The Bradyarrhythmias: Disorders of Sinus Node Function and AV Conduction Disturbances

Anatomy of the Conducting System

Under normal conditions, the pacemaker function of the heart resides in the sinoatrial (SA) node, which lies at the junction of the right atrium and superior vena cava. The SA node is approximately 1.5 cm long and 2 to 3 mm wide and is supplied by the sinus node artery, which arises from either the right coronary artery (60%) or the left circumflex coronary artery (40%). Once the impulse exits the sinus node and perinodal tissue, it traverses the atrium until it reaches the atrioventricular (AV) node. The blood supply of the AV node is derived from the posterior descending coronary artery (90%). The AV node lies at the base of the interatrial septum just above the tricuspid annulus and anterior to the coronary sinus. The electrophysiologic properties of the AV node result in slow conduction, which is responsible for the normal delay in AV conduction, i.e., the PR interval.

The bundle of His emerges from the AV node, enters the fibrous skeleton of the heart, and courses anteriorly across the membranous interventricular septum. It has a dual blood supply from the AV nodal artery and a branch of the anterior descending coronary artery. The branching (distal) portion of the bundle of His gives rise to a broad sheet of fibers that course over the left side of the interventricular septum to form the left bundle branch and a narrow cable-like structure on the right side that forms the right bundle branch. The arborization of both the right and left bundle branches gives rise to the distal His-Purkinje system, which ultimately extends throughout the endocardium of the right and left ventricles.

The SA node, atrium, and AV node are significantly influenced by autonomic tone. Vagal influences depress automaticity of the SA node, depress conduction, and prolong refractoriness in the tissue surrounding the SA node; inhomogeneously decrease atrial refractoriness and slow atrial conduction; and prolong AV nodal conduction and refractoriness. Sympathetic influences exert the opposite effect.

Electrophysiologic Principles

In the resting state, the interior of most cardiac cells, with the exception of the SA and AV nodes, is approximately -80 to -90 mV, negative with respect to a reference extracellular electrode. The resting membrane potential is determined primarily by the concentration gradient of potassium across the cell membrane. Activation of cardiac cells results from movement of ions across the cell membrane, causing a transient depolarization known as the action potential. The ionic species responsible for the action potential varies among the cardiac tissues, and the configuration of the action potential is therefore unique to each tissue (Fig. 229-1).

Figure 229-1

Figure 229-1: Action potential configurations in different regions of the mammalian heart.

The action potential of the His-Purkinje system and ventricular myocardium has five phases (Fig. 229-2). The rapid depolarizing current (phase 0) is mainly determined by an influx of sodium into myocardial cells followed by a secondary (slower) influx of calcium, which produces a slow inward current. The repolarization phases of the action potential (phases 1 to 3) are primarily related to outward flux of potassium. The resting membrane potential is phase 4.

Figure 229-2

Figure 229-2: Schematic representation of the action potential in normal ventricle depicting the direction, strength, and period of flow of the ionic currents underlying the action potential. The arrow's direction and size indicate whether current is inward- or outward-directed and the approximate current strength of the ion identified at the arrow's base. The horizontal position of the arrow corresponds to the same moment in the time course of action potential (see text). The five phases of the action potential are indicated by the numerals placed along the waveform.

The bradyarrhythmias result from abnormalities either of impulse formation, i.e., automaticity, or of conduction. Automaticity, which is normally observed in the sinus node, the specialized fibers of the His-Purkinje system, and some specialized atrial fibers, is the property of a cardiac cell that causes it to depolarize spontaneously during phase 4 of the action potential, leading to the generation of an impulse. To exhibit automaticity, the resting membrane potential must decrease spontaneously until threshold potential is reached and an all-or-none regenerative response occurs. The ionic currents producing spontaneous diastolic depolarization appear to involve the inward current of either sodium or calcium and a decreasing outward potassium current. The velocity of conduction, i.e., impulse propagation through cardiac tissues, depends on the magnitude of inward current, which is directly related to the rate of rise and amplitude of phase 0 of the action potential. The more positive the threshold potential and the slower the rate of depolarization toward threshold, the slower is the rate of rise of phase 0 of the action potential and the slower is the conduction velocity. Disease states or drugs may result in lower rates of rise of phase 0 at any given membrane potential. Passive membrane properties (e.g., intracellular resistance and intercellular coupling) can also affect impulse propagation. Propagation is more rapid parallel to fiber orientation than transverse to it, a property termed anisotropic conduction.

Refractoriness is a property of cardiac cells that defines the period of recovery that cells require after being discharged before they can be reexcited by a stimulus. The absolute refractory period is defined by that portion of the action potential during which no stimulus, regardless of its strength, can evoke another response. The effective refractory period is that part of the action potential during which a stimulus can evoke only a local, nonpropagated response. The relative refractory period extends from the end of the effective refractory period to the time that the tissue is fully recovered. During this time, a stimulus of greater than threshold strength is required to evoke a response, which is propagated more slowly than normal. In the normal His-Purkinje system or ventricular myocytes, excitability is recovered following completion of the action potential, and evoked responses have characteristics similar to the spontaneous normal response. In the AV node, recovery of excitability occurs well after completion of the action potential.

Intracardiac Recordings of the Specialized Conducting System

Electrode catheters allow the recording of activation of portions of the specialized conducting system, including the bundle of His. To obtain a recording from the bundle of His, the electrode catheter is positioned across the tricuspid valve (Fig. 229-3). The interval from local atrial depolarization in the His bundle recording to the onset of depolarization of the His bundle deflection is called the AH interval (normal = 60 to 125 ms) and represents an indirect method of assessing AV nodal conduction time. The interval from the beginning of the His bundle deflection to the earliest onset of ventricular activation, as measured from any of multiple-surface electrocardiogram (ECG) leads or the intracardiac ventricular electrogram, is called the HV interval (normal = 35 to 55 ms) and represents conduction time through the His-Purkinje system. Electrode catheters can be positioned in the area of the sinus node to record high right atrial activity. Left atrial activity may be recorded directly via a catheter placed across a patent foramen ovale or indirectly using a catheter inserted into the coronary sinus. The atrial activation sequence may be "mapped," and sites of intra- and interatrial conduction abnormalities may be ascertained.

Figure 229-3

Figure 229-3: Normal intracardiac recording. Surface ECG leads I, II, and V1 are displayed with intracardiac ECGs from the high right atrium (HRA), left atrium from the coronary sinus (CS), and AV junction to obtain a His bundle electrogram (HBE). T, time lines; A, atrial activation; H, His bundle activation; V, ventricular activation. Atrial activation begins in the HRA and spreads inferiorly to the low atrial septum, as recorded in the HBE, and the left atrium, as recorded in the CS. The AH and HV intervals represent AV nodal and His-Purkinje conduction times, respectively. Vertical lines = 0.10 s.

Sinus Node Dysfunction

The SA node is normally the dominant cardiac pacemaker because its intrinsic discharge rate is the highest of all potential cardiac pacemakers. Its responsiveness to alterations in autonomic nervous system tone is responsible for the normal acceleration of heart rate during exercise and the slowing that occurs during rest and sleep. Increases in sinus rate normally result from an increase in sympathetic tone acting via 0x0003b2-adrenergic receptors and/or a decrease in parasympathetic tone acting via muscarinic receptors. Slowing of the heart rate is normally due to opposite alterations. In adults, the normal sinus rate under basal conditions is 60 to 100 beats per minute. Sinus bradycardia is said to exist when the sinus rate is less than 60 beats per minute, and sinus tachycardia when it exceeds 100 beats per minute. However, there is wide variation among individuals, and rates less than 60 beats per minute do not necessarily indicate pathologic states. For example, trained athletes often exhibit resting rates under 50 beats per minute due to increases in vagal tone. Normal elderly individuals may also show marked sinus bradycardia at rest.


SA node dysfunction is most often found in the elderly as an isolated phenomenon. Although interruption of the blood supply to the SA node may produce dysfunction, the correlation between obstruction of the sinus node artery and clinical evidence of SA node dysfunction is poor. Specific disease states associated with SA node dysfunction include senile amyloidosis and other conditions associated with infiltration of the atrial myocardium. Sinus bradycardia is associated with hypothyroidism, advanced liver disease, hypothermia, typhoid fever, and brucellosis; it occurs during episodes of hypervagotonia (vasovagal syncope), severe hypoxia, hypercapnia, acidemia, and acute hypertension. However, most cases of SA node dysfunction are due to idiopathic degeneration or are secondary to pharmacologic agents.


Although marked (0x00226450 beats per minute) sinus bradycardia may cause fatigue and other symptoms due to inadequate cardiac output, more commonly sinus node dysfunction is manifest as paroxysmal dizziness, presyncope, or syncope. These symptoms usually result from abrupt, prolonged sinus pauses caused by failure of sinus impulse formation (sinus arrest) or block of conduction of sinus impulses to the surrounding atrial tissue (sinus exit block). In either case, the ECG manifestation is a prolonged period (>3 s) of atrial asystole. In some patients, SA node dysfunction is accompanied by abnormalities in AV conduction. In addition to the absence of atrial activity, lower pacemakers fail to emerge during the sinus pauses, resulting in periods of ventricular asystole and syncope. Occasionally, SA node dysfunction is manifested by an inadequate acceleration in sinus rate in response to a stress such as exercise or fever. In some patients, SA node dysfunction may become manifest only in the presence of certain cardioactive drugs: cardiac glycosides, 0x0003b2-adrenergic blocking drugs, calcium channel blockers, amiodarone, and other antiarrhythmic agents. These agents, which do not usually cause sinus node dysfunction in normal people, may unmask evidence of sinus node dysfunction in susceptible individuals.

The sick sinus syndrome refers to a combination of symptoms (dizziness, confusion, fatigue, syncope, and congestive heart failure) caused by SA node dysfunction and manifested by marked sinus bradycardia, sinoatrial block, or sinus arrest. Because these symptoms are nonspecific, and because ECG manifestations of sinus node dysfunction are often intermittent, it may be difficult to prove that such symptoms are actually caused by SA node dysfunction.

Atrial tachyarrhythmias such as atrial fibrillation, atrial flutter, or atrial tachycardia may be accompanied by SA node dysfunction. The bradycardia-tachycardia syndrome refers to paroxysmal atrial arrhythmia that upon termination is followed by prolonged sinus pauses (Fig. 229-4) or in which there are alternating periods of tachyarrhythmia and bradyarrhythmia. Syncope or presyncope may result from failure of the sinus node to recover function following suppression of automaticity by atrial tachyarrhythmia.

Figure 229-4

Figure 229-4: Tachycardia-bradycardia syndrome. Rhythm strip of ECG lead II showing spontaneous cessation of supraventricular tachycardia followed by a 6-s pause prior to resumption of sinus activity. The patient was asymptomatic during supraventricular tachycardia, but the sinus pause caused severe light-headedness.


First-degree sinoatrial exit block denotes a prolonged conduction time from the SA node to the surrounding atrial tissue. It cannot be recognized on a standard (surface) ECG but requires invasive intracardiac recordings, which can detect this condition indirectly, by measuring the sinus response to atrial premature beats, or directly, by recording SA node electrograms. Second-degree sinoatrial exit block denotes the intermittent failure of conduction of sinus impulses to the surrounding atrial tissue; it is manifested as the intermittent absence of P waves (Fig. 229-5). Third-degree, or complete, sinoatrial block is characterized by a lack of atrial activity or by the presence of an ectopic subsidiary atrial pacemaker. On the standard ECG it cannot be distinguished from sinus arrest, but direct intracardiac recordings of SA node activity permit this distinction. The bradycardia-tachycardia syndrome is manifested on the standard ECG as tachyarrhythmias (Fig. 229-4). Most often these are atrial flutter or fibrillation, although any tachycardia during which the atria are activated may cause overdrive suppression of the sinus node resulting in clinical appearance of this syndrome.

Figure 229-5

Figure 229-5: Second-degree sinoatrial exit block. Surface ECG denoting abrupt absence of P wave during sinus rhythm. Prior to the pause, the sinus rate is regular. The interval of the pause is exactly twice the basal sinus cycle length. The arrow marks the appropriate location for the absent P wave. SA exit block can be 2:1 as above or longer, as shown in Fig. 229-6.

The most important step in the diagnosis is to correlate symptoms with ECG evidence of SA node dysfunction. While ambulatory ECG (Holter) monitoring remains a mainstay in evaluating sinus node function, most episodes of syncope are paroxysmal and unpredictable. Single and even multiple 24-h Holter monitor recordings may fail to include a symptomatic episode.

Caution must be taken in interpreting the Holter monitor results. For instance, a pause during sleep is often a normal finding associated with heightened vagal tone. This should not be interpreted as sinus node dysfunction requiring pacemaker implantation.

Continuous-loop event records represent a more specific diagnostic tool. These devices may be worn for prolonged periods of time and allow close correlation between electrocardiographic findings and symptoms. They do require the patient's ability to activate the monitor at the time of symptoms. More recently, an implantable event recorder, which can be interrogated like a pacemaker, has been developed for patients with rare events.

The response to carotid sinus pressure and pharmacologic autonomic "denervation" of the heart may be helpful. Carotid sinus pressure can be particularly useful in patients in whom paroxysmal dizziness or syncope is compatible with the hypersensitive carotid sinus syndrome (Chap. 21). In such patients, the response can be dramatic, and sinus pauses in excess of 5 s may occur. Although pauses in excess of 3 s are considered abnormal, in elderly patients such pauses are common and do not necessarily signify a diagnostic response. This is a major limitation of the use of carotid sinus pressure as a diagnostic test in the elderly. The other noninvasive test of SA node function involves the use of pharmacologic agents to manipulate the autonomic nervous system and assess the balance of parasympathetic and sympathetic activity on the sinus node. Physiologic or pharmacologic maneuvers that are vagomimetic (Valsalva maneuver or phenylephrine-induced hypertension), vagolytic (atropine), sympathomimetic (isoproterenol or hypotension by nitroprusside), or sympatholytic (0x0003b2-adrenergic blocking agents) can be utilized, singly and in combination. These studies are designed to test the response of the sinus node to autonomic stimulation and inhibition and thereby characterize the status of autonomic regulation of the sinus node. Abnormalities of the autonomic control of sinus function are particularly common in patients in whom asymptomatic sinus bradycardia is documented.

Intrinsic Heart Rate

This is a manifestation of the primary activity of the SA node, and its determination requires chemical autonomic blockade of the heart with a combination of atropine and a beta blocker. Normal values of intrinsic heart rate (in beats per minute) are calculated by the formula 118.1 - (0.57 age). The use of autonomic blockade can separate patients with asymptomatic sinus bradycardia into a group with primary sinus node dysfunction (slow intrinsic heart rate) and a group with autonomic imbalance (normal intrinsic heart rate). Autonomic blockade is particularly useful when combined with invasive assessment of sinus node function. Autonomic blockade may depress conduction in patients with intrinsic disease of the conduction system and should be carried out only in a setting where arrhythmias can be monitored and treated rapidly.


The invasive electrophysiologic investigation of SA node dysfunction should be undertaken in patients who have had symptoms compatible with SA node dysfunction and in whom no documentation of the arrhythmia responsible for these symptoms has been obtained by prolonged Holter monitoring. Asymptomatic patients with sinus bradycardia need not be tested, since no therapy is indicated. Similarly, symptomatic patients with ECG documentation of asystole, sinoatrial block or arrest, or the bradycardia-tachycardia syndrome do not require electrophysiologic tests for diagnosis. However, in symptomatic patients without documentation of an arrhythmia, electrophysiologic assessment of SA node function can yield information that may be used to guide appropriate therapy.

The results of electrophysiologic tests of sinus node function must be interpreted with caution. SA node dysfunction coexists frequently with other disorders such as AV conduction disturbances, which may cause symptoms such as syncope. Electrophysiologic evaluation of patients with symptoms such as undiagnosed syncope must not stop with the demonstration of abnormalities of SA node dysfunction or carotid sinus hypersensitivity. Instead, complete evaluation, including His bundle recordings and programmed atrial and ventricular stimulation (Chap. 230), is necessary to search for additional electrophysiologic abnormalities that could be responsible for symptoms.


Permanent pacemakers (see Table 229-4) are the mainstay of therapy for patients with symptomatic SA node dysfunction. Patients with intermittent paroxysms of bradycardia or sinus arrest and with the cardioinhibitory form of the hypersensitive carotid sinus syndrome are usually adequately treated by demand ventricular pacemakers. These devices are reliable, relatively inexpensive, and suffice to prevent episodic symptoms due to abrupt bradycardia. Whether dual-chamber pacing offers any advantages to ventricular pacing in such circumstances remains uncertain. Patients with symptomatic chronic sinus bradycardia or frequent prolonged episodes of sinus node dysfunction do better with dual-chamber pacemakers that preserve the normal AV activation sequence. Although theoretically an atrial demand pacemaker should be adequate for patients with SA node dysfunction, the frequent accompaniment of dysfunction in other portions of the cardiac conduction system usually mandates placement of a pacemaker capable of ventricular pacing. Recent studies suggest that AV sequential pacing may also be useful in preventing atrial fibrillation, an important component of the bradycardia-tachycardia syndrome.

Table 229-4: Guidelines for Permanent Pacing*

Acquired AV Block in Adults

Class I

  1. Complete heart block, permanent or intermittent, at any anatomic level, associated with any anatomic level, associated with any one of the following complications:
    1. Symptomatic bradycardia. In the presence of complete heart block, symptoms must be presumed to be due to the heart block unless proved to be otherwise.
    2. Congestive heart failure.
    3. Ectopic rhythms and other medical conditions that require drugs that suppress the automaticity of escape pacemakers and result in symptomatic bradycardia.
    4. Documented periods of asystole 0x0022653.0 s or any escape rate < 40 beats per minute in symptom-free patients.
    5. Confusional states that clear with temporary pacing.
    6. Post-AV junction ablation, myotonic dystrophy.
  2. Second-degree AV block, permanent or intermittent, regardless of the type or the site of block, with symptomatic bradycardia.
  3. Atrial fibrillation, atrial flutter, or rare cases of supraventricular tachycardia with complete heart block or advanced AV block, bradycardia, and any of the conditions described under a. The bradycardia must be related to digitalis or drugs known to impair AV conduction.

Class II

  1. Asymptomatic complete heart block, permanent or intermittent, at any anatomic site, with ventricular rates of 40 beats per minute or faster.
  2. Asymptomatic type II second-degree AV block, permanent or intermittent.
  3. Asymptomatic type I second-degree AV block at infra-His or intra-His levels.

Class III

  1. First-degree AV block.
  2. Asymptomatic type I second-degree AV block at the supra-His (AV node) level.

After Myocardial Infarction

Class I

  1. Persistent advanced second-degree AV block or complete heart block after acute myocardial infarction with block in the His-Purkinje system (bilateral bundle branch block).
  2. Transient advanced AV block and associated bundle branch block.

Class II

  1. Persistent advanced block at the AV node.

Class III

  1. Transient AV conduction disturbances in the absence of intraventricular conduction defects.
  2. Transient AV block in the presence of isolated left anterior hemiblock.
  3. Acquired left anterior hemiblock in the absence of AV block.
  4. Persistent first-degree AV block in the presence of bundle branch block not demonstrated previously.

Bifascicular and Trifascicular Block

Class I

  1. Bifascicular block with intermittent complete heart block associated with symptomatic bradycardia.
  2. Bifascicular or trifascicular block with intermittent type II second-degree AV block without symptoms attributable to the heart block.

Class II

  1. Bifascicular or trifascicular block with syncope that is not proved to be due to complete heart block, but other possible causes for syncope are not identifiable.
  2. Markedly prolonged HV (>100 ms).
  3. Pacing-induced infra-His block.

Class III

  1. Fascicular block without AV block or symptoms.
  2. Fascicular block with first-degree AV block without symptoms.

Sinus Node Dysfunction

Class I

  1. Sinus node dysfunction with documented symptomatic bradycardia. In some patients this will occur as a consequence of long-term (essential) drug therapy of a type and dose for which there are no acceptable alternatives.

Class II

  1. Sinus node dysfunction, occurring spontaneously or as a result of necessary drug therapy, with heart rates < 40 beats per minute when a clear association between significant symptoms consistent with bradycardia and the actual presence of bradycardia has not been documented.

Class III

  1. Sinus node dysfunction in asymptomatic patients, including those in whom substantial sinus bradycardia (heart rate < 40 beats per minute) is a consequence of long-term drug treatment.
  2. Sinus node dysfunction in patients in whom symptoms suggestive of bradycardia are clearly documented not to be associated with a slow heart rate.

Hypersensitive Carotid Sinus and Neurovascular Syndromes

Class I

  1. Recurrent syncope associated with clear, spontaneous events provoked by carotid sinus stimulation; minimal carotid sinus pressure induces asystole of >3 s duration in the absence of any medication that depresses the sinus node or AV conduction.

Class II

  1. Recurrent syncope without clear, provocative events and with a hypersensitive cardioinhibitory response.
  2. Syncope with associated bradycardia reproduced by a head-up tilt with or without isoproterenol or other forms of provocative maneuvers and in which a temporary pacemaker and a second provocative test can establish the likely benefits of a permanent pacemaker.

Class III

  1. A hyperactive cardioinhibitory response to carotid sinus stimulation in the absence of symptoms.
  2. Vague symptoms, such as dizziness, light-headedness, or both, with a hyperactive cardioinhibitory response to carotid sinus stimulation.
  3. Recurrent syncope, light-headedness, or dizziness in the absence of a cardioinhibitory response.

*Class I: agreement that permanent pacemaker should be implanted. Class II: divergence of opinion regarding need for implantation. Class III: agreement that pacemaker is unnecessary.

Guidelines for The Implantation of Cardiac Pacemakers and Antiarrhythmic Devices. Am Coll Cardiol/Am Heart Assoc.


AV Conduction Disturbances

The specialized cardiac conducting system normally ensures synchronous conduction of each sinus impulse from the atria to the ventricles. Abnormalities of conduction of the sinus impulse to the ventricles may portend the development of heart block, which can ultimately lead to syncope or cardiac arrest. In order to evaluate the clinical significance of conduction abnormalities, the physician must assess (1) the site of conduction disturbance, (2) the risk of progression to complete block, and (3) the probability that a subsidiary escape rhythm arising distal to the site of block will be electrophysiologically and hemodynamically stable. This latter point is perhaps the most important, since the rate and stability of the escape pacemaker determine what symptoms result from heart block. The escape pacemaker following AV nodal block is usually in the His bundle, which generally has a stable rate of 40 to 60 beats per minute and is associated with a QRS complex of normal duration (in the absence of a preexisting intraventricular conduction defect). This contrasts with escape rhythms arising in the distal His-Purkinje system, which have lower intrinsic rates (25 to 45 beats per minute), manifest wide QRS complexes with prolonged duration, and are unstable. Thus, the most important issue is to assess the risk of infra- or intra-His block (which always mandates a pacemaker) or AV nodal block in which the frequency of the escape pacemaker is not sufficient to meet hemodynamic requirements (Table 229-1). Although prolonged QRS complexes are invariable when the distal His-Purkinje pacemakers form the escape mechanism, wide QRS complexes can also coexist with AV nodal block and a His bundle rhythm. Therefore, QRS morphology alone may not be adequate to identify the site of block.

Table 229-1: Atrioventricular Conduction Evaluation


    1. Atrial activation times: Measurement of intraatrial conduction times. Prolonged activation times may be associated with atrial flutter or fibrillation.


  1. Measurement of AH and HV intervals: Prolongation of AH interval (>125 ms) or prolongation of the HV interval (>55 ms) may help localize the site of delay.


Incremental atrial pacing: To determine the cycle length at which block occurs in the AV node and/or His-Purkinje system. Block below the His bundle at rates of <150 beats per minute portends the development of infra-His block.


The AV node is supplied by the parasympathetic and sympathetic nervous systems and is sensitive to variations in autonomic tone. Chronic slowing of AV nodal conduction may be seen in highly trained athletes who have hypervagotonia at rest. A variety of diseases and drugs can also influence AV nodal conduction. These include acute processes such as myocardial infarction (particularly inferior), coronary spasm (usually of the right coronary artery), digitalis intoxication, excesses of beta and/or calcium blockers, acute infections such as viral myocarditis, acute rheumatic fever, infectious mononucleosis, and miscellaneous disorders such as Lyme disease, sarcoidosis, amyloidosis, and neoplasms, particularly cardiac mesotheliomas. AV nodal block may also be congenital.

Two degenerative diseases are commonly responsible for damage to the specialized conducting system and produce AV block usually associated with bundle branch block (Chap. 226). In Lev's disease, there is calcification and sclerosis of the fibrous cardiac skeleton, which frequently involves the aortic and mitral valves, the central fibrous body, and the summit of the ventricular septum. Lenegre's disease appears to be a primary sclerodegenerative disease within the conducting system itself with no involvement of the myocardium or the fibrous skeleton of the heart. These two diseases are probably the most common causes of isolated chronic heart block in adults. Hypertension and aortic and/or mitral stenosis are specific disorders that either accelerate the degeneration of the conducting system or have a direct effect by calcification and fibrosis involving the conducting system.

First-degree AV block, more properly termed prolonged AV conduction, is classically characterized by a PR interval >0.20 s, but use of this value may be misleading in terms of clinical significance. Since the PR interval is determined by atrial, AV nodal, and His-Purkinje activation, delay in any one or more of these structures can contribute to a prolonged PR interval. In the presence of a QRS complex of normal duration, a PR interval >0.24 s almost invariably is due to a delay within the AV node. If the QRS is prolonged, delays may be present at any of the levels mentioned above. Delay within the His-Purkinje system is always accompanied by a prolonged QRS duration but can occur with a relatively normal PR interval (Fig. 229-6). However, as indicated below, it is only with intracardiac recordings that the exact site of delay can be determined.

Figure 229-6

Figure 229-6: Example of marked His-Purkinje system disease with a relatively normal PR interval. Surface leads I, aVF, and V1 are shown with electrograms from the high right atrium (HRA), His bundle electrogram (HBE), and time lines (T). The QRS shows right bundle branch block and left anterior hemiblock; the PR interval is minimally elevated at 205 ms, but the HV interval exceeds 100 ms. Such a prolonged HV interval mandates a pacemaker.

Second-degree heart block (intermittent AV block) is present when some atrial impulses fail to conduct to the ventricles. Mobitz type I second-degree AV block (AV Wenckebach block) is characterized by progressive PR interval prolongation prior to block of an atrial impulse (Fig. 229-7A). The pause that follows is less than fully compensatory (i.e., is less than two normal sinus intervals), and the PR interval of the first conducted impulse is shorter than the last conducted atrial impulse prior to the blocked P wave. Usually the difference between the longest and shortest PR intervals exceeds 100 ms. This type of block is almost always localized to the AV node and associated with a normal QRS duration, although bundle branch block may be present. It is seen most often as a transient abnormality with inferior wall infarction or with drug intoxication, particularly digitalis, beta blockers, and occasionally calcium channel antagonists. This type of block can also be observed in normal individuals with heightened vagal tone. Although Mobitz type I block can progress to complete heart block, this is uncommon, except in the setting of acute inferior wall myocardial infarction. Even when it does, however, the heart block is usually well tolerated because the escape pacemaker usually arises in the proximal His bundle and provides a stable rhythm. As a result, the presence of Mobitz type I second-degree AV block rarely mandates aggressive therapy. Therapeutic decisions depend on the ventricular response and the symptoms of the patient. If the ventricular rate is adequate and the patient is asymptomatic, observation is sufficient.

Figure 229-7

Figure 229-7

Figure 229-7: A. Mobitz type I second-degree AV block. Intracardiac recordings demonstrate that the PR prolongation (320, 615 ms) is localized to the AV node (AH 240, 535 ms, respectively). HBE, His bundle electrogram; A, atrium; H, His; V, ventricle. Time lines (T) = 100 ms. B. Mobitz type II second-degree AV block. Intracardiac recordings document block below the His bundle.
C. 2:1 heart block. Surface leads 1, aVF, V1, demonstrate 2:1 heart block. The intracardiac leads, high right atrium (HRA), coronary sinus (CS), and HBE, demonstrate a diseased His bundle with marked intra-His conduction delay (split-His = HH′) during conducted beats and block in the His bundle every other beat (i.e., between H and H′).

In Mobitz type II second-degree AV block, conduction fails suddenly and unexpectedly without a preceding change in PR intervals (Fig. 229-7B). It is generally due to disease of the His-Purkinje system and is most often associated with a prolonged QRS duration. When Mobitz type II block occurs with a normal QRS duration, an intra-His site of block should be expected (Fig. 229-7C). It is important to recognize this type of block because it has a high incidence of progression to complete heart block with an unstable, slow, lower escape pacemaker. Therefore, pacemaker implantation is necessary in this condition. Mobitz type II block may occur in the setting of anteroseptal infarction or in the primary or secondary sclerodegenerative or calcific disorders of the fibrous skeleton of the heart. In so-called high-degree AV block there are periods of two or more consecutively blocked P waves, but intermittent conduction can be demonstrated. Block is usually in the His-Purkinje system, but simultaneous block in the AV node may also be present. Regardless of the site of origin of the escape rhythm, if it is slow and the patient is symptomatic, a cardiac pacemaker is mandatory.

Third-degree AV block is present when no atrial impulse propagates to the ventricles. If the QRS complex of the escape rhythm is of normal duration, occurs at a rate of 40 to 55 beats per minute, and increases with atropine or exercise, AV nodal block is probable. Congenital complete AV block is usually localized to the AV node. If the block is within the His bundle, the escape pacemaker is usually less responsive to these perturbations. If the escape rhythm of the QRS is wide and associated with rates 0x00226440 beats per minute, block is usually localized in, or distal to, the His bundle and mandates a pacemaker, since the escape rhythm in this setting is unreliable (Fig. 229-8). Some patients with infra-His bundle block are capable of retrograde conduction. In such patients, a "pacemaker syndrome" (see below) may develop if a simple ventricular pacemaker is used. Dual-chamber pacemakers eliminate this potential problem.

AV Dissociation

AV dissociation exists whenever the atria and ventricles are under the control of two separate pacemakers and, while present in complete AV block, can occur in the absence of a primary conduction disturbance. AV dissociation unrelated to heart block may occur under two circumstances: First, it may develop with an AV junctional rhythm in response to severe sinus bradycardia. When the sinus rate and the escape rate are similar and the P waves occur just before, in, or following the QRS complex, isorhythmic AV dissociation is said to be present. Treatment usually consists of removal of the offending cause of sinus bradycardia (i.e., discontinuation of digitalis, beta blockers, or calcium antagonists), accelerating the sinus node by vagolytic agents, or insertion of a pacemaker if the escape rhythm is slow and results in symptoms. Second, AV dissociation can be caused by an enhanced lower (junctional or ventricular) pacemaker that competes with normal sinus rhythm and frequently exceeds it. This has been called interference AV dissociation because the rapid lower pacemaker results in bombardment of the AV node in a retrograde fashion, rendering it refractory to the normal sinus impulses. Thus failure of antegrade conduction is a physiologic response in this circumstance. Interference dissociation commonly occurs during ventricular tachycardia, accelerated junctional or ventricular rhythms seen with digitalis intoxication, myocardial ischemia and/or infarction, or local irritation following cardiac surgery. The accelerated rhythm should be treated with either antiarrhythmic drugs (Chap. 230), removal of an offending drug, or correction of the metabolic abnormality or ischemia.

Intracardiac Electrocardiographic Recordings in Diagnosis and Management

The main therapeutic decision in patients with AV conduction disturbance is whether or not a permanent pacemaker is required, and a number of circumstances exist in which His bundle electrocardiography can be a useful diagnostic tool upon which to base this decision. It is unquestionable that patients with symptomatic second- or third-degree AV block should be paced, and therefore, these patients do not require electrophysiologic study. However, intracardiac ECG recordings can be useful in at least the following four groups of patients:

Patients with syncope and bundle branch or bifascicular block without documentation of AV block. In such patients, the demonstration of marked infra-His bundle conduction disturbances, i.e., a prolonged HV interval (>100 ms), may usually be taken as an indication of the need for the insertion of the permanent pacemaker. Complete electrophysiologic evaluation, including atrial and ventricular programmed stimulation, is indicated to help identify other possible cardiac etiologies for the syncope. Since the incidence of significant advanced AV block is low in asymptomatic patients who have bifascicular block, electrophysiologic evaluation or permanent pacemakers are not cost-effective. In this group, observation appears most reasonable.

Patients with 2:1 AV conduction. Intracardiac recordings are necessary to ascertain the site of the conduction disturbance because the typical ECG features of Mobitz type I or Mobitz type II block cannot be discerned during a 2:1 pattern of AV conduction on the surface ECG. Intracardiac recordings may demonstrate that AV nodal block, intra-His bundle block, infra-His bundle block, or combinations of block may be responsible (Figs. 229-7 and 229-8). A surface ECG finding that suggests an infra-His bundle lesion is the presence of alternating bundle branch block associated with changing PR intervals. Intracardiac recordings in such patients confirm that the block is almost always in the His-Purkinje system. Increasing block with exercise or following atropine suggests intra- or infra-His block (Table 229-2). The finding of infra- or intra-His bundle block in patients with asymptomatic second-degree AV block mandates pacemaker therapy because of the high likelihood of the development of symptomatic high-grade AV block and syncope.

Table 229-2: Site of 2:1 Atrioventricular Block


Observation-Site of Block

1. QRS width

Normal QRS-in AV node or His bundle

2. PR interval of conducted P wave

>0.30 s-in AV node
0x0022640.16 s-in HPS or His bundlea

3. Atropine or exercise

Improve conduction-in AV node
Worsen conduction-in HPS or His bundlea

4. CSP

Worsen conduction-in AV node
Improve conduction-in HPS or His bundlea

5. Retrograde conduction

Present-in HPS or His bundlea
Absent-may be anywhere

aUse of a pacemaker is indicated.

NOTE: BBB, bundle branch block; HPS, His-Purkinje system; CSP, carotid sinus pressure.

Patients with Wenckebach block in the presence of bundle branch block. This situation, particularly when the maximal change in PR interval is 0x00226450 ms, can suggest intra- or infra-His Wenckebach block, in which case a pacemaker is mandated. Intracardiac recordings are necessary to make this diagnosis.

Asymptomatic patients with third-degree AV block. In such patients, electrophysiologic studies may be useful in assessing the stability of the junctional pacemaker. Pacing is indicated when the His bundle escape pacemaker is shown to be unstable by an inadequate response to exercise, atropine, or isoproterenol or by a prolonged junctional recovery time following ventricular pacing.

Figure 229-8

Figure 229-8: Third-degree AV block. The figure shows surface leads 1, aVF, V1, and an intracardiac His bundle recording (HBE). Complete heart block is evident on the surface leads. The intracardiac recording demonstrates an absence of QRS deflection (V) after a His bundle (H) spike. This indicates block below the His bundle. Note that following the second QRS complex (V), there is an atrial (A) deflection indicating retrograde conduction. Retrograde conduction is often present when block is in the His-Purkinje system but is virtually never present when block is in the AV node.


A number of congenital and familial syndromes involving the cardiac conduction system have been described. An example of a congenital condition that is transmitted but not genetic is congenital complete heart block associated with maternal systemic lupus erythematosus. This disorder is associated with maternal IgG autoantibodies to several ribonucleoproteins that are transplacentally transmitted to the fetus and damage the fetal AV node. The fetal conduction disease is generally clinically evident by the second trimester and is associated with significant fetal mortality and neonatal requirement of cardiac pacing.

The embryonic development of the cardiac septa and conduction system occur together, and clinical disorders have been described, including the Holt-Oram syndrome, an autosomal dominant disorder including upper limb dysplasia and atrial septal defect, often with conduction disturbances in the AV node. Studies of families with a high incidence of congenital heart disease, including ostium secundum atrial septal defect and conduction disorders in the AV node, have identified the gene NKX2-5 on chromosome 5q35 as important in the regulation of septation and in the development and function of the AV node. A familial syndrome of progressive complete heart block has also long been recognized. The gene for this disorder has been mapped to a region on chromosome 19q13. Familial disorders of SA node function have also been described, but specific details of abnormal genetic sites are not available.


Pharmacologic Therapy

Pharmacologic therapy is usually reserved for acute situations. Atropine (0.5 to 2.0 mg intravenously) and isoproterenol (1 to 4 0x0003bcg/min intravenously) are useful in increasing heart rate and decreasing symptoms in patients with sinus bradycardia or AV block localized to the AV node. They have an insignificant effect on lower pacemakers. In patients with neurovascular syncope, beta blockers and disopyramide have been suggested as methods to depress left ventricular function and decrease mechanoreceptor-related reflexes. Mineralocorticoids, ephedrine, and theophylline have also been reported to be of benefit to occasional patients. Unfortunately, no controlled study has shown that any of these pharmacologic modalities works in a predictable fashion in all patients. Further work on delineating different mechanisms in different patient groups may allow us to apply pharmacologic agents more appropriately. Long-term therapy of bradyarrhythmias is best accomplished by pacemakers.


External energy sources can be used to stimulate the heart when disorders in impulse formation and/or transmission lead to symptomatic bradyarrhythmias. Pacer stimuli can be applied to the atria and/or ventricles. Indications for pacemaker insertion are listed in the guidelines summarized in Table 229-4.

Temporary Pacing

This is usually instituted to provide immediate stabilization prior to permanent pacemaker placement or to provide pacemaker support when a bradycardia is precipitated by what is presumed to be a transient event such as ischemia or drug toxicity. Temporary pacing is usually achieved by the transvenous insertion of an electrode catheter with the catheter positioned in the right ventricular apex and attached to an external generator. This procedure is associated with a small risk of cardiac perforation, infection at the insertion site, and thromboembolism; the risk of the latter two complications increases markedly if the pacing wire is left in place for more than 48 h. The development of an entirely external transthoracic cardiac pacing system may preclude the need for transvenous pacing in selected patients. However, occasional failure of ventricular capture and significant discomfort related to the large current required for effective transthoracic ventricular stimulation preclude the uniform use of this approach.

Permanent Pacing

This mode of pacing is instituted for persistent or intermittent symptomatic bradycardia not related to a self-limiting precipitating factor or for documented infranodal second- or third-degree AV block. Permanent pacing leads are usually inserted transvenously through the subclavian or cephalic vein with the leads positioned in the right atrial appendage for atrial pacing and the right ventricular apex for ventricular pacing. The leads are then attached to the pulse generator, which is inserted into a subcutaneous pocket below the clavicle. Epicardial lead placement is used when (1) transvenous access cannot be obtained; (2) the chest is already open, i.e., in the course of a cardiac operation; and (3) adequate endocardial lead placement cannot be achieved. Most pacemaker generators are powered by lithium batteries. The life expectancy of the generator is related to (1) voltage output required for capture, (2) requirement for incessant or intermittent pacing, and (3) number of cardiac chambers paced. Life expectancy of the simple ventricular demand pacemaker can exceed 10 years.

Pacing Code

A code consisting of three to five letters has been developed for describing pacemaker type and function (Table 229-3). The first letter indicates the chamber(s) paced and is designated V for ventricular pacing, A for atrial pacing, or D for dual-chamber (both atrial and ventricular) pacing. The second letter indicates the chamber in which electrical activity is sensed and is also indicated by A, V, or D. An additional designation, O, has been used when pacemaker discharge is not dependent on a sensed electrical activity. The third letter refers to the response to a sensed electric signal. The letter O represents no response to an underlying electric signal, usually related to the absence of associated sensing function; I represents inhibition of pacing function; T represents triggering of pacing function; and D indicates a dual response, i.e., spontaneous atrial and ventricular activity inhibiting atrial and ventricular pacing and atrial activity triggering a ventricular response. Additional fourth and fifth letters of the pacing code have been recommended to indicate whether the pacemaker is programmable and has rate modulation (fourth) and whether special antitachycardia functions are available (i.e., antitachycardia pacing, T, and delivery of high- or low-energy shocks). In the fourth category, M represents multiprogrammability and R represents rate response ("physiologic") pacing. It follows from the described code that the standard VVIR (ventricular demand pacemaker) paces the ventricle, senses the ventricle, is inhibited by sensed spontaneous ventricular activity, and has rate modulation, while the DDDR pulse generator is capable of sensing and pacing both the atria and ventricles and has a dual response to the sensed atrial and ventricular activity as described above (Fig. 229-9). Both pacemakers have rate modulation (R). "Physiologic" pacemakers use sensors (muscular activity, respiratory rate, temperature, O2 saturation, QT interval, etc.) as methods to allow the pacemaker to increase the heart rate in response to physiologic demands, i.e., exercise. These pacemakers are essential when chronotropic incompetence is present and an increase in heart rate is required to enhance physiologic performance. Studies have shown that such "physiologic" pacemakers improve exercise tolerance and relieve symptoms to a greater degree than fixed-rate pacemakers.

Figure 229-9

Figure 229-9: Normally functioning DDD pacemaker. All three panels show a lead II rhythm strip at 50 mm/s. The programmed lower rate is approximately 55 beats per minute. (Top) AV sequential pacing with a paced AV interval of 160 ms is shown for the first two complexes. A VPC occurs and is sensed, resetting the cycle. (Middle) The first beat is AV paced, but spontaneous sinus P waves and APC trigger a ventricular paced complex with a sensed P to QRS of 120 ms. (Bottom) After the first AV paced complex, a paced atrial complex conducts to the ventricle with a PR of 120 ms, inhibiting the ventricular pacemaker.









Table 229-3: The NASPE/BPEG Generic Pacemaker Code











to Sensing

Rate Modulation



O, None

O, None

O, None

O, None

O, None


A, Atrium

A, Atrium

T, Triggered

P, Simple programmable

P, pacing (antitachyarrhythmia)


V, Ventricle

V, Ventricle

I, Inhibited

M, Multiprogrammable

S, Shock


D, Dual (A + V)

D, Dual (A + V)

D, Dual (T + I)

C, Communicating
R, Rate modulation

D, Dual (P + S)

Manufacturer's designation

S, single (A or V)

S, (A or V)





From DP Zipes, in E Braunwald (ed): Heart Disease: A Textbook of Cardiovascular Medicine, 5th ed. Philadelphia, Saunders, 1997.


Selection of the appropriate pacemaker and pacing mode depends on the clinical condition and the type of bradyarrhythmia being treated. The two most common pacing mode selections are DDD and VVI. DDD provides AV sequential pacing, which is ideally suited for the relatively young and active patient who has intact sinus node function or intermittent dysfunction and high-grade persistent or intermittent AV block. The DDD mode will allow for physiologic atrial sensed and ventricular paced rates and improve exercise tolerance. AV synchrony and dual-chamber pacing may also be desirable in patients with borderline hemodynamic reserve who are dependent on atrial contribution to cardiac output and in those patients who develop the pacemaker syndrome (see below) in response to ventricular demand pacing.

Rate-responsive DDD (i.e., DDDR) pacing is indicated when chronotropic incompetence is present in a patient who requires AV synchrony. The DDD pacing mode is contraindicated in chronic atrial fibrillation or flutter, because rapid and irregular ventricular pacing will occur to the upper rate limit. In some cases this will produce a more rapid ventricular rate than the patient's own rate in the absence of a pacemaker. DDD pacemakers must either automatically switch (i.e., mode-switching function) or be reprogrammed to the VVI mode. Almost all such pacemakers are now combined with some form of rate responsiveness so that when the device functions in the VVI mode, it also will respond to physiologic demands (VVIR).

Chronotropic insufficiency (i.e., the inability of the sinus rate to accelerate) is a contraindication for a DDD pacemaker, since such a pacemaker will act as a "fixed-rate" pacemaker at the programmed lower rate. In these situations, a rate-adaptive or "physiologic" pacemaker is indicated (VVIR or DDDR). In patients with impaired sinus node function or chronic atrial fibrillation, a sensor-driven, rate-adaptive pacemaker must be implanted. As mentioned earlier, these pacemakers automatically adjust ventricular pacing rates to a sensed indicator of exertion. The DDD pacing mode may also be contraindicated in patients with intermittent or persistent ventriculoatrial conduction, who may develop pacemaker-mediated tachycardia (see below).

Programmability of Pacemakers

This allows for modification of pacing function after implantation and for adaptation to changes in clinical needs. Pacemaker programming is accomplished by activation of the programming head positioned over the implanted pulse generator after making the desired changes in programmable parameters (Table 229-3). A radio frequency system is routinely used to communicate the program to the pacemaker. A high degree of sophistication is required to recognize the presence and causes of pacemaker malfunction and their treatment.


Adverse effects of permanent pacing are usually associated with failure or malfunction of the pacing system. These problems are usually secondary to over- or undersensing, output failure, and/or lead fracture or displacement. Two other problems may occur. The pacemaker syndrome consists of fatigue, dizziness, syncope, and distressing pulsations in the neck and chest and can be associated with adverse hemodynamic effects. The pathophysiologic contributors to the pacemaker syndrome include (1) loss of atrial contribution to ventricular systole; (2) vasodepressor reflex initiated by cannon a waves, which are caused by atrial contractions against a closed tricuspid valve and observed in the jugular venous pulse (Chap. 225); and (3) systemic and pulmonary venous regurgitation due to atrial contraction against a closed AV valve. The symptoms associated with the pacemaker syndrome can be prevented by maintaining AV synchrony by dual-chamber pacing or, in the case of a ventricular demand pacemaker, by programming an escape rate 15 to 20 beats per minute below that of the paced rate (i.e., hysteresis). As a result of this programming, sinus activity and thus atrial contraction will be less likely to occur at the same time as ventricular pacing and ventricular contraction. The second major problem peculiar to dual-chamber pacemakers is the development of pacemaker-mediated tachycardia. In this instance, retrograde depolarization of the atria, resulting from a premature ventricular depolarization or a paced ventricular complex, is sensed and leads to subsequent triggering of ventricular pacing. This, in turn, can result in repetition of the phenomenon of ventriculoatrial conduction with the development of an endless-loop, pacemaker-mediated tachycardia. It may be corrected by reprogramming the atrial refractory period.



The Tachyarrhythmias

Mechanisms of Tachyarrhythmias

Tachyarrhythmias may be divided into disorders of impulse propagation and disorders of impulse formation.


Disorders of impulse propagation (reentry) are generally considered to be the most common mechanism of sustained paroxysmal tachyarrhythmia. The requirements for initiating reentry include (1) electrophysiologic inhomogeneity (i.e., differences in conduction and/or refractoriness) in two or more regions of the heart connected with each other to form a potentially closed loop; (2) unidirectional block in one pathway; (3) slow conduction over an alternative pathway, allowing time for the initially blocked pathway to recover excitability; and (4) reexcitation of the initially blocked pathway to complete a loop of activation (Fig. 230-1). Repetitive circulation of the impulse over this loop can produce a sustained tachyarrhythmia. While anatomic obstacles may underlie reentry and provide an inexcitable center around which the impulse can circulate, they are not essential. Reentrant arrhythmias can be reproducibly initiated and terminated by premature complexes and rapid stimulation. The response of these arrhythmias to stimulation can help distinguish them from arrhythmias caused by triggered activity.

Figure 230-1

Figure 230-1: Schema of reentry. Y branching of the Purkinje system to ventricular muscle is shown in panels A through C. The right limb (gray area) of the Purkinje system has a longer refractory period than the left. A. During a slow stimulated rate (S1), conduction proceeds normally over both Purkinje fibers, resulting in collision in the ventricular muscle. B. An early premature stimulus (S2) results in block in the Purkinje fiber on the right and slow conduction down the left. The impulse conducts through the ventricle and attempts to reenter the initial site of block but fails because this site has not fully recovered excitability. C. An earlier stimulus (S3) again results in block on the left. The resulting slower propagation down the left fiber provides enough time for the initial site of block to recur and allows the impulse to conduct through it to produce a reentrant circuit.

Enhanced Automaticity

Disorders of impulse formation can be subdivided into tachyarrhythmias caused by enhanced automaticity and those caused by triggered activity. In addition to the sinus node, automatic pacemaker activity can be observed in specialized atrial fibers, fibers of the atrioventricular (AV) junction, and Purkinje fibers (Chap. 229). Myocardial cells do not normally possess pacemaker activity. Enhancement of normal automaticity in latent pacemaker fibers or the development of abnormal automaticity due to partial depolarization of the resting membrane occurs as a consequence of a variety of pathophysiologic states, which include (1) increased endogenous or exogenous catecholamines, (2) electrolyte disturbances (e.g., hyperkalemia), (3) hypoxia or ischemia, (4) mechanical effects (e.g., stretch), and (5) drugs (e.g., digitalis). Tachycardia caused by automaticity cannot be started or stopped by pacing.

Triggered Activity

Rhythms due to triggered activity are events that do not occur spontaneously but require a change in cardiac electrical frequency as a trigger. Triggered activity may be caused by early afterdepolarizations, which occur during phases 2 and 3 of the action potential, or delayed afterdepolarizations, which occur following completion of phase 3 of the action potential (Fig. 229-2). Triggered activity has been observed in atrial, ventricular, and His-Purkinje tissue under conditions such as increased local catecholamine concentration, hyperkalemia, hypercalcemia, and digitalis intoxication (delayed afterdepolarizations) or during bradycardia, hypokalemia, or other situations prolonging action potential duration (early afterdepolarizations). All of these conditions produce an accumulation of intracellular calcium. With increasing amplitude of the afterdepolarizations, threshold can be reached and repetitive activity produced. The exact role of triggered activity in spontaneous clinical arrhythmias is unknown, but tachyarrhythmias associated with digitalis intoxication, accelerated idioventricular rhythm in acute infarction and/or reperfusion, and exercise-induced ventricular tachycardia (VT) are believed to be caused by triggered activity due to delayed afterdepolarizations. Torsade de pointes ("twisting of the points"; polymorphic VT associated with long QT intervals) may be caused by triggered activity due to early afterdepolarizations, although reentry may also be operative.

The use of electrophysiologic studies, i.e., intracardiac recordings and programmed stimulation, has greatly expanded the understanding of the mechanisms of tachyarrhythmias. In addition to helping diagnose arrhythmias, these techniques may be of value in determining the most appropriate types of therapy because they allow the physician to observe the hemodynamic and symptomatic consequences of the arrhythmia in the presence or absence of therapy. Electrophysiologic studies of tachycardias require the positioning of multiple electrode catheters at critical areas within the heart. These electrodes must be capable of both stimulating and recording from multiple sites in the atria and/or ventricles.

Premature Complexes

Atrial Premature Complexes (APC)

APCs can be found on 24-h Holter monitoring in over 60% of normal adults. APCs are usually asymptomatic and benign, although at times they may be associated with palpitations. In susceptible patients, they can initiate paroxysmal supraventricular tachycardias. APCs may originate from any location in either atrium, and they are recognized on the electrocardiogram (ECG) as early P waves with a morphology that differs from the sinus P wave (Fig. 230-2). While APCs usually conduct to the ventricles when they occur late in the cardiac cycle, early APCs may reach the AV conduction system while it is still in its relative refractory period, resulting in a conduction delay manifested by prolonged PR interval following the premature P wave (Fig. 230-2). Very early APCs may even block in the AV node if this structure is encountered during its effective refractory period. APCs, whether conducted or not, are usually followed by a pause before a return to sinus activity. Most commonly, an APC enters and resets the sinus node, so the sum of the pre- and postextrasystolic PP intervals is less than the sum of two sinus PP intervals (Fig. 230-2). In this case, the pause is said to be less than fully compensatory. The QRS complex following most APCs is normal, although early APCs may be followed by aberrantly conducted QRS complexes due to the premature complex falling within the relative refractory period of the His-Purkinje system.

Figure 230-2

Figure 230-2: ECG lead II. Sinus rhythm with one atrial premature complex (arrow). Note the difference in P-wave configuration between sinus and the premature atrial complexes. In addition, note that the PR interval of the premature complex is prolonged, due to slowed conduction of the premature impulse through the AV conduction system.

Since most APCs are asymptomatic, treatment is not required. When they cause palpitations or trigger paroxysmal supraventricular tachycardias (see below), treatment may be useful. Factors that precipitate APCs, such as alcohol, tobacco, or adrenergic stimulants, should be identified and eliminated; in their absence, mild sedation or the use of a beta blocker may be tried.

AV Junctional Complexes

The site of origin of these complexes is thought to be in the bundle of His, since the normal AV node in vivo possesses no automaticity. AV junctional complexes are less common than either atrial or ventricular premature complexes and are more often associated with cardiac disease or digitalis intoxication. Junctional premature impulses can conduct both antegradely to the ventricles and retrogradely to the atrium and, on rare occasions, may fail to conduct in either direction. Premature AV junctional complexes can be recognized by normal-appearing QRS complexes that are not preceded by a P wave. Retrograde P waves (inverted in leads II, III, and aVF) may be observed after the QRS complex.

While often asymptomatic, junctional premature complexes may be associated with palpitations and cause cannon a waves, which may result in distressing pulsations in the neck. When symptomatic, they should be treated like APCs.


These are among the most common arrhythmias and occur in patients with and without heart disease. Of adult males, 0x00226560% will exhibit VPCs during a 24-h Holter monitoring. In patients without heart disease, VPCs have not been shown to be associated with any increased incidence in mortality or morbidity. VPCs may occur in up to 80% of patients with previous myocardial infarction, and in this setting, if frequent (>10 per hour) and/or complex (occurring in couplets), they have been associated with increased mortality. However, cardiac mortality in such patients usually occurs in association with significantly impaired ventricular function. While frequent and complex ventricular ectopy is an independent risk factor, it is not as strong a risk factor as is impaired ventricular function. Moreover, even though ventricular tachycardia and/or fibrillation may be the basis for the sudden death in these patients, this does not a priori establish a cause-and-effect relation between spontaneous ectopy and life-threatening ventricular tachycardia or fibrillation. Very early cycle (R-on-T) VPCs have been stated by some to increase the risk of sudden death. Although this has been observed during acute ischemia and in the setting of QT prolongation, frequently, VT or fibrillation is precipitated by VPCs that occur after the T wave of the prior beat.

VPCs are recognized by wide (usually >0.14 s), bizarre QRS complexes that are not preceded by P waves (Fig. 230-3A). They may bear a relatively fixed relationship to the preceding sinus complex (i.e., fixed coupled VPCs). When fixed coupling is not present and the interval between VPCs has a common denominator, ventricular parasystole is said to be present (Fig. 230-4). Under these circumstances, the VPCs are a manifestation of abnormal automaticity of a protected ventricular focus. Because this focus is not penetrated by sinus impulses, it is not reset by them, and the interectopic intervals remain relatively fixed (0x002264120 ms variation of mean RR cycle length).

Figure 230-3

Figure 230-3: A. Single ventricular ectopy. During sinus rhythm, five premature ventricular complexes (filled circles) occur. Note that the QRS configuration is bizarre and different from that during sinus rhythm. The premature ventricular complexes are not preceded by P waves. The QRS widths of the premature complexes are 120-160 ms and multiple morphologies are present. The pause following the premature complexes is fully compensatory, the sinus beat after the premature complex occurring on time. B. Nonsustained ventricular tachycardia (VT). Following two sinus beats, an atrial premature contraction with long PR interval initiates an 8-beat run of wide complex tachycardia. Atrial activity can be seen following the fourth and seventh beats. The greater number of QRS complexes compared with P waves confirms the diagnosis of VT.

Figure 230-4

Figure 230-4: Ventricular parasystole. At varying sinus cycle lengths during exercise, interectopic intervals remain constant at 1620 to 1640 ms. However, the coupling intervals between sinus and ectopic complexes vary between 510 and 310 ms.

VPCs may occur singly; in patterns of bigeminy, in which every sinus beat is followed by a VPC; in trigeminy, in which two sinus beats are followed by a VPC; in quadrigeminy, etc. Two successive VPCs are termed pairs or couplets, while three or more consecutive VPCs are termed ventricular tachycardia when the rate exceeds 100 beats per minute (Fig. 230-3B). VPCs may have similar morphologies (monomorphic, or uniform) or different morphologies (polymorphic, or multiformed).

Most commonly, VPCs are not conducted retrogradely to the atrium to reset the sinoatrial node. Thus they produce a fully compensatory pause; i.e., the interval between conducted sinus beats that bracket the VPC equals two basic RR intervals. Ventricular impulses may also manifest retrograde conduction to the atrium and cause inverted P waves in leads II, III, and aVF. This retrograde atrial activation can reset the sinus node, and the pause that results may therefore be less than compensatory. In many instances, the VPC will not be associated with retrograde ventriculoatrial (VA) conduction but may block retrogradely in the AV node. This renders the AV node refractory to the subsequent sinus beat and causes slowed conduction (i.e., prolonged PR interval) or block of the next sinus P wave. This prolonged PR interval is said to be a manifestation of concealed retrograde conduction of the ventricular impulse into the AV node. A VPC that does not produce any manifestation of retrograde concealed conduction and fails to influence the oncoming sinus impulse is termed an interpolated VPC.

VPCs can cause palpitations or neck pulsations secondary to either the occurrence of cannon a waves or the increased force of contraction due to postextrasystolic potentiation of ventricular contractility. Patients with frequent VPCs or bigeminy may rarely develop syncope or lightheadedness because the VPCs do not result in an adequate stroke volume and the cardiac output is reduced by the "halving" of the heart rate.


In the absence of cardiac disease, isolated asymptomatic VPCs, regardless of configuration and frequency, need no treatment. When arrhythmias are symptomatic, the symptoms should first be addressed by either allaying the patient's anxiety or, if this is not successful, reducing the frequency of the VPCs with antiarrhythmic agents. 0x0003b2-Adrenergic blockers may be successful in managing VPCs that occur primarily in the daytime or under stressful situations and in specific settings such as mitral valve prolapse and thyrotoxicosis. While other antiarrhythmic agents may be tried should this be unsuccessful, their risk may outweigh any benefits. In patients with cardiac disease, frequent VPCs are associated with an increased risk of sudden and nonsudden cardiac death, and many physicians have attempted to eliminate or reduce the frequency of these VPCs in an attempt to reduce this risk. However, the cause-and-effect relationship of the VPCs to fatal events has never been established. The ability of pharmacologic antiarrhythmic therapy guided by continuous ECG monitoring to reduce the risk of sudden death in postmyocardial infarction patients with frequent (0x0022656 per minute) VPCs was tested by the Cardiac Arrhythmia Suppression Trial (CAST). This study compared mortality in patients whose ectopy was suppressed by one of three agents (encainide, flecainide, or moricizine) and then randomized to treat with either the "effective" drug or placebo. After a mean follow-up of 2 years, the study was discontinued because both the sudden death and overall mortality rate were significantly increased in patients receiving antiarrhythmic agents. This study has shown that in patients having the characteristics of the study population, abolition of ventricular ectopy by pharmacologic therapy cannot be used as a marker to define reduction of the risk of sudden death after myocardial infarction and, in fact, may increase mortality. Recent studies have evaluated the use of electrophysiologic testing and implantable cardioverter/defibrillator (ICD) placement in the management of patients at high risk for sudden death (i.e., those with left ventricular ejection fractions <40% and nonsustained VT). These studies have found that induction of a sustained ventricular arrhythmia through programmed electrical stimulation selects a group of these patients whose prognosis is improved with implantation of a defibrillator. These studies have found no correlation between the rate, morphology, or duration of nonsustained episodes of VT and the likelihood of having a sustained ventricular arrhythmia.

Antiarrhythmic agents can also produce the lethal arrhythmias that they are given to prevent (proarrhythmic effects). Thus therapy directed toward VPCs in the setting of chronic cardiac disease may result in an inappropriate and costly use of agents without proven efficacy and with potential side effects in many patients. The high incidence of side effects and the frequent exacerbation of arrhythmias caused by all antiarrhythmic drugs make it mandatory to monitor patients being treated with such agents.

In acute myocardial infarction, the greatest incidence of primary ventricular fibrillation occurs within the first 24 h (Chap. 243). Temporary prophylactic antiarrhythmic therapy with lidocaine or procainamide was formerly recommended for all patients with acute infarction, regardless of the presence or degree of spontaneous ectopy. However, failure to improve overall survival and drug toxicity have led most physicians to recommend prophylactic antiarrhythmic therapy only to young patients with complicated infarctions, where a favorable risk-benefit ratio may be obtained. Other studies have shown that intravenous beta blockers may also reduce the incidence of primary ventricular fibrillation.


Tachycardias refer to arrhythmias with three or more complexes at rates exceeding 100 beats per minute; they occur more often in structurally diseased than in normal hearts. Those paroxysmal tachycardias that are initiated by APCs or VPCs are considered to be due to reentry, except some of the digitalis-induced tachyarrhythmias, which are probably due to triggered activity (see below).

If the patient is hemodynamically stable, an attempt should be made to determine the mechanism and origin of the tachycardia, since this will usually lead to an appropriate therapeutic decision. Information to be obtained from the ECG includes (1) the presence, frequency, morphology, and regularity of P waves and QRS complexes; (2) the relationship between atrial and ventricular activity; (3) a comparison of the QRS morphology during sinus rhythm and during the tachycardia; and (4) the response to carotid sinus massage or other vagal maneuvers. It is useful first to compare a 12-lead ECG during the tachycardia with one recorded during sinus rhythm. One can also utilize the electrodes situated at the end of a flexible pacing catheter inserted into the esophagus behind the left atrium to record atrial activity.

Observation of the jugular venous pulse can provide clues to the presence of atrial activity and its relationship to ventricular ectopy. Intermittent cannon a waves suggest AV dissociation, while persistent cannon a waves suggest 1:1 VA conduction. Flutter waves may be seen or no atrial activity may be apparent, as in the presence of atrial flutter and fibrillation, respectively. The arterial pulse may also manifest AV dissociation or atrial fibrillation by demonstrating variations in amplitude. A first heart sound of variable intensity during a regular rhythm also suggests AV dissociation or atrial fibrillation (AF).

Carotid sinus pressure should only be applied while the patient is electrocardiographically monitored with resuscitative equipment available to manage the rare episode of asystole and/or ventricular fibrillation associated with this procedure. Carotid sinus massage should not be performed in patients with carotid arterial bruits. The patient should be positioned flat with the neck extended. Massage of one carotid bulb at a time should be performed by applying firm pressure just underneath the angle of the jaw for up to 5 s. Alternative vagomimetic maneuvers include the Valsalva maneuver, immersion of the face in cold water, and administration of 5 to 10 mg edrophonium.

Sinus Tachycardia

In the adult, sinus tachycardia is said to be present when the heart rate exceeds 100 beats per minute (bpm): sinus tachycardia rarely exceeds 200 bpm and is not a primary arrhythmia; instead, it represents a physiologic response to a variety of stresses, such as fever, volume depletion, anxiety, exercise, thyrotoxicosis, hypoxemia, hypotension, or congestive heart failure. Sinus tachycardia has a gradual onset and offset. The ECG demonstrates P waves with sinus contour preceding each QRS complex. Carotid sinus pressure usually produces modest slowing with a gradual return to the previous rate upon cessation. This contrasts with the response of paroxysmal supraventricular tachycardias, which may slow slightly and terminate abruptly.


Sinus tachycardia should not be treated as a primary arrhythmia, since it is almost always a physiologic response to a demand placed on the heart. As such, the therapy should be directed to the primary disorder. This may involve institution of digitalis and/or diuretics for heart failure and oxygen for hypoxemia, treatment of thyrotoxicosis, volume repletion, aspirin for fever, or tranquilizers for emotional upset.

Atrial Fibrillation

AF is a common arrhythmia that may occur in paroxysmal and persistent forms. It may be seen in normal subjects, particularly during emotional stress or following surgery, exercise, acute alcoholic intoxication, or a prominent surge of vagal tone (i.e., vasovagal response). It may also occur in patients with heart or lung disease who develop acute hypoxia, hypercapnia, or metabolic or hemodynamic derangements. Persistent AF usually occurs in patients with cardiovascular disease, most commonly rheumatic heart disease, nonrheumatic mitral valve disease, hypertensive cardiovascular disease, chronic lung disease, atrial septal defect, and a variety of miscellaneous cardiac abnormalities. AF may be the presenting finding in thyrotoxicosis. So-called lone AF, which occurs in patients without underlying heart disease, often represents the tachycardia phase of the tachycardia-bradycardia syndrome.

The morbidity associated with AF is related to (1) excessive ventricular rate, which in turn may lead to hypotension, pulmonary congestion, or angina pectoris in susceptible individuals; (2) the pause following cessation of AF, which can cause syncope; (3) systemic embolization, which occurs most commonly in patients with rheumatic heart disease (Table 230-1); (4) loss of the contribution of atrial contraction to cardiac output, which may cause fatigue; and (5) anxiety secondary to palpitations. In patients with severe cardiac dysfunction, particularly those with hypertrophied, noncompliant ventricles, the combination of the loss of the atrial contribution to ventricular filling and the abbreviated filling period due to the rapid ventricular rate in AF can produce marked hemodynamic instability, resulting in hypotension, syncope, or heart failure. In patients with mitral stenosis, in whom ventricular filling time is critical, development of AF with a rapid ventricular rate may precipitate pulmonary edema (Chap. 236). AF may also cause a cardiomyopathy related to persistent rapid rates (so-called tachycardia-induced cardiomyopathy).

Table 230-1: Factors Associated with High Risk of Stroke in Patients with Atrial Fibrillation

1. Age >65

2. Hypertension

3. Rheumatic heart disease

4. Prior stroke or TIA

5. Diabetes mellitus

6. Congestive heart failure

7. Left atrial dimension >5 cm

NOTE: TIA, transient ischemic attack.











AF is characterized by disorganized atrial activity without discrete P waves on the surface ECG (Fig. 230-5A). Atrial activation is manifested by an undulating baseline or by more sharply inscribed atrial deflections of varying amplitude and frequency ranging from 350 to 600 beats per minute. The ventricular response is irregularly irregular. This results from the large number of atrial impulses that penetrate the AV node, making it partially refractory to subsequent impulses. This effect of nonconducted atrial impulses to influence the response to subsequent atrial impulses is termed concealed conduction. As a result, the ventricular response is relatively slow, considering the actual atrial rate. AF may convert to atrial flutter, especially in response to antiarrhythmic drugs like quinidine or flecainide. If AF converts to atrial flutter, which has a slower atrial rate, the effect of concealed conduction may be diminished, and a paradoxic increase in the ventricular response may occur. The main factor determining the rate of the ventricular response is the functional refractory period of the AV node or the most rapid paced rate at which 1:1 conduction through the AV node can be observed.

Figure 230-5

Figure 230-5: Atrial fibrillation and atrial flutter. A. Lead V1 demonstrating an irregular ventricular rhythm associated with poorly defined irregular atrial activity consistent with atrial fibrillation. B. Lead II demonstrates atrial flutter, identified by the regular "sawtooth-like" activity (arrows) at an atrial rate of 300 bpm with 2:1 ventricular response.

If, in the presence of AF, the ventricular rhythm becomes regular and slow (e.g., 30 to 60 bpm), complete heart block is suggested, and if the ventricular rhythm is regular and rapid (e.g., 0x002265100 bpm), a tachycardia arising in the AV junction or ventricle should be suspected. Digitalis intoxication is a common cause of both phenomena.

Patients with AF exhibit a loss of a waves in the jugular venous pulse and variable pulse pressures in the carotid arterial pulse. The first heart sound usually varies in intensity. On echocardiography, the left atrium is frequently enlarged, and in patients in whom the left atrial diameter exceeds 4.5 cm, it may be difficult to convert AF to sinus rhythm and/or maintain the latter, despite therapy.


In acute AF, a precipitating factor such as fever, pneumonia, alcoholic intoxication, thyrotoxicosis, pulmonary emboli, congestive heart failure, or pericarditis should be sought. When such a factor is present, therapy should be directed toward the primary abnormality. If the patient's clinical status is severely compromised, electrical cardioversion is the treatment of choice. In the absence of severe cardiovascular compromise, slowing of ventricular rate becomes the initial therapeutic goal. This may be most rapidly accomplished with 0x0003b2-adrenergic blockers and/or calcium channel antagonists. Both prolong the refractory period of the AV node and slow conduction within it. When catecholamine levels or sympathetic nervous system tone is likely to be elevated, beta blockers may be favored. Digitalis preparations are less effective, take longer to act, and are associated with more toxicity. Conversion to sinus rhythm may then be attempted. Prior to cardioversion, precautions must be taken to reduce the risk of systemic embolization. Patients should be anticoagulated to an INR of at least 1.8 for the prior 3 consecutive weeks or have had AF for <48 h. Alternatively, for those patients with AF for >48 h who are not anticoagulated, a transesophageal echocardiogram can exclude the presence of left atrial thrombus and allow safe cardioversion. Following cardioversion, anticoagulation must be maintained for at least 4 weeks until atrial mechanical function returns to normal.

Antiarrhythmic medications in either oral or intravenous form may be employed but are only modestly effective in restoring sinus rhythm. When antiarrhythmic agents such as the quinidine-like drugs (type 1A) or the flecainide-like agents (type 1C) are used (Table 230-2), it is important to increase AV node refractoriness prior to administering such drugs because their vagolytic effect and/or their ability to convert AF to atrial flutter may reduce the concealed conduction in the AV node and lead to an excessively rapid ventricular response. 0x0003b2-Adrenergic blockers are especially useful in this regard.

Table 230-2: Classification of Antiarrhythmic Drugs

Class I

Drugs that reduce maximal velocity of phase of depolarization (Vmax) due to block of inward Na+ current in tissue with fast response action potentials


A 0x002193Vmax at all heart rates and 0x002191action potential duration, e.g., quinidine, procainamide, disopyramide


B Little effect at slow rates on Vmax in normal tissue; 0x002193Vmax in partially depolarized cells with fast response action potentials


Effects increased at faster rates


No change or 0x002193in action potential duration, e.g., lidocaine, phenytoin, tocainide, mexiletine


C 0x002193Vmax at normal rates in normal tissue


Minimal effect on action potential duration, e.g., flecainide, propafenone, moricizine

Class II

Antisympathetic agents, e.g., propranolol and other 0x0003b2-adrenergic blockers: 0x002193SA nodal automaticity, 0x002191AV nodal refractoriness, and 0x002193AV nodal conduction velocity

Class III

Agents that prolong action potential duration in tissue with fast-response action potentials, e.g., bretylium, amiodarone, sotalol

Class IV

Calcium (slow) channel blocking agents: 0x002193conduction velocity and 0x002191refractoriness in tissue with slow-response action potentials, e.g., verapamil, diltiazem

Drugs that cannot be classified by this schema:





NOTE: SA, sinoatrial; AV, atrioventricular.

Direct-current electrical cardioversion is a highly effective method to restore sinus rhythm, either as a primary method of therapy or following the failure of antiarrhythmic medications. Electrical cardioversion is accomplished through the delivery of at least 200 W s of energy between electrodes placed to the right of the sternum and the cardiac apex or to the left of the scapula. If external cardioversion is unsuccessful, internal cardioversion with energy delivered between two catheters inside the heart or one inside and a patch outside the heart may prove effective.

It is unlikely that patients with chronic AF will convert to and remain in sinus rhythm in the presence of long-standing rheumatic heart disease and/or when the atria are markedly enlarged. It is also unlikely for patients with recurrent, paroxysmal lone AF to be converted to and maintained in sinus rhythm.

The goal of therapy in patients in whom AF cannot be converted to sinus rhythm is control of the ventricular response. This can usually be accomplished by digitalis, beta blockers, or calcium channel blockers singly or in combination. In occasional patients, the ventricular response cannot be controlled by pharmacologic therapy alone. In such patients, the creation of complete heart block by radiofrequency catheter ablation of the AV junction followed by permanent pacemaker implantation is appropriate. Surgical or direct-current catheter ablation of the AV junction is rarely required to achieve AV block.

If sinus rhythm is restored electrically or pharmacologically, quinidine or related agents as well as the class IC agents (e.g., flecainide), sotalol, or amiodarone may be used to prevent recurrence. In patients in whom cardioversion is unsuccessful or in whom AF has recurred or is likely to recur despite antiarrhythmic therapy, it is probably wisest to allow the patient to remain in AF and to control the ventricular response with calcium antagonists, 0x0003b2-adrenergic blockers, or digitalis glycosides. Since such patients are always at risk of systemic embolization, particularly in the presence of organic heart disease, chronic anticoagulation must be considered (Table 230-3). Chronic anticoagulation is particularly important in the elderly, where the attributable risk of AF for stroke approaches 30%. Several studies have now demonstrated conclusively that the incidence of embolization in patients with AF not associated with valvular heart disease is reduced by chronic anticoagulation with warfarin-like agents. Aspirin also may be effective for this purpose in patients who are not at high risk for stroke. Although anticoagulation may be associated with hemorrhagic complications, the risk is largely associated with INRs above the recommended range of 1.8 to 3.0. Recommendations for the selection of antiarrhythmic medications to prevent the recurrence of AF are shown in Fig. 230-6.

Figure 230-6

Figure 230-6: Recommendations for the selection of antiarrhythmic medications to prevent the recurrence of atrial fibrillation. See Tables 230-2 and 230-4 for definition of types IA and IC drugs. An atrioventricular nodal blocking agent (i.e., beta blocker, calcium channel blocker, or digoxin) should be added to all type IC and IA agents as well as to dofetilide. LVEF, left ventricular ejection fraction; CHF, congestive heart failure; CAD, coronary artery disease; EF, ejection fraction.

Table 230-3: Recommendations for Long-Term Anticoagulation in Patients with Chronic Atrial Fibrillation

Age, years

Risk Factorsa




Warfarin [target INR 2.5 (range 2.0-3.0)]



Aspirin or warfarin
Warfarin [target INR 2.5 (range 2.0-3.0)]


All patients

Warfarin [target INR 2.5 (range 2.0-3.0)]

aRisk factors are prior transient ischemic attack, systemic embolus or stroke, hypertension, poor left ventricular function, rheumatic mitral valve disease, prosthetic heart valve.

From A Laupacis et al: Chest 114:579S, 1998.


Ablation therapy for cure of AF is an active area of investigation. This therapy is particularly attractive for the small subset of patients who have a focal atrial tachycardia that degenerates into AF. These automatic foci are often located in the pulmonary veins, and a targeted ablation in these areas may be curative. While ablation of these foci is possible, the procedure can result in pulmonary vein stenosis, pulmonary hypertension, and stroke. Further technologic advances are necessary before this procedure can be more widely and safely performed. A more morbid approach involves making multiple lesions in the right and left atria (MAZE procedure) to compartmentalize the electrical conductance of these chambers and disallow the propagation of fibrillatory waves. The morbidity, mortality, and success rate of such catheter-based procedures renders them experimental at this time.

Atrial Flutter

This arrhythmia occurs most often in patients with organic heart disease. Flutter may be paroxysmal, in which case there is usually a precipitating factor, such as pericarditis or acute respiratory failure, or it may be persistent. Atrial flutter (as well as AF) is very common during the first week following open-heart surgery. Atrial flutter is usually less long-lived than is AF, although on occasion it may persist for months to years. Most commonly, if it lasts for more than a week, atrial flutter will convert to AF. Systemic embolization is less common in atrial flutter than in AF.

Atrial flutter is characterized by an atrial rate between 250 and 350 bpm. Typically, the ventricular rate is half the atrial rate, i.e., approximately 150 bpm. If the atrial rate is slowed to <220 beats per minute by antiarrhythmic agents such as quinidine, which also possess vagolytic properties, the ventricular rate may rise suddenly because of the development of 1:1 AV conduction. Classically, flutter waves are seen as regular sawtooth-like atrial activity, most prominent in the inferior leads (Fig. 230-5B). When the ventricular response is regular and not a simple fraction of the atrial rate, complete AV block is present, which may be a manifestation of digitalis toxicity. Activation mapping suggests that atrial flutter is a form of atrial reentry localized to the right atrium.


The most effective treatment of atrial flutter is direct-current cardioversion, which can be accomplished at low energy (25 to 50 W s) under mild sedation. Higher energies (100 to 200 W s) are often used because they are less likely to cause AF, which not infrequently occurs following lower energy delivery. Although atrial flutter is associated with a slightly lower risk of embolization than AF, the same precautions should be followed in regard to anticoagulation as are used with AF. In patients who develop atrial flutter following open-heart surgery or recurrent flutter in the setting of acute myocardial infarction, particularly if they are being treated with digitalis, atrial pacing (using temporary pacing wires implanted at the time of operation or a pacing lead inserted into the atrium pervenously) at rates of 115 to 130% of the atrial flutter rate can usually convert the atrial flutter to sinus rhythm. Atrial pacing may also result in the conversion of atrial flutter to AF, which allows for easier control of the ventricular response. If immediate conversion of atrial flutter is not mandated by the patient's clinical status, the ventricular response should first be slowed by blocking the AV node with a beta blocker, calcium antagonist, or digitalis. Digitalis is the least effective and occasionally converts atrial flutter into AF. Once AV nodal conduction is slowed with any of these drugs, an attempt to convert flutter to sinus rhythm using a class I (A or C) agent or amiodarone should be made. Increasing doses of the drug selected are administered until the rhythm converts or side effects occur. Ibutilide is a new antiarrhythmic agent that is administered intravenously and appears to be particularly effective for conversion of atrial flutter to sinus rhythm.

Quinidine, other Class IA drugs, flecainide, propafenone, sotalol, and amiodarone (Table 230-4) may be useful in preventing recurrences of atrial flutter. Radiofrequency ablation is a highly effective treatment for patients with the most typical forms of atrial flutter, which are due to reentry around the tricuspid valve in a counterclockwise or clockwise fashion. The coronary sinus and inferior vena cava cause the wavefront of activation to pass between them and the tricuspid valve. Ablation of the narrowed isthmus using radiofrequency energy can cure flutter in >85% of cases.

Table 230-4: Drugs Used to Treat Cardiac Tachyarrhythmias


Mode of Administration

t1/2 (oral), h

Route of Metabolism

Clinical Effects and/or Indications for Use


IV, 0.25-1.5 mg
Oral, 0.75-1.5 mg loading dose over 12-24 h
Maintenance, 0.23-0.50 mg/kg



Slowing of ventricular rate during AF, flutter, and other atrial tachycardias in the absence of preexcitation; slowing, termination, and/or prevention of SVT due to AV nodal reentry and AV reentry utilizing bypass tracts; may terminate or prevent intraatrial reentrant tachycardias; ineffective in prevention of automatic atrial tachycardias


IV bolus, 6-12 mg



Acute termination of regular reentrant SVT involving the AV node

Quinidine (class IA)

Oral, 200-400 mg q6h


Hepatic, 80%
Renal, 20%

Atrial and ventricular tachyarrhythmias; all types of SVT; control of ventricular rate in patients with preexcitation and AF and flutter

Procainamide (class IA)

IV, 40-50 mg/min to total of 10-20 mg/kg.
Oral, 500-1000 mg q6h (sustained-release forms)


Hepatic, 50%
Renal, 50%

Same as quinidine

Disopyramide (class IA)

Oral, 100-300 mg q6h


Hepatic, 50%
Renal, 50%

Same as quinidine

Lidocaine (class IB)

IV, 20-50 mg/min to total of 5 mg/kg loading dose, followed by 1-4 mg/kg



VT and VF, especially during acute ischemia and myocardial infarction

Phenytoin (class IB)

IV, 20 mg/kg to total dose of 1000 mg
Oral, 1000-mg loading dose over 24 h
Maintenance, 100-400 mg/d



Tachyarrhythmias induced by digitalis; occasionally effective for ventricular tachyarrhythmias not induced by digitalis alone or in combination with other antiarrhythmic agents; polymorphic VT associated with increased QT interval

Mexiletine (class IB)

Oral, 100-300 mg q6-8h



Ventricular tachyarrhythmias; secondary agent in combination with other class 1 medication

Flecainide (class IC)

Oral, begin at 50-100 mg bid, increase by 0x00226450 mg in 4-day intervals to a maximum of mg daily


Hepatic, 75%
Renal, 25%

Supraventricular tachyarrhythmias including atrial fibrillation and flutter; also ventricular arrhythmias refractory to other medications or radiofrequency ablation

Propafenone (class IC)

Oral, 150-300 mg q8h



Same as flecainide

Moricizine (class IC)

Oral, 200-400 mg q8h



Same as flecainide

Beta blockers (class II) e.g., metoprolol

IV, load with 5-10 mg q5min for 3 doses, then 3 mg q6h
Oral, 25-100 mg bid



Slowing of ventricular rate during AF, atrial flutter, and other atrial tachyarrhythmias in the absence of preexcitation; SVT due to AV nodal reentry; reentry utilizing bypass tracts; arrhythmias (e.g., VT) induced by exercise or occurring in the presence of hyperthyroidism; polymorphic VT associated with congenital long QT syndrome

Bretylium (class III)

IV, 1-2 mg/kg per min to total load, 5-10 mg/kg
Maintenance, 0.5-2 mg/kg



Refractory VT and VF, especially due to acute ischemia

Amiodarone (class III)

IV, 5-10 mg/kg load over 20 min, then 1 g/24 h



Sustained VT and VF


Oral, load 800-1600 mg/d for 1 week, then 400-600 mg/d for 3 weeks, then 200-400 mg/d thereafter



AF and atrial flutter, other types of SVT, VT, VF

Sotalol (class III)

Oral, 80-320 mg q12h


Renal, 90%
Hepatic, 10%

Atrial and ventricular tachyarrhythmias

Ibutilide (class III)

IV, <60 kg: 0.01 mg/kg over 10 min
IV, 0x00226560 kg: 1 mg over 10 min, repeat after 10 min if no effect



AF, atrial flutter, and other SVTs including preexcitation tachycardias


125-250 mg PO bid



AF, atrial flutter, and other SVTs

Calcium channel blockers (class IV) e.g., verapamil

IV, 2.5-10 mg over 1-2 min to total of 0.15 mg/kg
Oral, 240-480 qd



Slowing of ventricular rate during AF and flutter, and other SVTs in the absence of preexcitation; idiopathic VT


IV, load with 0.25 mg/kg over 2 min; if needed, repeat after 15 min with 0.35 mg over 2 min
Maintenance, 10-15 mg/h



Same as verapamil

NOTE: AF, atrial fibrillation; AV, atrioventricular; SVT, supraventricular tachycardia; VF, ventricular fibrillation; VT, ventricular tachycardia.

Paroxysmal Supraventricular Tachycardias (PSVT)

In most cases, functional differences in conduction and refractoriness in the AV node or the presence of an AV bypass tract provide the substrate for the development of PSVT (previously termed paroxysmal atrial tachycardia). Electrophysiologic studies have demonstrated that reentry is responsible for the vast majority of cases of PSVT (Fig. 230-7). Reentry has been localized to the sinus node, atrium, AV node, or a macroreentrant circuit involving conduction in the antegrade direction through the AV node and retrograde through an AV bypass tract. Such a bypass tract may also conduct antegradely, in which case the Wolff-Parkinson-White (WPW) syndrome is said to be present. When the bypass tract manifests only retrograde conduction, it is termed a concealed bypass tract (Fig. 230-7B). In these cases, the QRS complex during sinus rhythm is normal. In the absence of the WPW syndrome, reentry through the AV node or through a concealed bypass tract makes up more than 90% of all PSVTs.

Figure 230-7

Figure 230-7: Examples of reentrant supraventricular tachycardia (SVT). A. AV nodal reentry. No P waves are visible. B. AV reentry using a concealed bypass tract. Inverted retrograde P waves are superimposed on the T wave. C. Intraatrial reentry. Inverted P waves follow the T waves and precede the QRS complex.

AV Nodal Reentrant Tachycardia

There is no age or disease predisposition for the development of AV nodal reentrant tachycardia, the most common cause of supraventricular tachycardia. It is, however, more commonly observed in women. It usually presents as a regular narrow QRS complex tachycardia at rates of 120 to 250 bpm. APCs that initiate the arrhythmia are almost always associated with a prolonged PR interval. Retrograde P waves may be absent, buried in the QRS complex, or appear as distortions at the terminal parts of the QRS complex (Fig. 230-7A).

AV nodal reentrant PSVT (Fig. 230-8) can be reproducibly initiated and terminated by appropriately timed atrial premature stimuli. The onset of the tachycardia is almost always associated with prolongation of the PR interval due to marked AV nodal conduction delay (prolonged AH interval) following the APC that is critical for the genesis of the arrhythmia. The sudden prolongation of the AH interval is consistent with the concept of dual AV nodal pathways: a fast pathway, which exhibits rapid conduction and a long refractory period, and a slow pathway, which has a short refractory period but conducts slowly. During sinus rhythm, only conduction over the fast pathway is manifest, resulting in a normal PR interval (Fig. 230-8). Atrial extrastimuli at a critical coupling interval are blocked in the fast pathway because of its longer refractory period and are conducted slowly through the slow pathway. If conduction down the slow pathway is slow enough to allow the previously refractory fast pathway time to recover excitability, a single atrial (echo) reentrant beat or sustained tachycardia ensues. A critical balance between conduction velocity and refractoriness within the node is required to sustain AV nodal reentry. Retrograde atrial and antegrade ventricular activation occur simultaneously, explaining why P waves may not be apparent on the surface ECG.

Figure 230-8

Figure 230-8: Mechanism of AV nodal reentry: The atrium, AV node (AVN), and His bundle are shown schematically. The AV node is longitudinally dissociated into two pathways, slow and fast, with different functional properties (see text). In each panel of this diagram, blue lines denote excitation in the AV node, which is manifest on the surface electrocardiogram, while black lines denote conduction, which is concealed and not apparent on the surface electrocardiogram. A. During sinus rhythm (NSR) the impulse from the atrium conducts down both pathways. However, only conduction over the fast pathway is manifest on the surface ECG, producing a normal PR interval of 0.16 s. B. An atrial premature depolarization (APD) blocks in the fast pathway. The impulse conducts over the slow pathway to the His bundle and ventricles, producing a PR interval of 0.24 s. Because the impulse is premature, conduction over the slow pathway occurs more slowly than it would during sinus rhythm. C. A more premature atrial impulse blocks in the fast pathway, conducting with increased delay in the slow pathway, producing a PR interval of 0.28 s. The impulse conducts retrogradely up the fast pathway producing a single atrial echo. Sustained reentry is prevented by subsequent block in the slow pathway. D. A still more premature atrial impulse blocks initially in the fast pathway, conducting over the slow pathway with increasing delay producing a PR interval of 0.36 s. Retrograde conduction occurs over the fast pathway and reentry occurs, producing a sustained tachycardia (SVT).

Clinical Features

AV nodal reentry may produce palpitations, syncope, and heart failure depending on the rate and duration of the arrhythmia and the presence and severity of any underlying heart disease. Hypotension and syncope may occur because of the sudden loss of the atrial contribution to ventricular filling; this can also lead to a marked increase in atrial pressure, acute pulmonary edema, and a reduction in ventricular filling. Simultaneous atrial and ventricular contraction produces cannon a waves with each heartbeat.


In patients without hypotension, vagal maneuvers, particularly carotid sinus massage, can terminate the arrhythmia in 80% of cases. If hypotension is present, raising the blood pressure by the cautious use of intravenous phenylephrine in 0.1-mg increments may terminate the arrhythmia alone or in combination with carotid sinus pressure. If these maneuvers are unsuccessful, verapamil (2.5 to 10 mg intravenously) or adenosine (6 to 12 mg intravenously) is the agent of choice. We prefer to use adenosine because of its extremely short half-life, lessening the consequences of any side effects. Beta blockers may also be used to slow or terminate the tachycardia but are agents of second choice. Digitalis glycosides have a slower onset of action and should not be used for acute therapy. When these drugs fail to terminate the tachycardia, or when the tachycardia is recurrent, atrial or ventricular pacing via a temporary pacemaker inserted pervenously may be used to terminate the arrhythmia. However, if severe ischemia and/or hypotension is caused by the tachycardia, dc cardioversion should be considered.

AV nodal reentry can usually be prevented by the use of drugs that act primarily on the antegrade slow pathway (such as digitalis, beta blockers, or calcium channel antagonists) or on the fast pathway (class IA or IC; Table 230-4). We favor initial therapy with beta blockers, calcium channel antagonists, or digoxin because the risk-benefit ratio associated with treatment with these agents is more favorable than that of IA or IC agents. Drugs most likely to avert recurrences prevent induction of the arrhythmias by programmed stimulation. This technique utilizes temporary pacemaker catheters connected to a physiologic stimulator capable of variable rate pacing and stimulation with one or more precisely timed premature impulses. In symptomatic patients who require chronic therapy, radiofrequency catheter modification of the AV node should be considered. This technique can cure AV nodal reentry in >90% of cases and has been proven to be safe, although a 1 to 2% risk of AV block requiring a permanent pacemaker exists.

AV Reentrant Tachycardia

PSVT due to AV reentry incorporates a concealed AV bypass tract as part of the tachycardia circuit. Thus the impulse passes antegradely from the atria through the AV node and His-Purkinje system to the ventricles and then retrogradely through the (concealed) bypass tract back to the atrium. Patients with this disorder manifest the same type of PSVT as do patients with the WPW syndrome (see below), but the bypass tract cannot conduct in an antegrade direction during sinus rhythm or other atrial tachyarrhythmias.

AV reentrant tachycardia can be initiated and terminated by either APCs or VPCs. Initiation of PSVT by a VPC is virtually diagnostic of AV reentry. Alternation of the QRS complexes occurs in approximately one-third of such tachycardias. Since atrial activation must follow ventricular activation during AV reentry, the P wave usually occurs after the QRS complex (Fig. 230-7B).

Atrial activation mapping is of major value in evaluating the origin of these tachycardias. Most concealed bypass tracts are left-sided. Thus, during PSVT or during ventricular pacing, the earliest activation sequence is recorded in the left atrium, usually via a catheter in the coronary sinus. This eccentric atrial activation is quite distinct from the normal retrograde activation sequence in which the earliest activation of the atria is in the area of the AV junction. The ability of a ventricular stimulus to conduct to the atrium at a time when the bundle of His is refractory and the termination of the tachycardia by a ventricular stimulus that does not reach the atrium are diagnostic of retrograde conduction over a concealed bypass tract.


This is similar to the treatment for AV nodal reentry tachycardia. Although pharmacologic agents may be used, patients who require chronic therapy should be considered candidates for radiofrequency catheter ablation of the bypass tract. This requires detailed electrophysiologic study to exclude other arrhythmias that may be responsible for patients' symptoms and to determine the location of the bypass tract(s). The efficacy of this procedure exceeds 90%, with minimal risks. In the remaining small number of patients failing catheter ablation, surgical ablation or pharmacologic therapy can be used.

Sinus Node Reentry and Other Atrial Tachycardias

Reentry in the region of the sinus node or within the atria is invariably initiated by APCs. These arrhythmias are less common than AV nodal or AV reentry and are more often associated with underlying cardiac disease. During sinus node reentry, the P-wave morphology is identical to that occurring in sinus rhythm, but the PR interval is prolonged. This is in contrast to sinus tachycardia, in which the PR interval tends to shorten. With intraatrial reentry, the P-wave configuration differs from that during sinus rhythm, and the PR interval is prolonged (Fig. 230-7C).


Sinus node and atrial reentrant arrhythmias are managed like other reentrant PSVTs, except that catheter ablation is less successful because multiple foci may be present.

Nonreentrant Atrial Tachycardias

These may be a manifestation of digitalis intoxication or may be associated with severe pulmonary or cardiac disease, with hypokalemia, or with the administration of theophylline or adrenergic drugs. Multifocal atrial tachycardia (MAT) (Fig. 230-9) is particularly common following theophylline administration. By definition, MAT requires three or more consecutive P waves of different morphologies at rates greater than 100 beats per minute. MAT usually has an irregular ventricular rate because of varying AV conduction. There is a high incidence of atrial fibrillation (50 to 70%) in patients with MAT. Treatment should be directed at the underlying disorder. The digitalis-induced arrhythmias are caused by triggered activity. In such atrial tachycardias with AV block secondary to digitalis intoxication, the atrial rate rarely exceeds 180 bpm, and typically 2:1 block is present. Atrial arrhythmias precipitated by digitalis can usually be treated by withdrawal of the drug.

Figure 230-9

Figure 230-9: Multifocal atrial tachycardia. A lead I rhythm strip demonstrates a multifocal atrial tachycardia defined by 0x0022653 consecutive P waves of variable morphology and rate >100 bpm (arrows).

Automatic atrial tachycardias not caused by digitalis are difficult to terminate, and in such cases the main goal of therapy should be to control the ventricular response, either by drugs that affect the AV node, such as digitalis, beta blockers, or calcium channel antagonists, or by ablation techniques. Catheter ablation and surgery have been employed to eradicate the arrhythmia's focus or create heart block for rate control.

Preexcitation (WPW) Syndrome

The most frequently encountered type of ventricular preexcitation is that associated with AV bypass tracts (Fig. 230-20). These connections are composed of strands of atrial-like muscle which may occur almost anywhere around the AV rings. The term Wolff-Parkinson-White syndrome is applied to patients with both preexcitation on the ECG and paroxysmal tachycardias. AV bypass tracts can be associated with certain congenital abnormalities, the most important of which is Ebstein's anomaly.

Figure 230-20

Figure 230-20: Conduction over an accessory pathway. The morphology of a QRS complex in patients with an accessory pathway (AP) is an example of fusion. If there is no antegrade conduction over the AP (top) the AP may still conduct in the retrograde direction but is considered concealed. When conduction over the AP is minimal and atrioventricular (AV) node conduction predominates, the QRS becomes a fusion of conduction over the A V nOde-His-Purkinje system and the AP. When conduction to the ventricle over the AP predominates compared with AV nodal conduction, the QRS represents a fusion of conduction over the AV node-HPS and the AP, but the larger the portion of the ventricle activated by the AP, the wider the QRS complex appears. H-P, His Purkinje; LA, left atrium; LV, left ventricle; PVC, premature ventricular complex; RA, right atrium; RV, right ventricle. [HR Grogin: Supraventricular tachycardia, in M Scheinman (volume ed): Arrhythmias: Electrophysiologic Principles, in E Braunwald (series ed): Atlas of Heart Diseases, vol 9. Philadelphia, Current Medicine, 1996, p 5.9.]

AV bypass tracts that conduct in an antegrade direction produce a typical ECG pattern of a short PR interval (<0.12 s), a slurred upstroke of the QRS complex (delta wave), and a wide QRS complex. This pattern results from a fusion of activation of the ventricles over both the bypass tract and the AV nodal His-Purkinje system (Fig. 230-10). The relative contribution of activation over each system determines the amount of preexcitation.

Figure 230-10

Figure 230-10: ECG in Wolff-Parkinson-White syndrome. There is a short PR interval (0.11 s), a wide QRS complex (0.12 s), and slurring on the upstroke of the QRS produced by early ventricular activation over the bypass tract (delta wave, d in lead I). The negative delta waves in V1 are diagnostic of a right-sided bypass tract. Note the Q wave (negative delta wave) in lead III, mimicking myocardial infarction.

During PSVT in WPW, the impulse is usually conducted antegradely over the normal AV system and retrogradely through the bypass tract. Rarely (approximately 5%), tachycardias occurring in patients with WPW will exhibit a reverse pattern with antegrade conduction through the bypass tract and retrograde conduction through the normal AV system. This produces a tachycardia with a wide QRS complex in which the ventricles are totally activated by the bypass tract. Atrial flutter and AF also occur commonly in patients with WPW syndrome. Since the bypass tract does not have the same decremental conducting properties as the AV node, the ventricular responses during atrial flutter or fibrillation may be unusually rapid and may cause ventricular fibrillation (VF).

The goals of electrophysiologic evaluation in patients suspected of having the WPW syndrome are (1) to confirm the diagnosis, (2) to localize the bypass tract and determine how many bypass tracts are present, (3) to demonstrate the role of the bypass tract in the genesis of the arrhythmias, (4) to determine the potential for the development of possibly life-threatening rates during atrial flutter or fibrillation, and (5) to evaluate therapeutic options.


Pharmacologic therapy is aimed at altering the electrophysiologic properties (i.e., refractoriness or conduction velocity) of one or more components of the reentrant circuit. This is most often accomplished by agents such as beta blockers or calcium channel blockers that slow conduction and increase refractoriness of the AV node or by agents such as quinidine or flecainide that slow conduction and increase refractoriness primarily in the bypass tract. Some drugs may affect multiple sites (Fig. 230-11).

Figure 230-11

Figure 230-11: Site of action of antiarrhythmic agents in the Wolff-Parkinson-White syndrome. The atrium, ventricle, antegrade conduction through the AV node (0x002193), retrograde conduction through the AV node (0x002191), and the bypass tract are shown. Drugs on the left affect antegrade AV nodal conduction. Type IA drugs on the upper right affect retrograde conduction over the node and antegrade conduction over the bypass tract. Drugs on the lower right affect conduction in both directions in the AV node and the bypass tract.

Acute management of episodes of PSVT in patients with WPW syndrome is similar to that of PSVT in patients with concealed bypass tracts.

In patients with the WPW syndrome and AF, dc cardioversion should be carried out if there is a life-threatening, rapid ventricular response. In non-life-threatening situations, lidocaine (3 to 5 mg/kg) or procainamide (15 mg/kg) administered intravenously over 15 to 20 min will usually slow the ventricular response. More recently, ibutilide has become available as an alternative therapy for preexcitation tachycardia. Caution should be employed when using digitalis or intravenous verapamil in patients with the WPW syndrome and AF, since these drugs can shorten the refractory period of the accessory pathway and can increase the ventricular rate, thereby placing the patient at increased risk for VF. Chronic oral therapy with verapamil is not associated with this risk. In addition to these drugs, beta-blocking agents are of no utility in controlling the ventricular response during AF when conduction proceeds over the bypass tract. Although atrial or ventricular pacing can almost always terminate PSVT in patients with the WPW syndrome, they can induce AF. As such, chronic pacemaker therapy is to be discouraged.

While surgical ablation of bypass tracts offers a permanent cure of supraventricular tachycardia (SVT) and most AFs associated with SVT, the advent of radiofrequency catheter ablation has virtually eliminated the need for surgery. Catheter ablation of bypass tracts is possible in >90% of patients and is the treatment of choice in patients with symptomatic arrhythmias. It is safer, more cost-effective, and just as successful as surgery. Nevertheless, surgical ablation may be required in the occasional patient in whom catheter ablation fails.

Nonparoxysmal Junctional Tachycardia

This rhythm usually results from conditions that produce enhanced automaticity or triggered activity in the AV junction and is most commonly due to digitalis intoxication, inferior wall myocardial infarction, myocarditis, endogenous or exogenous catecholamine excess, acute rheumatic fever, or valve surgery.

The onset of nonparoxysmal junctional tachycardia is usually gradual, with a "warm-up" period prior to stabilization of the rate, which can range from 70 to 150 bpm, faster rates usually being associated with digitalis intoxication. Nonparoxysmal junctional tachycardia is recognized by a QRS complex identical to that of sinus rhythm. The rate can be influenced by autonomic tone and can be increased by catecholamines, vagolytic agents, or exercise and slowed somewhat by carotid sinus pressure. When this rhythm is due to digitalis intoxication, it usually is associated with AV block and/or dissociation. Soon after cardiac surgery, retrograde conduction is more likely to be present because of the heightened sympathetic state.


This is directed toward elimination of the underlying etiologic factors. Since digitalis is the most common cause of this rhythm, discontinuation of this drug is indicated. If the rhythm is associated with other serious manifestations of digitalis intoxication, such as ventricular or atrial irritability, active intervention with lidocaine or a beta blocker may be useful, and in some instances, use of digitalis antibodies (Fab fragments) should be considered. Cardioversion of this rhythm should not be attempted, particularly in the setting of digitalis intoxication. When AV conduction is intact, atrial pacing can capture and override the junctional focus and provide the AV synchrony necessary to maximize cardiac output. Nonparoxysmal junctional tachycardia is usually not a chronic, recurrent problem, and attention to the acute precipitating events can often resolve the tachycardia.

Ventricular Tachycardia

Sustained ventricular tachycardia is defined as VT that persists for more than 30 s or requires termination because of hemodynamic collapse. VT generally accompanies some form of structural heart disease, most commonly chronic ischemic heart disease associated with a prior myocardial infarction. Sustained VT may also be associated with nonischemic cardiomyopathies, metabolic disorders, drug toxicity, or prolonged QT syndrome, and it occurs occasionally in the absence of heart disease or other predisposing factors. Nonsustained VT (three beats to 30 s) is also associated with cardiac disease but occurs in its absence more often than the sustained arrhythmia. While nonsustained VT usually does not produce symptoms, sustained VT is almost always symptomatic and is often associated with marked hemodynamic compromise and/or the development of myocardial ischemia. A fixed anatomic substrate, not acute ischemia, is responsible for most recurrent episodes of sustained uniform VT. Acute ischemia appears to have little role in the genesis of sustained uniform VT associated with chronic infarction but may play a role in the degeneration of stable VT into VF or initiation of polymorphic VT. Most episodes of VF begin with VT.

The ECG diagnosis of VT is suggested by a wide-complex QRS tachycardia at a rate exceeding 100 bpm. The QRS configuration during any episode of VT may be uniform (monomorphic), or it may vary from beat to beat (polymorphic). Bidirectional tachycardia refers to VT that shows an alternation in QRS amplitude and axis. Typically this appears as a QRS with a right bundle branch block pattern with alternating superior (leftward) and inferior axes (rightward). While the rhythm is usually quite regular, slight irregularity may exist. Atrial activity may be dissociated from ventricular activity, or the atria may be depolarized retrogradely. The onset of the tachycardia is generally abrupt, but in nonparoxysmal tachycardias it can be gradual. Paroxysmal VT is usually initiated by a VPC.

It is important to distinguish SVT with aberration of intraventricular conduction from VT because the clinical implications and management of these two arrhythmias are totally different. The most important clinical predictor of VT is the presence of structural heart disease. The observation of intermittent cannon a waves and varying first heart sounds suggests AV dissociation and is diagnostic of VT. In a majority of cases, the diagnosis can and should be made by close examination of the 12-lead ECG. Pharmacologic maneuvers, such as administration of intravenous verapamil or adenosine, can be hazardous and should be avoided. It is always useful to have a 12-lead ECG recorded during sinus rhythm for comparison with that during tachycardia. When the tracing obtained during sinus rhythm demonstrates the same morphologic features as those during the tachycardia, the diagnosis of PSVT with aberration is favored. An infarction pattern on the sinus rhythm tracing suggests the potential presence of the anatomic substrate necessary for VT. Characteristics of the 12-lead ECG during the tachycardia that suggest a ventricular origin for the arrhythmia are (1) a QRS complex >0.14 s in the absence of antiarrhythmic therapy, (2) AV dissociation (with or without fusion or captured beats) or variable retrograde conduction (Fig. 230-12), (3) a superior QRS axis in the presence of a right bundle branch block pattern, (4) concordance of the QRS pattern in all precordial leads (i.e., all positive or all negative deflections), and (5) other QRS patterns (morphology) with prolonged duration that are inconsistent with typical right or left bundle branch block patterns. (See Table 230-5 for a detailed synopsis of ECG criteria that favor the diagnosis of VT over SVT for wide complex tachycardia.) A wide, complex, bizarre tachycardia that is very irregular suggests AF with conduction over an AV bypass tract. Similarly, a QRS complex in excess of 0.20 s is uncommon during VT in the absence of drug therapy and is more common with preexcitation. Intravenous verapamil will stop most recalcitrant SVTs involving the AV junction, but it is rarely effective for VT. Because of this property, verapamil has been utilized to attempt to differentiate SVT with aberrant conduction from VT. However, this is extremely hazardous, since intravenous verapamil can precipitate cardiac arrest in patients with VT.

Figure 230-12

Figure 230-12: Ventricular tachycardia with AV dissociation. P waves are dissociated from the underlying wide complex rhythm (best seen on lead V1).

Table 230-5: Wide Complex Tachycardia

ECG Criteria That Favor Ventricular Tachycardia

  1. AV dissociation
  2. QRS width:
    >0.14 s with RBBB configuration
    >0.16 s with LBBB configuration
  3. QRS axis:
    Left axis deviation with RBBB morphology
    Extreme left axis deviation (northwest axis) with LBBB morphology
  4. Concordance of QRS in precordial leads
  5. Morphologic patterns of the QRS complex
    0x002003RBBB: Mono- or biphasic complex in V1
    RS (only with left axis deviation) or QS in V6

    Broad R wave in V1 or V2 0x0022650.04 s
    Onset of QRS to nadir of S wave in V1 or V2 of 0x0022650.07 s
    Notched downslope of S wave in V1 or V2
    Q wave in V6

NOTE: AV, atrioventricular; BBB, bundle branch block.

It has been possible to replicate sustained uniform VT in more than 95% of patients with this arrhythmia using programmed electrical stimulation. In most patients the tachycardia is initiated with ventricular premature stimuli. A sustained monomorphic VT with a morphology identical to that of the spontaneous arrhythmia is the rule. The clinical significance of polymorphic VT initiated by programmed stimulation is not clear, since more aggressive stimulation (i.e., the use of three or four extrastimuli) can induce polymorphic VT and even VF in some normal subjects and in patients who have never had a clinical arrhythmia.

Sustained uniform VT can be terminated by programmed stimulation or rapid pacing in at least 75% of patients; the remainder require cardioversion. The ability to reproducibly initiate and terminate a sustained, uniform VT permits assessment of pharmacologic and electrical therapy of these arrhythmias.

The reproducible termination of VT by programmed stimulation permits evaluation of the effectiveness of antitachycardia pacemakers for long-term therapy of paroxysmal episodes of arrhythmia. Unfortunately, rapid pacing, the most effective form of therapy, can accelerate the tachycardia and/or produce VF. Therefore, antitachycardia pacing is a viable form of therapy only when the pacing device includes backup defibrillation capabilities.

Clinical Features

Symptoms resulting from VT depend on the ventricular rate, duration of the tachycardia, and presence and extent of underlying cardiac disease. When the tachycardia is rapid and associated with severe myocardial dysfunction and cerebrovascular disease, hypotension and syncope are common. However, the presence of hemodynamic stability does not preclude a diagnosis of VT. The rate, loss of the atrial contribution to ventricular filling, and abnormal sequence of ventricular activation are important factors producing a decreased cardiac output during VT.

The prognosis of VT depends on the underlying disease state. If sustained VT develops within the first 6 weeks following acute myocardial infarction, the prognosis is poor, with a 75% mortality rate at 1 year. Patients with nonsustained VT following myocardial infarction have a threefold greater risk of death than a comparable group of patients without this arrhythmia. However, a cause-and-effect relationship between the nonsustained tachycardia and subsequent sudden death has not been established. Patients without heart disease who have uniform VT have a good prognosis and an extremely low risk of sudden death.


The risk-benefit ratio of treating each specific type of VT should be considered before beginning therapy. This is important because antiarrhythmic agents can produce or exacerbate the very arrhythmias that they are given to prevent. In general, patients with VT but without organic heart disease have a benign course; such patients with asymptomatic, nonsustained VT need not be treated because their prognosis will not be affected. An exception is the patient with congenital long QT syndrome. Such patients have recurrent polymorphic VT and a high mortality from sudden death if untreated. Patients with sustained VT in the absence of heart disease usually require therapy because the arrhythmia causes symptoms. These tachycardias may respond to beta blockers; verapamil; class IA, IC, or III agents (Fig. 230-21); or amiodarone. In patients with VT and organic heart disease, if marked hemodynamic compromise is present or if there is evidence of ischemia, congestive heart failure, or central nervous system hypoperfusion, the rhythm should be promptly terminated by dc cardioversion (see below). If the patient with organic heart disease tolerates the VT well, pharmacologic therapy may be tried. Procainamide is probably the most effective agent for acute therapy. It may or may not terminate the tachycardia but almost always slows the rate. In stable patients in whom these drugs do not terminate the arrhythmia, a pacing catheter can be inserted pervenously into the right ventricular apex, and the tachycardia can be terminated by overdrive pacing.

Figure 230-21

Figure 230-21: The effect of a drug with class III antiarrhythmic action on a reentry circuit by sufficiently prolonging the refractory period of path Ot, thus preventing reentry from occurring (B).

Programmed stimulation is probably the most effective way to select the appropriate antiarrhythmic agent to prevent recurrent, sustained VT. After demonstrating that the tachycardia can be initiated reproducibly in the absence of antiarrhythmic agents, drugs can be studied serially, and the drug that prevents initiation of the tachycardia can be selected; long-term (>2 years) successful prevention of the arrhythmia can then be expected in 80% of patients if a complete stimulation protocol is used following drug administration. Failure to perform a complete protocol will lead to recurrences, which are often blamed on the lack of utility of programmed stimulation as a method of evaluating drug efficacy. Drug levels demonstrated to be successful in the laboratory need to be maintained chronically. Unfortunately, prevention of inducible VT is expected in only 50% of cases. Use of Holter monitor for guided therapy, although advocated by some, is of less value.

Antitachycardia pacing has been used as a means to terminate tachycardias that have been reproducibly terminated by pacing in the electrophysiology laboratory. Automatic antitachycardia pacing devices are not used alone because pacing during VT may accelerate tachycardia, converting a stable arrhythmia into an unstable one and resulting in severe hemodynamic compromise. However, devices combining antitachycardia pacing with an ICD (see below) afford a "backup" means of terminating unstable arrhythmias.

The advent of endocardial catheter and intraoperative mapping led to the development of surgical techniques for the management of VT. Activation mapping permits localization of the site of origin of the arrhythmia. In centers in which expertise in mapping is available, operation has been successfully employed to cure tachycardias in the majority of patients in whom it has been undertaken. Even though most patients with VT and ischemic heart disease have markedly impaired left ventricular function and multivessel coronary artery disease, the operative mortality rate has ranged between 8 and 15%. Following operation, >90% of survivors are controlled either off (two-thirds of patients) or on (one-third) antiarrhythmic agents that were previously ineffective in controlling these rhythms. With the development of radiofrequency ablation and refinement of mapping criteria to locate critical sites of the VT circuit, precisely, catheter ablation can be performed as a curative procedure in selected patients. In experienced centers cure of VT in these selected patients approaches 75%.

Specific Types of VT

Torsade de pointes (Fig. 230-13) refers to VT characterized by polymorphic QRS complexes that change in amplitude and cycle length, giving the appearance of oscillations around the baseline. This rhythm is, by definition, associated with QT prolongation. The latter may result from electrolyte disturbances (particularly hypokalemia and hypomagnesemia), use of a variety of antiarrhythmic drugs (especially quinidine), phenothiazines and tricyclic antidepressants, liquid protein diets, intracranial events, and bradyarrhythmias, particularly third-degree AV block. It also may occur as a congenital anomaly that most often presents with torsade de pointes (syncope or sudden death) at a young age.

Figure 230-13

Figure 230-13: Rhythm strips of patients with drug (disopyramide)-induced torsade de pointes. The polymorphic ventricular tachycardia is associated with very long QT intervals.

The electrocardiographic hallmark is polymorphic VT preceded by marked QT prolongation, often in excess of 0.60 s. These patients often have multiple episodes of nonsustained polymorphic VT associated with recurrent syncope, but they also may develop VF and sudden cardiac death.

Therapy should be directed at removing the precipitating factors, i.e., correcting metabolic abnormalities and removing drugs that have induced the prolonged QT interval. In the setting of drug-induced torsade de pointes, atrial or ventricular overdrive pacing and the administration of magnesium have also been useful in terminating and preventing the arrhythmia. For patients with the congenital prolonged QT interval syndrome, 0x0003b2-adrenergic blocking agents have been the mainstay of therapy; agents that shorten the QT interval may also be useful (e.g., phenytoin). Cervicothoracic sympathectomy has been proposed as a form of therapy for congenital prolonged QT syndrome, but it is not often effective as the sole therapy. Pacing in combination with beta blockers and sympathectomy has been used by some investigators when beta blockers fail, but it is not uniformly successful and results in a Horner's syndrome. More recently, ICDs with dual chambered pacing capability and beta blockers have become the treatment of choice for patients with recurrent episodes despite beta blockers.

Polymorphic tachycardias associated with normal QT intervals in patients with ischemic heart disease that are initiated by "R-on-T" VPCs are probably caused by reentry, and their treatment is totally different. This is not true torsade de pointes. In such cases, class I or III agents may be the most effective form of therapy and should be administered in full antiarrhythmic doses. However, these arrhythmias may also result from acute, severe ischemia and will only respond to abolition of the ischemia, usually by revascularization.

Accelerated idioventricular rhythm, also termed slow VT, with a rate that ranges from 60 to 120 bpm, usually occurs in acute myocardial infarction, often during reperfusion. It may also be seen following cardiac operations; in patients with cardiomyopathy, rheumatic fever, or digitalis intoxication; and in patients with no evidence of heart disease. The rhythm is usually transient and rarely causes significant hemodynamic compromise or symptoms.

Treatment is rarely necessary and should usually be considered only if symptoms arise due to impaired hemodynamics, most commonly due to AV dissociation. In most cases, atropine can accelerate the sinus rate to overdrive the ventricular rhythm.

Ventricular Flutter and Ventricular Fibrillation (  Fig. 230-14;)

These arrhythmias occur most often in patients with ischemic heart disease. They also occur following administration of antiarrhythmic drugs, particularly those that induce prolonged QT intervals and torsade de pointes (see above), in patients with severe hypoxia or ischemia, and in those with WPW who develop AF with an extremely rapid ventricular response (p. 1299). Electrical accidents frequently cause cardiac arrest due to the development of VF. The onset of these arrhythmias is rapidly followed by loss of consciousness and, if untreated, death. Episodes of cardiac arrest recorded during Holter monitoring reveal that approximately three-fourths of the sudden deaths are due to VT or VF.

Figure 230-14

Figure 230-14: Ventricular fibrillation. In a patient with coronary disease, ventricular fibrillation is initiated by an early ventricular premature complex that produces a rapid polymorphic ventricular tachycardia which rapidly degenerates to ventricular fibrillation (note the undulating baseline with indistinguishable systole and diastole).

In patients with nonischemic VF, the onset usually begins with a short run of rapid VT, which is initiated by a relatively late coupled VPC. In patients with acute myocardial infarction or ischemia, however, VF is usually precipitated by a single early ventricular complex beat falling on the T wave (the vulnerable period), which produces a rapid VT that degenerates into VF (Fig. 230-14).

The clinical setting in which VF occurs is important. Most patients who have primary VF within the first 48 h of the onset of acute infarction have a good long-term prognosis, with a very low rate of recurrence or sudden cardiac death. Their short-term mortality may, however, be slightly increased. In contrast, patients who experience VF unassociated with the development of acute myocardial infarction have a recurrence rate of 20 to 30% in the year following the event (Chap. 39).

Ventricular flutter usually appears as a sine wave with a rate between 150 and 300 bpm. These oscillations make it impossible to assign a specific morphology to the arrhythmia and in some cases to distinguish it from rapid VT. VF is recognized by grossly irregular undulations of varying amplitudes, contours, and rates (Fig. 230-14). Electrophysiologic studies have demonstrated that regardless of the apparent gross irregularity on the surface ECG, VF usually starts out with a rapid repetitive sequence of VT that ultimately breaks down into multiple wavelets of reentry.

Electrophysiologic studies have been useful in patients who have been resuscitated from cardiac arrest. In approximately 70% of patients with prior infarction, programmed stimulation can reproducibly initiate a sustained VT. Ablation may be possible in some of these patients, particularly if the VT can be slowed so that it can be mapped. Several recent secondary prevention trials have demonstrated superior survival (3 years) in patients treated with ICDs versus amiodarone (Table 230-6). However, in patients with ejection fractions >35% or <20%, survival was comparable. Further subgroup analysis is necessary to identify those patients most likely to be benefited by ICDs.

Table 230-6: Trials of ICD Therapy vs. Antiarrythmic Drugs (AAD): VT/VF Patients






ICD vs. empiric amiodarone or sotolol (mainly amiodarone)

ICD vs. empiric amiodarone

ICD vs. empiric amiodarone, metoprolol, and propafenonea

Sample size

n = 1016
AAD = 509
ICD = 507

n = 659
Amiodarone = 331
ICD = 328

n = 346
Amiodarone = 92
Metoprolol = 97
Propafenone* = 58
ICD = 99

Patient inclusion criteria

Survivors of VF
with syncope
VT with EF 0x00226440%

Survivors of VF
with syncope
VT with EF 0x00226435% and cycle length 0x002264400 ms

Survivors of VF (no EF requirement)

Mortality in 'drug' or 'control' arm

1 year0x0020032 years0x0020033 years

3 years

2 years

Mortality in ICD arm

1 year0x0020032 years0x0020033 years

3 years

2 years

Reduction in mortality with ICD

1 year0x0020032 years0x0020033 years

3 years

2 years

aFollowing an interim analysis in March, 1992, enrollment in propafenone arm was discontinued because mortality was increased significantly over mortality in the ICD arm.

NOTE: EF, ejection fraction; ICD, implanted cardioverter/defibrillator; VF, ventricular fibrillation; VT, ventricular tachycardia.


AVID Investigators: N Engl J Med 337(22):1576, 1997; K Kuck, S Connolly: ACC NewsOnline, 1998.



Many advances have been made in the identification of genes responsible for syndromes associated with ventricular tachycardias and sudden cardiac death. Four specific examples include the congenital long QT syndrome (LQTS), hypertrophic obstructive cardiomyopathy (Chap. 238), arrhythmogenic right ventricular dysplasia, and the Brugada syndrome. The latter is a recently described disorder characterized by the electrocardiographic profile of a pseudo bundle branch block pattern with ST elevation and terminal T-wave inversion in leads V1-V3 (Fig. 230-15). The clinical presentation is VF in patients with structurally normal hearts. A mutation in the cardiac sodium channel, SCN 5A, is believed to be responsible. While the same gene is responsible for the LQTS, the mutation is different in the two syndromes.

Figure 230-15

Figure 230-15: Brugada syndrome. Note ST elevation with terminal T wave inversion in leads V1-V3 mimicking right bundle branch block.


Pharmacologic Antiarrhythmic Therapy

Prior to initiation of pharmacologic antiarrhythmic therapy, potential aggravating factors such as transient metabolic abnormalities, congestive heart failure, or acute ischemia must be corrected; in some cases this may suffice to control arrhythmias. In addition, the potential role of drugs as a cause or exacerbating factor in the development of the arrhythmia must be considered. It must be recognized that we do not have a good understanding of the effects of antiarrhythmic agents on the spontaneous onset of tachyarrhythmias. In some cases, they may facilitate the onset.

Antiarrhythmic drugs are used in three principal situations: (1) to terminate an acute arrhythmia; (2) to prevent recurrence of an arrhythmia; and (3) to prevent a life-threatening arrhythmia for which the patient is perceived to be at risk but which has never occurred.

Most currently available antiarrhythmic agents (Table 230-4) have a relatively low toxic/therapeutic ratio; all can exert proarrhythmic effects (Table 230-7), and therefore they may exacerbate underlying arrhythmias. Serum levels can be determined for most currently available antiarrhythmic agents. Standards for therapeutic and toxic levels can serve only as a rough guide for selecting the appropriate dose in any individual patient. In the final analysis, the therapeutic level in a given patient is the concentration that achieves the desired antiarrhythmic effect, and the toxic level for each patient is the concentration at which undesirable side effects occur. Since many adverse effects are directly related to drug concentrations, the lowest serum level that achieves an effective antiarrhythmic response should be chosen.

Table 230-7: Toxicity of Most Frequently Used Antiarrhythmic Agents



Proarrhythmic Toxicity




Nonarrhythmic Toxicity


A Flutter 1:1




Anorexia, nausea, vomiting, visual changes

Atrial tachycardia, VT, AV nodal block, accelerated junctional rhythms, atrial and ventricular premature depolarizations; acceleration of ventricular rate during atrial fibrillation or flutter in the presence of preexcitation


Anorexia, nausea, vomiting, diarrhea, cinchonism, tinnitus, hearing and visual changes, thrombocytopenia, hemolytic anemia, rash, potentiation of digoxin levels






Lupus erythematosus-like syndrome, anorexia, nausea






Anticholinergic actions: dry mouth, urinary retention, visual disturbances (avoid in narrow-angle glaucoma) constipation, congestive heart failure






Dizziness, confusion, delirium, seizures, coma; side effects potentiated by liver and heart failure






Ataxia, tremor, gait disturbances, rash, vomiting






Dizziness, nausea






Taste disturbance, bronchospasm






Pulmonary infiltrates and fibrosis, hepatitis, hypo- and hyperthyroidism, photosensitivity, peripheral neuropathy, tremor











aTDP (torsade de pointes) occurs most often in the setting of slow heart rates, QT prolongation, and hypokalemia or hypomagnesemia and at the time of conversion from atrial fibrillation to sinus rhythm. QT prolongation and torsade de pointes are not dose-related phemonema. QRS prolongation is a dose-related phenomena and will occur at toxic concentrations. QT and WRS intervals should be monitored and dose reductions made for interval prolongations.
bMay suppress sinus node function in patients with underlying sinus node dysfunction. May suppress escape foci in patients with complete heart block.
cAvoid in patients with prior myocardial infarction and depressed left ventricular function. Use in combination with AV nodal blocking agent to limit risk of atrial flutter with 1:1 conduction.
NOTE: A flutter 1:1, atrial flutter with 1:1 atrioventricular (AV) conduction; VT/VF, ventricular tachycardia/ventricular fibrillation.

In order to determine the therapeutic level for a patient, one must have a standard to judge drug efficacy. For a patient with an incessant arrhythmia, antiarrhythmic drugs may be administered empirically until the arrhythmia is suppressed. If a reproducible precipitating factor such as exercise can be identified, serial drug testing during such a provocative maneuver may be performed. Unfortunately, most arrhythmias are sporadic and occur unpredictably without identifiable precipitating factors. In these cases, if one waits to observe spontaneous recurrences on each antiarrhythmic drug, assessment of drug efficacy may require months. This type of assessment of efficacy may be adequate for arrhythmias that are not life-threatening. However, this mode of assessment is inadequate for arrhythmias that compromise hemodynamic stability, result in syncope, or cause cardiac arrest. In such cases, two methods for determination of arrhythmic drug efficacy have been utilized. The first, which consists of continuous ECG monitoring in the control state and then in the presence of antiarrhythmic drugs, has been used in order to determine the effect that each drug has on spontaneous atrial or ventricular ectopy. This method presupposes that the mechanism responsible for sustained arrhythmias is the same as that causing isolated premature depolarizations (which may or may not be true) and that therefore eradication of isolated ectopy will correlate with prevention of sustained arrhythmias. This method has a number of limitations. First, patients frequently show marked degrees of spontaneous variation in frequency of ectopy, which may mimic antiarrhythmic drug effects. Second, 25 to 30% of patients with sustained ventricular arrhythmias such as VT or VF demonstrate only rare spontaneous ectopy. Finally, many patients demonstrate a dissociation between the effects of antiarrhythmic agents on spontaneous ectopy and the effects of the same agent on sustained arrhythmias.

An alternative method to assess drug efficacy is programmed stimulation. Numerous studies have demonstrated that most clinically occurring supraventricular and ventricular tachyarrhythmias may be reproducibly initiated and terminated safely using this technique. Studies are performed initially in a baseline state in the absence of antiarrhythmic drugs. If the patient's clinical arrhythmia can be reproducibly initiated, then the ability of individual antiarrhythmic drugs to prevent reinduction of the arrhythmia can be assessed either after the drug is administered intravenously or after several days of oral loading in order to achieve a steady-state serum concentration. Use of this method assumes that (1) the induced and spontaneous arrhythmias are identical, and (2) prevention of induction of arrhythmias will correlate with prevention of recurrent spontaneous tachycardias on the same drug regimen. This technique has been validated in patients with a variety of reentrant PSVTs, VT, and VF. The technique is safe when carefully performed, the potential complications being those of any intravascular catheterization. Appropriate interpretation of the results of programmed stimulation is critically dependent on correlating the patient's spontaneous arrhythmias with those induced in the laboratory, with regard to rate and morphology, in order to be certain that the arrhythmia induced in the laboratory represents the same arrhythmia that occurred spontaneously and caused symptoms.

Classification of Antiarrhythmic Drugs

A number of classifications of antiarrhythmic drugs have been proposed; the most frequently used is a modification of one proposed by Vaughan-Williams (Table 230-2). This classification is based in part on the ability of antiarrhythmic drugs to modify the cardiac cellular (1) excitatory currents (Na+ or Ca2+), (2) action potential duration, and (3) automaticity (phase 4 depolarization). These effects of the drugs on isolated cardiac cells are thought to account for some of the antiarrhythmic properties of the drugs. Thus depression of excitatory currents by class I and class IV antiarrhythmics results in slowing of conduction velocity and may interrupt arrhythmias by blocking conduction in areas of marginal excitability, where conduction velocity is already slow. Class III antiarrhythmics allegedly exert their action by increasing refractoriness through prolongation of the action potential duration. However, this classification has a number of limitations. The electrophysiologic effects of these drugs in vivo may differ from their effects on isolated cells. Also, the effects of heart rate and fiber geometry are not considered. Not all drugs (e.g., adenosine) fit into the classifications. Finally, some drugs (e.g., amiodarone) exhibit properties consistent with multiple classes. The uses, actions, and toxic actions of currently available antiarrhythmic drugs are summarized in Tables 230-4 and 230-7.

Electrical Therapy of Tachyarrhythmias


Cardiac pacing can be used to terminate and in selected cases prevent recurrent supraventricular and ventricular arrhythmias. Because many tachyarrhythmias appear to be due to a reentrant mechanism with the impulse traveling in a circuit, a properly timed paced impulse can penetrate and prematurely depolarize part of the circuit, rendering it refractory to the next circulating wavefront and thereby interrupting the circus movement. Pacing therapy for arrhythmias is generally reserved for patients whose arrhythmias are refractory to drug therapy and who remain hemodynamically stable during the tachycardia. All forms of pacing therapy require repeated demonstration of their effectiveness and reliability in terminating the arrhythmias during electrophysiologic testing prior to implantation of the pacing device.

The type of pacing device and modality selected for arrhythmia termination depends on (1) the rate of the tachycardia (rates >160 bpm are rarely terminated by a single premature stimulus), (2) the type of arrhythmia (atrial flutter and VT are rarely terminated by single extrastimuli), and (3) concomitant drug therapy.

Because many tachycardias cannot be terminated by single premature stimuli, pacemakers have been developed that allow for multiple extrastimuli (burst pacing) to be introduced. In the current era, antitachycardia pacing is almost exclusively for ventricular arrhythmias because of the success of radiofrequency ablative therapy for supraventricular arrhythmias.

Cardiac pacing has also been used to prevent ventricular tachyarrhythmias. Polymorphic VT associated with a long QT interval and bradycardia (torsade de pointes, p. 1304) is most likely to respond. Pacing the atrium and/or ventricle at rates between 90 and 120 bpm appears to increase the homogeneity of electrical recovery and markedly reduces the propensity for a recurrence of arrhythmias.

Pacemakers may be self-contained or energized by an external radiofrequency source. The self-contained pacemaker may function automatically [i.e., it incorporates an arrhythmia recognition program (circuit)], or it may be activated by an external magnet. The major advantage of a fully automatic system is that there is no need for the patient to recognize the arrhythmia in order for termination to occur. The advantages of the externally activated system (rarely used today) include (1) the decreased risk of unnecessary treatment because of faulty sensing, and (2) the opportunity to initiate monitoring at the time of attempted termination of arrhythmia. This type of monitoring is frequently helpful if pacing techniques are employed to terminate VT, given the risk of acceleration of the arrhythmia by pacing.

The limitations of pacing therapy are primarily related to (1) the changes in the characteristics of the arrhythmia over time such that programmed pacing parameters no longer terminate the tachycardia, (2) the risk of acceleration of the tachycardia with the development of AF when stimulating the atrium and the development of rapid VT and VF when stimulating the ventricles, and (3) inappropriate recognition of supraventricular tachyarrhythmias as ventricular tachycardias, leading to delivery of therapy unnecessarily, which can initiate VT or VF. Future pacing generators that can perform cardioversion and defibrillation will increase the applicability of pacing therapy for the treatment of arrhythmias (see below).

Cardioversion and Defibrillation

Electrical cardioversion and defibrillation remain the most reliable methods for terminating arrhythmias. By depolarizing all or at least a large portion of excitable myocardium in a near homogeneous fashion, the electrical shock can interrupt reentrant arrhythmias. External cardioversion is routinely performed by placing two paddles 12 cm in diameter in firm contact with the chest wall, with one paddle usually located to the right of the sternum at the level of the second rib and the other in the left anterior axillary line in the fifth intercostal space. If the patient is conscious, a short-acting barbiturate to act as an anesthetic or an amnesic drug such as diazepam or medazolam should be administered to prevent patient discomfort. A person skilled in maintaining an airway should be present.

Energy is delivered synchronously with the QRS complex for all arrhythmias except ventricular flutter and VF, since asynchronous shocks can produce VF. The amount of energy used will vary with the type of tachycardia being treated. With the exception of AF, SVTs can frequently be terminated with energy levels in the range of 25 to 50 W s, while AF usually requires 0x002265100 W s for termination. For terminating VT, energy levels 0x002265100 W s should probably be employed. While energies as low as 25 W s may be used successfully, they also have a higher incidence of producing VF or AF. At least 200 W s of energy should be used for initial attempts at terminating VF. If the initial shock fails, all repeated attempts at defibrillation should be with the maximum energy that the defibrillator is capable of delivering (320 to 400 W s).

Indications for cardioversion depend on the clinical setting and the patient's general condition. Any tachycardia (except sinus tachycardia) that produces hypotension, myocardial ischemia, or heart failure warrants consideration of prompt termination using external cardioversion. Arrhythmias that fail to terminate with pharmacologic therapy may also be terminated by electrical cardioversion. Transient bradycardias and supraventricular and ventricular irritability following cardioversion are common and usually do not warrant antiarrhythmic intervention.

Implanted Cardioverter/Defibrillator (Fig. 230-22)

ICD devices have been developed that will promptly recognize and terminate life-threatening ventricular arrhythmias. These devices can deliver <1 to 40 W s, the amount of which can be programmed. Current devices have antitachycardia pacing capabilities such that VT can be sensed and terminated without resorting to a painful shock. In such devices, high-energy shocks are reserved for hypotensive VT, acceleration of VT, or failure to terminate VT after a programmed duration (Fig. 230-16). ICDs now can be implanted transvenously, and some are small enough to be implanted in a manner similar to pacemakers. Clinical trials testing the function of these devices in patients with drug-refractory ventricular arrhythmias have demonstrated survival from sudden death at 1 year ranging between 92 and 100%. Currently, ICDs should be considered for patients with VT that is not hemodynamically tolerated. As mentioned earlier, recent randomized trials suggest that ICDs confer improved mortality over amiodarone in patients with hemodynamically untolerated VT and a cardiac arrest not due to reversible causes (Table 230-6). Finally, they are indicated for patients with depressed left ventricular function, prior myocardial infarction, nonsustained and sustained VT at electrophysiologic study (Table 230-8). Guidelines for their use are given in Table 230-9.

Figure 230-16

Figure 230-16: Normally functioning implantable defibrillators. A continuous Holter monitoring tracing is shown. On the top strip, a rapid polymorphic tachycardia is initiated which beats more uniformly. The automatic implantable cardioverter/defibrillator (ICD) senses the rhythm and delivers a shock which restores sinus rhythm.

Figure 230-22

Figure 230-22: Nonthoracotomy lead system for implantable defibrillator. [JL Cockrell, A Siu: Implantable defibrillators for the management of cardiac rhythm disorders, in M Scheinman (volume ed): Arrhythmias: Electrophysiologic Principles, in E Braunwald (series ed): Atlas of Heart Diseases, vol 9. Philadelphia, Current Medicine, 1996, p 9.7 (A only). Adapted from: Cardiac Pacemakers, Inc, St. Paul, MN)]

Table 230-8: ICD Therapy for Primary Prevention of Sudden Cardiac Death





ICD vs. conventional (AAD, primarily empiric amiodarone)

EP-guided Rx (AAD or ICD) vs. control

Sample size

n = 196

n = 704


0x002003Conventional = 101
0x002003ICD = 95

0x002003EP-guided Rx = 351
0x002003Control = 353

Patient inclusion

S/P MI, EF 0x00226435% NSVT, inducible sustained VT not suppressible by procainamide

CAD, EF 0x00226440%, NSVT, inducible sustained VT

Total mortality

Conventional = 39%
ICD = 16% (27 months)

Control = 48%
EP-guided Rx = 42%
AAD = 55%
ICD = 24% (60 months)

Reduction in mortality by ICD


55% (vs. control or AAD)

SCD or cardiac arrest

Conventional = 13%
ICD = 3.2%

Control = 32%
EP-guided Rx = 25%
AAD = 37%
ICD = 9%

Reduction in SCD or cardiac arrest by ICD


75% (vs. control or AAD)

NOTE: AAD, antiarrhythmic drug; CAD, coronary artery disease; EF, ejection fraction; EP, electrophysiology; ICD, implantable cardioverter/defibrillator; MADIT, multicenter automatic defibrillator trial; MUSTT, multicenter unsustained tachycardia trial; NSVT, nonsustained ventricular tachycardia; RX, therapy; SCD, sudden cardiac death; S/P MI, status post-myocardial infarction; VT, ventricular tachycardia.



Table 230-9: ACC/AHA Guidelines for ICD Implantation

Class 1a


1.                     Cardiac arrest due to VF or VT not due to a transient or reversible cause.

2.                  Spontaneous sustained VT.


Syncope of undetermined origin with clinically relevant, hemodynamically significant sustained VT or VF induced at EP study when drug therapy is ineffective, not tolerated, or not preferred.


Nonsustained VT with coronary disease, prior MI, LV dysfunction, and inducible VF or sustained VT at EP study that is not suppressible by a class I antiarrhythmic drug.

Class 2b


    1. Cardiac arrest presumed to be due to VF when EP testing is precluded by other medical conditions.
  1. Severe symptoms attributable to sustained ventricular tachyarrhythmias while awaiting cardiac transplantation.


Familial or inherited conditions with a high risk for life-threatening ventricular tachyarrhythmias such as long QT syndrome or hypertrophic cardiomyopathy.


Nonsustained VT with coronary artery disease, prior MI, and LV dysfunction, and inducible sustained VT or VF at EP study.


Recurrent syncope of undetermined etiology in the presence of ventricular dysfunction and inducible ventricular arrhythmias at EP study, when other causes of syncope have been excluded.

Class 3c


    1. Syncope of undetermined cause in a patient without inducible ventricular tachyarrhythmias
  1. Incessant VT or VF


VF or VT resulting from arrhythmias amenable to surgical or catheter ablation; for example, atrial arrhythmias associated with the Wolff-Parkinson-White syndrome, right ventricular outflow tract VT, idiopathic LV tachycardia, or fascicular VT.


Ventricular tachyarrhythmias due to a transient or reversible disorder.

aEvidence and/or agreement that procedure is indicated.

bDivergence in evidence opinion that procedure is indicated.

cEvidence/agreement that procedure is not indicated or is harmful.

NOTE: EP, electrophysiology; LV, left ventricular; MI, myocardial infarction; VF, ventricular fibrillation, VT, ventricular tachycardia.

Adapted from American College of Cardiology/American Heart Association: J Am Coll Cardiol 31:1175, 1998.











The most frequent problem with the ICD has been its inappropriate discharge in the absence of sustained ventricular arrhythmias. Additional potential problems include an increase in defibrillation threshold and decrease in tachycardia rates below the rate cut-off of the device in response to many antiarrhythmic drugs. Permanently implanted ventricular pacemakers may interfere with the device's ability to sense VF. This can be avoided by using committed bipolar pacing systems that are better able to sense local ventricular activity. Diagnostic features of newer, all-in-one devices are able to identify the probable cause of an ICD discharge (e.g., AF, SVT, fractured lead) and to adjust pharmacologic therapy or reprogram the device to avoid such inappropriate shocks. These newer devices have the capability to take a "second look" prior to shock delivery and thus may abort delivery for self-terminating arrhythmias. In addition, the range of candidates suitable for implantation will be expanded because the newer devices have the capability of shock therapy for patients whose arrhythmias do not cause loss of consciousness.

Newer generations of ICDs are smaller and frequently allow placement of a second lead in the right atria. This lead senses atrial activity and provides enhanced discrimination of atrial from ventricular electrical activity. This enhanced discrimination of SVT from VT prevents inappropriate shocks for SVT that may be misinterpreted as VT and allows the device to switch from a dual-chamber to a single-chamber device should an SVT-like AF develop. These dual-chamber devices also allow AV sequential pacing. Finally, ICDs are now available that have defibrillation coils in the right atrium as well as right ventricle. These devices are suited for patients with infrequent but highly symptomatic atrial fibrillation. Patients with these atrial defibrillators can activate the device themselves and terminate their atrial fibrillation without going to the hospital.

Ablative Therapy for Arrhythmias

Catheter-based mapping techniques have provided a nonoperative approach to the identification and cure of a variety of arrhythmias. In fact, catheter ablation techniques are now the procedures of choice for symptomatic patients with (1) concealed or manifest (WPW) bypass tracts, (2) AV nodal reentrant SVT, (3) typical atrial flutter, and (4) poorly controlled ventricular responses to atrial arrhythmias, most commonly AF. Successful ablation of bypass tracts and modifications of the AV node by radiofrequency energy are extremely successful and cost-effective and are the procedure of choice for patients with recurrent episodes. The creation of AV block with implantation of a pacemaker is the method of choice in managing patients with AF and poorly controlled ventricular response. Idiopathic VTs (Fig. 230-17) and some VTs that are associated with coronary artery disease are also amenable to ablation, but the result is less successful than for ablation of SVTs.

Figure 230-17

Figure 230-17: Radiofrequency ablation of idiopathic ventricular tachycardia in a patient with prior infarction. Leads I, II, and III are shown. Ventricular tachycardia with a right bundle branch block and left axis deviation is shown in a patient with a prior inferior wall infarction. Radiofrequency applied to the site of origin terminates the tachycardia.

Surgical therapy is now relegated to cases of sustained VT associated with coronary artery disease when operative intervention is needed for coronary bypass surgery and/or aneurysmectomy or VT associated with specific structural abnormalities (e.g., idiopathic left ventricle aneurysm, s/p surgery for tetralogy of Fallot). It also may be undertaken for the unusual instances of failed catheter ablation for SVTs associated with bypass tracts.