involves an extensive biatrial ablation strategy
that combines linear ablation and the targeting of
complex fractionated activity beyond pulmonary vein
isolation.
 Automatic ATs start with a "warm-up" period
over the first 3–10 complexes and, similarly, slow
in rate before termination.
 They may respond to adenosine not only with
evidence of AV block but also with gradual slowing of
the atrial rhythm and termination.
 The initiation of automatic ATs frequently can be
provoked by isoproterenol infusion.
 The first P wave of the tachycardia has the same
morphology as the remaining waves.
 Some of the ATs may be triggered or provoked by
burst atrial pacing but are not reliably initiated by
programmed atrial stimulation.
 Focal reentrant AT
 Includesthe initiation of the tachycardia with
programmed atrial stimulation or spontaneous
premature beats.
 The P wave initiating the tachycardia will

characteristically have a different morphology than
the P wave during the sustained AT.
 In response to adenosine, reentrant ATs will

demonstrate AV block but typically do not slow
and/or terminate
 Most focal ATs in the absence of structural heart
disease originate from specific anatomic locations.
 These anatomic locations appear to be associated

with anatomic ridges, such as the crista terminalis,
the valve annuli, and the limbus of the fossa ovalis.
 ATs also appear to originate from the muscular

sleeves associated with the cardiac thoracic veins,
i.e., the SVC, the coronary sinus, and the
pulmonary veins.
 Sites of origin — Focal ATs do not occur randomly throughout the atria,
but rather cluster at predefined anatomic locations . These locations are
characterized by alterations in myocardial fiber orientation or sites of
automatic tissue. In a series of 186 patients with clinically documented
paroxysmal or incessant AT, 63 percent of ATs arose in the right atrium
(RA) and 37 percent in the left atrium (LA)The distribution of sites of
origin among the right atrial tachycardias was:
 Tricuspid annulus (35 percent)
 Crista terminalis (34 percent)
 Coronary sinus ostium (17 percent)
 Perinodal tissues(9 percent)
 RA appendage (4 percent)
 Left atrial tachycardias were predominantly located around the

pulmonary veins (67 percent) . Less common sites of origin include the
mitral annulus (17 percent), coronary sinus body (6 percent), left
intraatrial septum (6 percent), and the LA appendage (4 percent)
 As was indicated, repetitive firing of these foci
also appears to serve as the triggering mechanism
for AF in most patients.
 It is important to distinguish focal ATs from

reentrant tachycardias that incorporate the AV
node in the circuit
 The primary distinction is related to the

persistence of the AT in the presence of AV block
that occurs spontaneously or is created by carotid
sinus massage or the administration of adenosine
 Atrial activity drives the ventricles in AT and all
changes in the PP interval accompanied by
correlative changes in the RR intervals
 In addition, the V–A relationship changes when

the atrial rate changes.
 The P wave in AT is characteristically distinct from
the sinus P-wave morphology, and unless there is
significant AV nodal conduction delay
 The PR interval is shorter than the measured RP
interval when there is a 1:1 relationship between
atria and ventricles
 The P wave for ATs depends on the anatomic site of origin.
 Observation over several minutes with multiple ECGs is
invaluable in distinguishing focal AT from sinus
tachycardia. Although focal ATs are regular, the rate may
accelerate or "warm up" in the first few beats of the
tachycardia and decelerate in the last few beats. An
abrupt onset or termination (eg, over three to four beats)
favors a focal AT. Sinus tachycardia requires 30 seconds
to several minutes to speed up or slow down
 In addition to attempting to create AV block to establish
the diagnosis of AT, analysis of the P-wave morphology on
the 12-lead ECG may help exclude AV nodal reentry, AV
bypass tract–mediated reentrant tachycardias, and
physiologic or inappropriate sinus tachycardia
ATRIAL TACHYCARDIA
 Focal AT generally have atrial rates of 150 to 200 beats/min,
with a P wave contour different from that of the sinus P
wave.
 Automatic ATs vs Reenterant ATs
 Start with a "warm-up" period over the first 3–10 complexes and
similarly, slow in rate prior to termination and same P wave
morphology at initiation and maintenance in automatic ATs
 Programmed stimulation increases reentrant ATs; P wave
variability
 P waves are usually found in the second half of the
tachycardia cycle (long RP–short PR tachycardia).
 The ECG distinction between focal automatic or
microreentrant and macroreentrant AT or
atypical AFL is not always possible.
 Although sustained focal ATs tend to be slower,
the atrial rates frequently overlap.
 Focal ATs, which are more common in the absence of
structural heart disease, tend to demonstrate an
isolectric baseline between P waves
 Whereas macroreentrant ATs represent atrial
activation that is continuous and an isoelectric
baseline between P waves frequently is absent
 In patients with a history of prior atrial surgery,
one must suspect a macroreentrant mechanism.
 These distinctions are less important with

respect to acute management but have
importance related to ablation strategies and
anticipated outcome
CLINICAL FEATURES
Atrial tachycardia occurs commonly in patients with significant
structural heart disease such as coronary artery disease, with
or without myocardial infarction, heart failure, and cor
pulmonale, as well as in patients without structural heart
disease. It can also occur with digitalis intoxication, often
precipitated by potassium depletion. The signs, symptoms, and
prognosis are usually related to the underlying cardiovascular
status and the rate of the tachycardia. Atrial tachycardias
frequently occur in short recurrent bursts but on occasion can
be incessant. When they are incessant, tachycardia-induced
cardiomyopathy can result. This may be partially or totally
reversible with elimination of the tachycardia. In some
patients, exercise or stress can provoke the tachycardia; in
others, the tachycardia may be positional. Stimulants such as
caffeine, chocolate, and ephedrine can also provoke episodes.
FOCAL ATRIAL TACHYCARDIA-
TREATMENT
 Pharmacologic treatment of AT generally is
approached in a similar fashion to that of AF and
AFL.
 AV nodal blocking agents are administered in the
setting of rapid ventricular rates.
 Acute IV administration of procainamide or
amiodarone may terminate the tachycardia.
 Tachycardias that do not respond to
pharmacologic therapy may be terminated with
electrical cardioversion
TREATMENT
 Typically, anticoagulation before treatment is
not needed unless there is evidence of severe
atrial dilatation, >5 cm left atrial diameter with a
high risk of AF, and/or a history of coincident
paroxysmal AF
 Most focal ATs are readily amenable to catheter

ablative therapy.
 In patients who fail to respond to medical therapy or
who are reluctant to take chronic drug therapy, this
option should be considered, with an anticipated 90%
cure rate
TREATMENT
 A parahisian location for the AT and/or a focus
that is located in the left atrium may modestly
increase the risk related to the procedure
 And for this reason, every effort should be

made to determine the likely origin of the AT
based on an analysis of the P-wave morphology on
12-lead ECG before the procedure.
WITH THESE LIMITATIONS IN MIND, WE SUGGEST THE FOLLOWING APPROACH
FOR CHRONIC TREATMENT OF PATIENTS WITH FREQUENT OR SYMPTOMATIC
AT, WHICH IS IN GENERAL AGREEMENT WITH THE
2003 ACC/AHA/ESCGUIDELINES
 We suggest initial therapy with oral beta blockers or

nondihydropyridine calcium channel blockers (ie,
diltiazem orverapamil ). Patients who do not respond to
one of these agents may have successful suppression
with another. Therefore, we suggest switching from
one drug to another before considering class I or III
antiarrhythmic drugs or catheter ablation.
 In patients with recurrent symptomatic AT despite
therapy with beta blockers, diltiazem , or verapamil ,
we suggest catheter ablation. The threshold for
considering catheter ablation is lower for younger
patients and in patients with tachycardia-mediated
cardiomyopathy.
 More aggressive antiarrhythmic drugs may be
considered for patients who fail beta blockers,
diltiazem , and verapamilwho do not want or are
not good candidates for ablation therapy. In
patients with significant comorbidities and
structural heart disease, amiodarone is
frequently the preferred agent. As with acute
therapy of ATs however, other class Ic (eg,
flecainide ), or class III (eg, sotalol )
antiarrhythmic drugs can be used in
appropriately selected patients.
 However, because of the unique risk profiles of
each of these agents, decisions regarding the use
of antiarrhythmic drugs, other than amiodarone,
should be made with the assistance of a
cardiologist experienced in arrhythmia
management.
 Patients with recurrent symptomatic AT in whom
all other therapeutic options have been
unsuccessful (including catheter ablation) may
also be considered for pacemaker implantation
followed by AV nodal ablation. This typically
provides symptomatic relief although generally
leaves the patient pacemaker dependent.
 Treatment of incessant AT — As described
above, patients with incessant AT may present
with a cardiomyopathy. Even patients with
normal left ventricular systolic function on initial
presentation are at risk of developing a
cardiomyopathy following extended periods of
tachycardia. This LV systolic dysfunction
typically reverses weeks to months following the
restoration of sinus rhythm. As such, aggressive
efforts should be made to restore normal sinus
rhythm in an attempt to prevent or reverse LV
systolic dysfunction.
 While there have been occasional reports of the
successful treatment of incessant AT using beta
blockers and Class IC antiarrhythmic drugs (ie,
flecainide ), pharmacologic therapy is
generally ineffective in incessant AT. For this
reason, if medical therapy with rate-controlling
medications and antiarrhythmic drugs is
unsuccessful, patients with AT and concomitant LV
systolic dysfunction should undergo catheter ablation
. Success rates vary according to the site of AT
origin, with successful ablation more likely for AT
originating in the right atrium . Only 10 to 15 percent
of patients will have recurrence of AT following
catheter ablation
AV NODAL TACHYCARDIAS
AV NODAL REENTRANT TACHYCARDIA
 Atrioventricular nodal reentrant tachycardia is
the most common paroxysmal regular SVT.
 It is more commonly observed in women than in

men and is typically manifest in the second to
fourth decades of life.
 In general, because AVNRT tends to occur in the

absence of structural heart disease, it is usually
well tolerated.
 Neck pulsations are usually felt because of the
simultaneous atrial and ventricular contraction,
and a "frog sign" can be identified on physical
examination during the arrhythmia.
 In the presence of hypertension or other forms

of structural heart disease that limit ventricular
filing, hypotension or syncope may occur.
 AVNRT- develops because of the presence of
two electrophysiologically distinct pathways for
conduction in the complex syncytium of muscle
fibers that make up the AV node
 The fast pathway in the more superior part of the
node has a longer refractory period,
 Whereas the pathway lower in the AV node region

conducts more slowly but has a shorter refractory
period
KOCH'S TRIANGLE
 Anatomy — The exact anatomic distribution of
these pathways is uncertain. Koch's triangle is
bounded by the tricuspid ring and the tendon of
Todoro, which bracket the coronary sinus at the
base of the triangle and are in close proximity
forming the apex near the His bundle at the
membranous septum. As an approximation, Koch's
triangle can be divided into thirds: the anterior,
which contains the compact AV node and the
fast pathways; the middle; and the posterior,
which is associated with the coronary sinus
AV NODAL REENTRANT
TACHYCARDIA
 Two types
 Commonform (80%)- Slow-fast pathway
 Uncommon form (20%)- Fast-slow pathway
 Fig.
 Representation of dual pathway physiology involving the
atrioventricular (AV) node and perinodal atrial tissue in
the common form of AVNRT.
 Left panel: A normal sinus beat (A1) is conducted through

the fast pathway (F) to the final common pathway (fcp) in
the AV node and into the Bundle of His. The conduction
through the slow pathway (S) runs into the refractory
period of the impulse through the fast pathway and is
extinguished.
 Middle panel: A critically timed atrial premature beat (A2)

finds the fast pathway refractory but is able to conduct
through the slow pathway which has a shorter refractory
period.
 If excitability in the fast pathway has recovered by the time
the impulse reaches the fcp, there may be retrograde
activation of the fast pathway.
 Fig ctd
 Right panel: The retrograde impulse throws off an
echo to the atrium (A*), and, if the slow pathway has
recovered its excitability, the impulse reenters the
slow pathway and produces ventricular depolarization
V*.
 If the mechanism persists, a repetitive circuit is
established that creates a sustained reentrant
tachycardia. The sequence of antegrade (S) and
retrograde (F) conduction is called the slow-fast
form of AVNRT.
 As a result of the inhomogeneities of conduction
and refractoriness, a reentrant circuit can
develop in response to premature stimulation.
 Although conduction occurs over both pathways

during sinus rhythm, only the conduction over
the fast pathway is manifest, and as a result,
the PR interval is normal.
 APCs occurring at a critical coupling interval are
blocked in the fast pathway because of the longer
refractory period and are conducted slowly over the
slow pathway
 When sufficient conduction slowing occurs, the
blocked fast pathway can recover excitability
and atrial activation can occur over the fast
pathway to complete the circuit.
 Repetitive activation down the slow and up the

fast pathway results in typical AV nodal
reentrant tachycardia
 The APC initiating AVNRT is characteristically
followed by a long PR interval consistent with
conduction via the slow pathway.
 AVNRT is manifest typically as a narrow QRS

complex tachycardia at rates that range from
120 to 250 beats/min.
 The QRS-P wave pattern associated with typical

AVNRT is quite characteristic, with simultaneous
activation of the atria and ventricles from the
reentrant AV nodal circuit
 The P wave frequently is buried inside the QRS
complex and either will not be visible or will
distort the initial or terminal portion of the QRS
complex.
 Because atrial activation originates in the region

of the AV node, a negative deflection will be
generated by retrograde atrial depolarization
when recording ECG leads II, III, or AVF.
It should first be noted that the P-wave axis for both
types is similar. In both, activation of the atria occurs
in an inferiorto- superior direction (retrograde
conduction of the fast pathway in typical or the slow
pathway in atypical AVNRT). This produces a negative
(inverted) P-wave axis in the inferior leads II, III,
and aVF. The AV node is located posteriorly, creating
posterior-to-anterior activation of the atria and
therefore producing a positive (upright) P-wave axis in
lead V1. P-wave width, on the other hand, differs in
the two forms. In typical AVNRT, the P wave tends to
be narrow, whereas in atypical AVNRT, it is wider
because of the differences in anatomic location of the
fast and slow pathways that activate the atria.
Typical AVNRT can be distinguished from atypical
AVNRT on an ECG by comparing the location of the
P wave in relation to the QRS complex. In typical
AVNRT, near-simultaneous conduction to the
ventricles via the slow pathway anterogradely and
to the atria via the fast pathway retrogradely may
rarely make P wave visible on the ECG because
they are inscribed in the QRS complex. When
visualized, the P waves occur in close proximity to
the QRS, creating a short RP interval (RP interval
less than half the RR interval). This can sometimes
manifest as a “pseudo-S wave” in the inferior leads
II, III, and aVF, and a “pseudo-R wave” in lead V1 .
Typical AVNRT, therefore, is an example of a “short-RP”
tachycardia. In contrast, P waves are clearly visible in
atypical AVNRT. Due to retrograde conduction through
a slow pathway, the presence of the P wave occurs later
than the QRS complex, resulting in an RP interval that is
frequently longer than half the RR interval, called a long
RP tachycardia Another ECG feature that may help to
distinguish typical from atypical AVNRT is the mode of
initiation of the reentrant circuit. Though obviously
difficult to obtain on a standard 12-lead ECG, should a
rhythm strip be available that demonstrates an initiating
atrial premature beat, the diagnosis is more likely
typical AVNRT. A ventricular premature beat is more
likely to precipitate an atypical AVNRT
 The first two complexes are normal sinus beats with a normal P wave followed by
a QRS complex. The third complex, an atrial premature beat (APB), has a
prolonged PR interval; it initiates a common or typical atrioventricular nodal
reentrant tachycardia (AVNRT) in which antegrade conduction to the ventricle
is via the slow pathway and retrograde atrial activation is by the fast pathway.
Although no distinct P wave is seen, the QRS complex has a small terminal
deflection, known as a pseudo r', which is the P wave superimposed upon the
terminal portion of the QRS complex
 The12 lead ECG shows a regular narrow complex tachycardia
with a rate of 135 beats per minute; no P waves can be seen.
The QRS morphology is identical to that seen during sinus
rhythm.
 Occasionally (in ~20%), AVNRT occurs with
activation in the reverse direction, conducting
down the fast pathway and returning up the slow
pathway.
 This form of AVNRT occurs much less commonly

and produces a prolonged RP interval during the
tachycardia with a negative P wave in leads II,
III, and aVF.
 This atypical form of AVNRT is more easily

precipitated by ventricular stimulation
AV NODAL REENTRANT
TACHYCARDIA
 In this uncommon form AVNRT, conduction
through the reentrant circuit is so slow that the
HR is less than 100 bpm.
 Despite the absence of tachycardia, patients can

be symptomatic and may be treated with a slow
pathway ablation.
 This arrhythmia, sometimes referred to as AV

nodal reentrant arrhythmia (AVNRA), has been
mistaken for a junctional rhythm
AVNRT FIGURE 1-P WAVES BURRIED IN QRS ,THUS NOT VISIBLE.
FIGURE 2-RETROGRADE P-WAVES
FIGURE 3-SUPERIMPOSED P WAVES ON QRS AS LITTLE BLIPS
THERAPY — THE GENERAL APPROACH TO THE THERAPY OF
AVNRT INCLUDES TWO COMPONENTS, ACUTE TERMINATION
OF THE ARRHYTHMIA AND PREVENTION OF RECURRENT
EPISODES.
 Acute termination — The recommended approach to acute

termination of AVNRT depends upon the severity of the arrhythmia.
 Hemodynamic collapse or severe symptoms — Severe hemodynamic
decompensation is uncommon in AVNRT. Hemodynamic compromise may
be manifested clinically by one or more of the following features:
 Hypotension and shock
 Angina pectoris
 Shortness of breath and/or heart failure
 Syncope or near-syncope
 In such cases, immediate restoration of normal sinus rhythm is

essential. Based upon their speed of onset and high therapeutic
efficacy, treatment options in this setting include:
 Adenosine
 DC cardioversion
AV NODAL REENTRANT TACHYCARDIA- RX
 Treatment is directed at altering conduction
within the AV node.
 Vagal stimulation, such as that which occurs with

the Valsalva maneuver or carotid sinus massage,
can slow conduction in the AV node sufficiently
to terminate AVNRT.
 In patients in whom physical maneuvers do not

terminate the tachyarrhythmia, the
administration of adenosine, 6–12 mg IV,
frequently does so.
AV NODAL REENTRANT TACHYCARDIA- RX
 Intravenous beta blockade or calcium channel
therapy should be considered as second-line
treatment.
 If hemodynamic compromise is present, R-wave

synchronous DC cardioversion using 100–200 J
can terminate the tachyarrhythmia.
CHRONIC THERAPY — NOT ALL AVNRT
PATIENTS REQUIRE LONG-TERM SUPPRESSIVE
THERAPY
The decision to treat is based upon the following factors:
 The frequency of the arrhythmia
 The significance of the symptoms
 Patient tolerance of medications
 Patient preference
 Patients with symptomatic and/or frequent episodes of

AVNRT are generally treated with either catheter ablation
or chronic suppressive pharmacologic therapy. There are few
data to guide the selection of a specific therapy, and choices
are influenced by patient preference. The
2003 ACC/AHA/ESCguidelines on the management of
supraventricular arrhythmias included recommendations for
the chronic therapy of AVNRT, and as with acute therapies,
our recommendations are in general agreement with those
guidelines [.
 No treatment — Patients with infrequent and well-tolerated
episodes of AVNRT may choose no chronic therapy. Such patients
can be taught to terminate the arrhythmia using safe vagotonic
maneuvers, particularly the Valsalva maneuver and its variants
 Pharmacologic therapy , the medications that are most commonly
used for the chronic suppression of AVNRT are the
nondihydropyridine calcium channel blockers verapamiland
diltiazem , and ß-blockers.
 Among patients who do not respond to diltiazem , verapamil or ß-
blockers and who do not want to pursue EP study and ablation, the
following antiarrhythmic drugs may be considered:
 Flecainide (class IC)
 Propafenone (class IC)
 Sotalol (class III)
 Amiodarone (class III)
AV NODAL REENTRANT TACHYCARDIA-
PREVENTION
 Prevention may be achieved with drugs that slow

conduction in the antegrade slow pathway, such
as digitalis, beta blockers, and calcium channel
blockers.
 In patients who have a history of exercise-
precipitated AVNRT, the use of beta blockers
frequently eliminates symptoms.
 In patients who do not respond to drug therapy
directed at the antegrade slow pathway,
treatment with class IA or IC agents directed at
altering conduction of the fast pathway may be
considered
AV NODAL REENTRANT TACHYCARDIA-
PREVENTION
 Catheter ablation, directed at elimination or

modification of slow pathway conduction, is very
effective in permanently eliminating AVNRT.
 Patients with recurrent AVNRT that produces
significant symptoms or heart rates >200 beats/min
and patients reluctant to take chronic drug therapy
should be considered for ablative therapy.
 Catheter ablation can cure AV nodal reentry in >95%
of patients with a single procedure.
 The risk of AV block requiring a permanent
pacemaker is ~1% with the ablation procedure.
AV JUNCTIONAL TACHYCARDIAS
 It is uncertain if the AV node itself has
pacemaker cells, but it is clear that the AV
junction does have pacemaker cells and is
capable of exhibiting automaticity.
 AV junction is an area that includes atrial tissue,
the AV node and His-Purkinje tissue
 Automaticity of the AV junction appears to arise

via a mechanism similar to that which occurs in
the SA node
 These can occur in the setting of enhanced
normal automaticity, abnormal automaticity, or
triggered activity.
 These tachycardias may or may not be

associated with retrograde conduction to the
atria, and the P waves may appear dissociated or
produce intermittent conduction and early
activation of the junction.
 Junctional ectopic rhythm is most often the
result of an acceleration of impulse generation
from the AV junction which, if more rapid than
the sinus node rate, assumes control as the
dominant pacemaker of the heart
 In such cases, there are no P waves seen before

the QRS complexes; instead, they occur either
simultaneously with the QRS complexes or more
commonly are retrograde (seen after the QRS
complex located in the ST segment or T wave).
 Sinus node activity is suppressed by the retrograde
atrial activation.
 If there is retrograde VA block of the impulse
to the atrium, sinus node activity is not
suppressed by the junctional rhythm, and sinus P
waves can be seen occurring independently at a
slower rate than the QRS complexes.
 This is known as AV dissociation
 When the junctional rhythm is faster than

100 beats/min, it is called junctional tachycardia.
 In some cases, the junctional ectopic rhythm
develops because there is failure of the sinus
node and of an atrial focus to assume pacemaker
function, which is therefore assumed by the AV
junction.
 This is known as a junctional escape rhythm.
 These arrhythmias may occur as a manifestation
of increased adrenergic tone or drug effect in
patients with sinus node dysfunction or after
surgical or catheter ablation.
 The arrhythmia may also be a manifestation of

digoxin toxicity.
 The most common manifestation of digoxin
intoxication is the sudden regularization of the
response to AF.
 A junctional tachycardia due to digoxin toxicity
typically does not manifest retrograde
conduction.
 Sinus activity may appear dissociated or result in
intermittent capture beats with a long PR
interval.
 If the rate is >50 beats per minute and <100
beats per minute, the term accelerated
junctional rhythm applies.
 Occasionally, automatic rhythms are mimicked by
AVNRT that fails to conduct to the atrium
 The triggering events associated with the onset
of the tachycardia may provide a clue to the
appropriate diagnosis.
 Initiation of the tachycardia without an atrial

premature beat with a gradual acceleration in
rate suggests an automatic focus.
AV JUNCTIONAL TACHYCARDIAS-
TREATMENT
 Treatment of automatic/triggered junctional
tachycardias is directed at decreasing
adrenergic stimulation and reversing digoxin
toxicity, if present.
 Digoxin therapy can be withheld if toxicity is

suspected, and the administration of digoxin-
specific antibody fragments can rapidly reverse
digoxin toxicity if the tachycardia is producing
significant symptoms and rapid termination is
indicated.
AV JUNCTIONAL TACHYCARDIAS-
TREATMENT
 Junctional tachycardia due to abnormal
automaticity can be treated pharmacologically
with beta blockers.
 A trial of class IA or IC drugs may also be

attempted. For incessant automatic junctional
tachycardia, focal catheter ablation can be
performed but is associated with an increased
risk of AV block.
PAROXYSMAL SVT
 The term paroxysmal supraventricular
tachycardia (PSVT) is applied to intermittent
SVTs with abrupt onset and offset other than
AF, atrial flutter, and MAT.
 PSVT occurs with an incidence of 35 per 100,000

person-years
 Because they have distinct clinical

characteristics, these narrow complex
tachycardias are usually considered separately.
PAROXYSMAL SVT
 PSVTs are often due to reentry, although the
sites of reentry vary
 The major causes are
 AVNRT- ~60 percent of cases;
 AVRT- ~30 percent of cases; and,
 AT or SANRT- ~ 10 percent of cases
 Junctional ectopic tachycardia and

nonparoxysmal junctional tachycardia are rare in
adults but can represent a larger portion of
PSVTs in children
 Reentry may occur around a fixed anatomic
obstacle or may be functional, developing in the
absence of an anatomic obstacle and resulting
from the intrinsic heterogeneity of
electrophysiologic properties of the myocardial
tissue.
 Reentrant circuits leading to a supraventricular
tachyarrhythmia may develop in various parts of
the heart:
 Within and around the SA node (sinus node reentry);
 Within the atrial myocardium (atrial tachycardia,
atrial flutter, or atrial fibrillation);
 Within the atrioventricular (AV node) due to the
presence of a slow and fast pathway
(atrioventricular nodal reentrant tachycardia); or
 Involving the AV node and an accessory pathway (AP)
(atrioventricular reentrant tachycardia) which
include Kent, Mahaim, James, and atriohisian (AH)
fibers.
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SUPRAVENTRICULAR

 The incidence of APCs frequently increases with

 Atrial premature complexes typically are

 A very early APC may not conduct to the

 This wide QRS pattern and the failure to

 For extremely symptomatic patients who do not

 The use of class IC antiarrhythmic agents may

 The complexes originate from the AV node and

 Pathologic conditions such as thyrotoxicosis,

 It is important to distinguish sinus tachycardia

The key features pointing to sinus tachycardia are:

 Excluding the diagnosis of an automatic AT that

 Frequently, patients are misdiagnosed as having an

 For severely symptomatic patients who are

 In comparison, intraatrial reentry has a

 ECG: P waves with a rate between 100 and 150

 Patients should undergo continuous ECG monitoring

 The terms AFL and macroreentrant AT

 Counterclockwise right AFL represents ~80%

 Macroreentrant left AFL also may develop,

 Classic or typical right AFL has an atrial rate of

 In this setting, a 1:1 rapid ventricular response

 Because lead V1 is frequently monitored in a

 The timing of atrial activation is much more

 Frequently, an individual patient may alternate

 Control of the ventricular rate in patients

 Prevention of systemic embolization, particularly

 Patients presenting with an initial episode of atrial flutter should have

 The organized atrial flutter activity frequently

 Asymptomatic patients with AFL may develop heart

 Owing to the typically faster ventricular rate,

 In selected patient with AF and typical right

 The atrial rhythm is characterized by at least three distinct P-

 Associated arrhythmias — MAT (and wandering atrial

 Discrete P waves with at least three different

 The absence of any intervening sinus rhythm

 The judicious use of flecainide or propafenone

but more experience with this drug is need

 Low-dose amiodarone therapy may also control

 The two general mechanisms for focal ATs can

 The Joint Expert Group defined focal AT as

 Enhanced automaticity — Enhanced automaticity refers to an acceleration

 The P wave initiating the tachycardia will

 In response to adenosine, reentrant ATs will

 These anatomic locations appear to be associated

 ATs also appear to originate from the muscular

 Crista terminalis (34 percent)

 Coronary sinus ostium (17 percent)

 Perinodal tissues(9 percent)

 Left atrial tachycardias were predominantly located around the

 It is important to distinguish focal ATs from

 The primary distinction is related to the

 In addition, the V–A relationship changes when

 These distinctions are less important with

 Most focal ATs are readily amenable to catheter

 And for this reason, every effort should be

 We suggest initial therapy with oral beta blockers or