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ES2
SECOND EDITION
ARRHYTHMIA
ESSENTIALS
Brian Olshansky, MD
Professor Emeritus of Medicine
University of Iowa Hospitals
Iowa City, Iowa
Cardiac Electrophysiologist
Mercy Hospital, North Iowa
Mason City, Iowa
Mina K. Chung, MD
Professor of Medicine
Cleveland Clinic Lerner College of Medicine
Case Western Reserve University
Cardiac Electrophysiology and Pacing
Department of Cardiovascular Medicine, Heart and Vascular Institute
Department of Molecular Cardiology, Lerner Research Institute
Cleveland Clinic
Cleveland, Ohio
Steven M. Pogwizd, MD
Featheringill Endowed Professor
in Cardiac Arrhythmia Research
Professor of Medicine, Physiology and Biophysics, and
Biomedical Engineering
Director, Center for Cardiovascular Biology
Associate Director, Cardiac Rhythm Management Laboratory
University of Alabama at Birmingham
Birmingham, Alabama
Nora Goldschlager, MD
Professor of Clinical Medicine
University of California, San Francisco
Chief, Clinical Cardiology
Director, Coronary Care Unit
ECG Laboratory and Pacemaker Clinic
San Francisco General Hospital
San Francisco, California
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899
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iii
Preface
Brian Olshansky, MD
Mina K. Chung, MD
Steven M. Pogwizd, MD
Nora Goldschlager, MD
iv
Chapter 1
Sinus Node: Normal and
Abnormal Rhythms
NORMAL SINUS NODE
Description
Normal sinus rhythm (NSR) is an atrial rhythm caused by electrical
activation that originates from the sinus node, a structure located in the
area of the junction of the right atrium and superior vena cava. NSR
P waves, representing atrial depolarization (but not sinus node activity
itself), are upright in leads I and aVL and the inferior leads (II, III, aVF),
indicating the high to low atrial activation pattern (Fig. 1.1). The P wave
in leads V1-V2 may be upright, biphasic, or slightly inverted, whereas
the P waves in leads V3-V6 tend to be upright, indicating right to left
atrial activation. The P-wave morphology may change with alterations in
autonomic tone, heart rate, and atrial abnormalities such as hypertrophy.
High vagal tone can be associated with a more inferior exit of the impulse
from the sinus node, whereas high sympathetic tone can be associated
with a more superior exit from the node.
1
2 Chapter 1 Sinus Node: Normal and Abnormal Rhythms
I V1 V4
aVR
II V2 V5
aVL
III aVF V3 V6
V1
II
V5
FIGURE 1.1
Normal sinus rhythm. Normal sinus rhythm is characterized by P waves that are usually upright in leads I, aVL, II, III, aVF, and V3-V6
at a rate between 60 and 100 bpm.
Chapter 1 Sinus Node: Normal and Abnormal Rhythms 3
V1
II
FIGURE 1.2
Normal sinus rhythm with sinus arrhythmia. This lead V1 and II rhythm strip shows normal sinus rhythm with sinus arrhythmia, in which the P-P intervals
vary by greater than 0.16 seconds. Sinus arrhythmia is often related to respiratory cycles.
4 Chapter 1 Sinus Node: Normal and Abnormal Rhythms
Approach to Management
Although sinus rhythm generally does not require any treatment, an
inability to increase the sinus rate appropriately in response to increases in
metabolic needs (“chronotropic incompetence”) may require permanent
rate responsive cardiac pacing when it is documented to cause symptoms.
Definitions of chronotropic incompetence are many and varied, and there
is no general agreement as to its parameters.
Associated Conditions
SB is often associated with sinus arrhythmia, escape rhythms (junctional
and ventricular), accelerated rhythms (junctional and ventricular), atrial
arrhythmias, WAP, or SA or AV Wenckebach-like periods. SB is usually
benign but can be associated with certain conditions and diseases,
including hypothyroidism, vagal stimulation, carotid sinus hypersensitivity,
Chapter 1 Sinus Node: Normal and Abnormal Rhythms 5
V1
II
V5
FIGURE 1.3
Wandering atrial pacemaker. This lead V1 II, and V5 rhythm strip shows wandering atrial pacemaker. There are at least three P wave
morphologies.
6 Chapter 1 Sinus Node: Normal and Abnormal Rhythms
V1
II
FIGURE 1.4
Sinus bradycardia. This lead II rhythm strip shows SB, which is characterized by sinus P waves (usually upright in leads II, III, aVF) with rate less
than 60 bpm.
I aVR V1 V4
III V3 V6
aVF
V1
II
V5
FIGURE 1.5
Sinus bradycardia with a wide QRS complex. Although the QRS complex is normally narrow (<0.12 seconds), the QRS can be wide
in the setting of bundle branch block or intraventricular conduction delay. This 12-lead ECG with rhythm strips of leads V1, II, and V5
shows sinus bradycardia with sinus arrhythmia (rates 53-56 bpm) and left bundle branch.
8 Chapter 1 Sinus Node: Normal and Abnormal Rhythms
N N N N N N
25 mm/sec
10 mm/mV
2
25 mm/sec
FIGURE 1.6
Tachycardia-bradycardia syndrome. This rhythm strip tracing shows an atrial tachyarrhythmia (atrial flutter/tachycardia) that suddenly terminates.
The tachycardia is followed by a 3.4-second pause and then sinus bradycardia. The combination of a tachycardia that is suddenly followed by a
bradycardia is characteristic of tachy-brady syndrome.
Chapter 1 Sinus Node: Normal and Abnormal Rhythms 9
Approach to Management
Evaluation or treatment often is unnecessary if the patient is asymptomatic.
Treatment depends on the nature of the rhythm disturbance and is usually
directed toward prevention of symptoms. Asystole can be life-threatening,
but more often it causes symptoms and is due to vagal surges or SND.
Asystolic pauses in a young, otherwise healthy person are generally due to
vagal surges related to a neurocardiogenic response. An asystolic response
after cardioversion, after a tachycardia, and in a patient who is older or has
heart disease is often due to SND. Because SND can be subclinical but
exacerbated by medical therapy, rate-slowing drugs should be avoided if
possible.
10 Chapter 1 Sinus Node: Normal and Abnormal Rhythms
TABLE 1.1
SINUS NODE DYSFUNCTION AND SINUS BRADYCARDIA MANAGEMENT
Setting Therapy
Asymptomatic • No therapy required. There is some relationship between the presence of
sleep apnea and sinus node dysfunction; some reports have suggested that
permanent pacing, even in asymptomatic patients, may benefit sleep apnea.
• Identify and treat associated medical conditions such as hypothyroidism.
• Avoid rate-slowing drug if feasible.
Symptomatic— • Treat reversible causes. Consider drugs as the cause (β-adrenergic
acute blockers, calcium channel blockers, and digoxin, antiarrhythmic drugs
[sotalol, amiodarone, flecainide, and propafenone]). A drug may be a
contributor, but until the problem resolves, treatment will be required.
• Atropine 0.6-2 mg intravenous every 5 min, up to a total of 2 mg. Low doses
and slow infusion may cause paradoxical bradycardia due to increase in
sinus rate and degree of AV block. Atropine will not work for heart transplant
patients. This is only a short-term solution.
• Isoproterenol 1-5 mcg/min is effective but can exacerbate myocardial
ischemia. Do not give to patients with unstable coronary artery disease.
Isoproterenol is rarely indicated and should only be considered in extreme
conditions when a temporary pacemaker is not available.
• Temporary pacemaker (preferably atrial, if AV conduction is intact and the
bradycardia is not due to high vagal tone) when unstable and episodes are
prolonged, persistent, highly symptomatic, recurrent, or unresponsive to
acute medical therapy, such as atropine or isoproterenol, or with bradycardia-
associated ventricular arrhythmias (e.g., torsades de pointes). Temporary
pacing may be used if permanent pacing is not possible, not indicated, or
dangerous (such as the presence of an ongoing infection). Temporary pacing
can be accomplished by epicardial wires (after cardiovascular surgery) or by
temporary balloon-tipped catheters placed percutaneously with or without
fluoroscopy (unreliable) or a temporary bipolar lead (screw in or not) that is
more reliable. Placement of a temporary pacemaker can be associated with
adverse events. It should be undertaken only if there is a long-term need to
pace but there is no immediate permanent pacemaker placement availability
(e.g., patients with recurrent syncope who on monitoring have pauses of
5 s or more, symptomatic or not). Temporary pacing is not indicated if there
are prolonged pauses caused by neurocardiogenic reasons (e.g., vasovagal
syncope, suctioning, endoscopy, vomiting, and cough).
Continued on following page
12 Chapter 1 Sinus Node: Normal and Abnormal Rhythms
TABLE 1.1
SINUS NODE DYSFUNCTION AND SINUS BRADYCARDIA MANAGEMENT (Continued)
Setting Therapy
• Transcutaneous pacing may be used emergently prior to placement of a
temporary pacing lead. It is highly unreliable and painful. It is not very
effective over time and is hardly ever indicated. It could be used for a
patient who has precipitous hemodynamic collapse due to persistent
or recurrent asystole. It has not been shown to reduce the risk of death
but occasionally can be used until an adequate temporary pacemaker is
placed. Most patients with episodic asystole do not fit into the category
of having a life-threatening arrhythmia, but patients with prolonged and
recurrent asystole might fit into this category, especially if the patient
is older and has underlying heart disease. Transcutaneous pacing is
not stable over time because of impedance changes between the large
electrodes and myocardium; moreover, adequate sedation is usually
necessary to prevent pain.
Symptomatic— • Permanent pacemaker:
chronic • Class I (ACC/AHA recommended) indications: Documented symptomatic
SB, including frequent pauses that cause symptoms; symptomatic
bradycardia occurring as a consequence of essential long-term
drug therapy at a dose and type for which there are no acceptable
alternatives; symptomatic chronotropic incompetence.
• Class IIa (ACC/AHA accepted, not mandatory, well substantiated)
indications: Sinus node dysfunction from necessary drug therapy with
HR <40 bpm when a clear association between presence of bradycardia
and significant symptoms has not been documented; syncope of
undetermined origin with major abnormalities in sinus node dysfunction
found at electrophysiology (EP) study.
• Class IIb (ACC/AHA accepted, not mandatory, less well substantiated):
Minimally symptomatic patients with chronic awake HR <40 bpm.
• Temporary transvenous pacemaker, if severe symptoms associated with
HR <30 bpm, unresponsive to acute medical therapy (e.g., atropine,
isoproterenol) or bradycardia-associated ventricular arrhythmias
(e.g., torsades de pointes). Temporary pacing is rarely indicated for
chronic symptomatic problems unless there are frequent recurrences of
symptomatic pauses or bradycardia.
ACC, American College of Cardiology; AHA, American Heart Association; AV, atrioventricular; HR, heart rate; SB, sinus
bradycardia.
TABLE 1.2
SINUS NODE DYSFUNCTION MANAGEMENT IN SPECIFIC
CLINICAL CIRCUMSTANCES
Setting Therapy
MI • Common causes for SB in setting of an acute MI: β-adrenergic blockers,
calcium channel blockers, amiodarone, morphine, lidocaine, chronic
antiarrhythmic drugs, pain, increased vagal tone (especially with
inferior MI), atrial ischemia. Usually resolves.
• In addition to symptomatic SB, additional indications for treatment of SB
include recurrent or worsening ischemia (evident by ST segment changes
on the ECG), poor cardiac output, hypotension, or bradycardia-related
ventricular arrhythmias. These are more common in the first 3-5 days after
infarction.
• Temporary pacing if there is symptomatic SB (despite stopping medications,
including β-adrenergic blockers), prolonged pauses (>3 s recurrently or
occasional ones >5 s), hypotension, heart failure symptoms. Permanent
pacing is rarely needed. In some instances, a wait of 5-7 days may not be
long enough to know if there is complete resolution of bradycardia. In that
case, a permanent pacemaker is indicated when there are continued pauses
or heart rates <40 per minute. Treadmill exercise testing can be used to
ascertain chronotropic competence after MI.
Pre-op • Atropine should be available, especially at induction of anesthesia and
during intubation when vagal tone is high.
• SB is very common intraoperatively due to maneuvers that increase vagal
tone such as intubation. If hypothermia is planned, SB can be expected.
No treatment is required.
• Even if asymptomatic, patients who cannot increase cardiac output because
of SB may require temporary pacing.
Post-op • SB is common, often due to pain, opiates, or effect of surgery itself, and is
usually not treated.
• Temporary pacing (preferably atrial but with ventricular backup pacing
if there is a vagal component) at 80-100 bpm can be used in cases of
hemodynamic decompensation. Permanent pacing should be considered if
SB does not resolve after 3-5 post-op days.
Heart • One to three weeks after transplant, SND, including SB, may resolve and
transplant require no chronic therapy.
• Acutely, isoproterenol is first-line therapy, as opposed to atropine, which will
not work in the denervated heart.
• Theophylline 150-200 mg PO bid may work in the subacute setting. Although
effective in the short term, it has not been proven effective over the long term.
• After 10-20 days, if persistent, symptomatic, and not expected to resolve,
SND may require treatment with a permanent pacemaker. An atrial pacing
device might be considered to avoid tricuspid valve damage (patient may
need repeated biopsies that may dislodge pacing leads), but make sure it
is secure in the transplanted donor (not recipient) atrium, such that paced
atrial beats will conduct intrinsically to the ventricles.
bid, Twice daily; ECG, electrocardiogram; MI, myocardial infarction; PO, per os; SB, sinus bradycardia;
SND, sinus node dysfunction.
14 Chapter 1 Sinus Node: Normal and Abnormal Rhythms
After cardiac surgery, sinus node function that fails to recover may also
necessitate a permanent pacemaker. Because it can take 5 to 6 weeks
before full return of sinus node function, frequently a decision is made to
implant a pacemaker by the fifth to seventh post-op day before hospital
discharge. It is best to make that decision while temporary pacing
wires are still in place so that temporary pacing can be instituted if it is
necessary.
Associated Conditions
SA exit block is usually related to drug therapy (digoxin, calcium
channel blockers, β-adrenergic blockers), vagal stimulation, SND with
degenerative disease of the sinus node and atrium, or hyperkalemia.
It is unusual after MI but may be caused by vagal excess (Bezold-
Jarisch reflex) from an inferoposterior MI. If unrelated to an acute cause
that is reversible or transient, SA exit block may cause progressive
bradycardia.
FIGURE 1.7
Sinoatrial exit block type I. This is a lead II rhythm strip of sinus rhythm with slight P-P interval shortening followed by a pause that is less than
twice the prevailing P-P interval. This represents SA exit block (type I) in a patient who has sinus node dysfunction.
V1
II
FIGURE 1.8
Sinoatrial exit block type II. This is a rhythm strip of leads V1 and II showing sinus rhythm (rate 67 bpm) with sinus pauses that are twice the
prevailing P-P interval. There is also left bundle branch block.
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V.
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