Current Indications for Temporary and Permanent Cardiac Pacing

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Chapter 33 Current Indications for Temporary and Permanent Cardiac Pacing

In the past few decades, improvements in device technology and surgical techniques have made permanent pacemaker implantation a readily performed minor surgery with a low likelihood of major complications. Similarly, temporary pacemaker insertion can often be performed at the bedside quickly and safely with a relatively limited set of tools. Nevertheless, employing cardiac pacing in a given situation remains a major clinical decision, as it has the potential for life-altering consequences for the patient. In 2008, the American College of Cardiology, the American Heart Association, and the Heart Rhythm Society (ACC/AHA/HRS) jointly issued an updated set of guidelines for cardiac pacing on the basis of a comprehensive review of available clinical data and expert opinion.¹ This chapter refers to this document frequently and makes use of the ACC/AHA/HRS conventional division of indications into class I, class IIa, class IIb, and class III. The European Society of Cardiology separately released a set of guidelines for pacemaker implantation in 2007, making use of the same system for classifying indications.²

The ACC/AHA/HRS and ESC guidelines also classify the supportive data for each recommendation by assigning a level of evidence (LOE, see Appendix Table 33-1).* It is notable that of the 71 specific ACC/AHA/HRS recommendations relating to permanent cardiac pacing in adults, only 3 have LOE A, 29 have LOE B, and 39 have LOE C. In some instances, the lack of randomized trials reflects a broad consensus on the standard of care and the absence of alternatives to cardiac pacing for symptomatic bradycardia. In many other instances, however, particularly for class II indications, data from large clinical trials are scarce. The guidelines should, therefore, not be adhered to blindly but should be seen as a framework to assist with clinical decision making. Accordingly, the aim of this chapter is to review the indications for cardiac pacing in adults, including temporary pacing, permanent pacing, and multiple-site pacing, with special attention to clinical dilemmas and specific clinical situations. Device therapy in pediatric and adolescent patients and in patients with congenital heart disease will be reviewed separately.

Indications for Permanent Pacing

Bradyarrhythmias

Permanent pacing is most commonly employed to treat bradyarrhythmias, which can result from dysfunction of the specialized cardiac conduction system or dysfunction of the autonomic nervous system or from iatrogenesis. Therefore, the aim of this section is to provide a pathophysiologic framework for considering cardiac pacing in terms of the anatomic compartments required for normal cardiac rhythmicity.

Disorders of Sinoatrial Conduction

The functions of the sinus node are impulse generation, impulse transmission, and modulation of heart rate in response to autonomic inputs. Patients suffering from sinus node dysfunction manifest one or more of several distinct electrocardiographic abnormalities, including sinus bradycardia, sinus pauses, bradycardia alternating with tachyarrhythmias, and failure to augment heart rate appropriately with exercise (see Appendix Table 33-2). Typically, such patients will complain of lightheadedness, fatigue, syncope, or activity intolerance. The main diagnostic tool for establishing the diagnosis of sinus node dysfunction is continuous ambulatory electrocardiographic monitoring for a period determined by the frequency of the patient’s symptoms.

No randomized trials demonstrating that pacing improves survival in patients with sinus node dysfunction have been conducted, and at least one small series suggests that short-term prognosis is good in this patient population.³ Thus, the primary role for pacing is to treat symptoms, prevent adverse events such as syncope, and permit therapy with drugs that slow heart rate, as required to treat other medical conditions. Before considering pacemaker implantation, reversible causes of sinus node dysfunction should be ruled out (Table 33-1). The indications for permanent pacing in sinus node dysfunction are summarized in Appendix Table 33-3. When sinus pauses or bradycardia coincide temporally with the patient’s symptoms and a causal link can be established, a pacemaker is indicated; this is a class I indication. Conversely, when the patient’s typical symptoms occur during periods when monitoring reveals a normal heart rate, pacemaker implantation would not be expected to provide any benefit; this is, therefore, a class III indication.

Table 33-1 Reversible Causes of Sinus Bradycardia and Atrioventricular Block

TYPE OF CAUSE	SPECIFIC CAUSE
Cardiac	Myocardial ischemia
	Viral myocarditis
	Lyme disease
	Rheumatic fever
	Endocarditis
	Post–cardiac surgery
	Post–cardiac transplant
	Athletic training
Autonomic nervous system	Neurocardiogenic syncope
	Carotid hypersensitivity
	Vagal stimulation
Drugs and medications	β-Adrenergic blockers
	Calcium channel blockers
	Clonidine
	Digitalis
	Ivabradine
	Reserpine, methyldopa
	Class IA antiarrhythmic drugs
	Class IC antiarrhythmic drugs
	Class III antiarrhythmic drugs
	General anesthetics
	Tricyclic antidepressants
	Phenothiazines
	Lithium
	Phenytoin
	Cholinesterase inhibitors
Hypothermia
Hypothyroidism
Neurologic	Elevated intracranial pressure
	Spinal cord injury
Electrolyte imbalances	Hypokalemia
	Hyperkalemia
	Hypercalcemia
Pulmonary	Obstructive sleep apnea
	Prolonged hypoxia

It should be emphasized that when the vagal tone is high, particularly during sleep, episodes of sinus bradycardia are common in healthy individuals. Thus, in inpatients or outpatients with cardiac monitors, pauses and periods of slow heart rate are frequently seen and can be of uncertain clinical significance. Similarly, symptoms of lightheadedness, syncope, and activity intolerance are not specific and can occur for a number of reasons. Thus, the decision to implant a pacemaker in a patient with evidence of sinus bradycardia and suggestive symptoms but without a clear causal link can be a difficult one. In such situations, we favor a thorough workup for other cardiac and noncardiac causes of the patient’s symptoms. Particularly in older adults, we have found that polypharmacy is an often-overlooked cause for lightheadedness and syncope and should be ruled out before pacemaker implantation is considered. When no other cause can be identified, pacemaker implantation is a class IIa indication. Such patients should be advised that when a causal link has not been established between bradycardia and their symptoms, a pacemaker might not provide any benefit.

In patients with suspected sinus node dysfunction, particularly in those manifesting some degree of activity intolerance, exercise testing can be a very helpful adjunctive assessment of sinus node function. Chronotropic incompetence is often defined as failure to achieve a heart rate of 80% of age-adjusted maximum predicted heart rate with exercise.⁴ However, the critical issue in such cases is whether heart rate is sufficient to meet physiologic demands. The clinician should, therefore, not place too much importance on the specific rate achieved but should determine whether sinus node function is the main factor limiting the patient’s ability to exercise. Where this is the case, pacemaker implantation is warranted; this is a class I indication, even when heart rate is normal at rest and sinus pauses are not identified on monitoring.

The usefulness of invasive electrophysiology testing in determining the need to implant a pacemaker is limited, primarily because abnormalities in electrophysiologic parameters are not, in general, predictive of clinical events. Nevertheless, for patients with syncope who are undergoing electrophysiology testing and in whom other causes have not been identified, profound abnormalities of sinus node function may tip the balance of considerations in favor of pacemaker implantation; this is a class IIa indication.

Finally, a clinical situation frequently encountered is evidence of sinus node dysfunction manifested by sinus pauses or resting bradycardia in the absence of symptoms. At present, data suggesting that implantation of a pacemaker in such patients prevents adverse events or prolongs life are not available. Pacemaker implantation in the asymptomatic patient with sinus node dysfunction is therefore not recommended (class III). However, when sinus node dysfunction is marked (resting heart rate persistently less than 40 beats/min while awake), the ACC/AHA/HRS guidelines do recognize a class IIb indication for pacing in those who are at least minimally symptomatic. Often, a simple exercise test is sufficient in these patients to establish whether clinically significant sinus node dysfunction is present. However, in patients who cannot exercise because of comorbidities, pacemaker implantation can be considered.

Disorders of Atrioventricular Conduction

The function of the atrioventricular (AV) node is to delay impulse propagation from atria to ventricles to the extent necessary to optimize ventricular filling. This delay varies physiologically over a large range and is heavily influenced by autonomic tone and heart rate. The function of the bundle of His, which passes from the AV node to the ventricle through the central fibrous body, is to transmit the electrical impulse rapidly from the atrium to the ventricle. Conduction time through the bundle of His is rapid and does not vary with heart rate under normal conditions. Conduction slowing or block can occur in the AV node, the bundle of His, or both, and characteristic electrocardiogram (ECG) patterns are present, as well as differences in prognosis, depending on the location and severity of the block. In general, when the block is above the level of the His bundle (supra-His), prognosis for progression to a high-grade block is better than when the block is at or below the level of the His bundle (intra-His or infra-His).⁵ Symptoms caused by an AV block can include fatigue, lightheadedness, and syncope; a persistent high-grade AV block can result in heart failure caused by bradycardia and loss of AV synchrony and can predispose to ventricular arrhythmias.

First-Degree Atrioventricular Block

First-Degree AV block is defined as P-R interval exceeding 0.2 seconds and is often reflective of incipient AV nodal disease, though it can be a normal finding in patients at rest with high vagal tone. Recent data from the Framingham cohort suggest that in the long term, patients with first-degree AV block have a significantly higher risk of requiring pacemaker implantation and have a higher mortality rate.⁶ However, with a few exceptions (discussed below), the short-term prognosis for those with isolated first-degree AV block is excellent, so pacemaker implantation is, in general, not indicated in asymptomatic patients as a prophylactic measure (class III). However, a few indications for pacing are recognized for first-degree AV block (summarized in Appendix Table 33-4).

Some patients with marked first-degree AV block (P-R interval >0.3 seconds) have symptoms that may warrant pacemaker implantation.⁷ In these patients, ventricular activation is so delayed that the subsequent atrial activation occurs shortly after the QRS complex on the surface ECG, resulting in atrial contraction against closed AV valves (Figure 33-1). Patients with severe left ventricular dysfunction and markedly prolonged P-R intervals may experience hemodynamic compromise caused by impaired ventricular filling and diastolic AV valvular regurgitation.⁸ Often, reducing the dosages of AV nodal blocking medications in these patients can shorten the P-R interval and improve symptoms. Where this is not possible, restoration of AV synchrony with dual-chamber pacing and a normal AV delay can solve the problem, and this is a class IIa indication. However, ventricular pacing under these circumstances carries with it the potential deleterious effects of intraventricular dyssynchrony, so consideration should be given to biventricular pacing in such instances, especially when left ventricular function is not normal (see below).

FIGURE 33-1 Twelve-lead electrocardiogram showing sinus rhythm with a prolonged P-R interval of 400 ms. This can lead to symptoms caused by atrioventricular dyssynchrony that improve after implantation of a dual-chamber pacemaker.

Finally, patients with several neuromuscular diseases (see Appendix Table 33-5) often have rapidly progressive AV conduction system disease. Even in asymptomatic patients with these disorders, marked first-degree AV block should prompt consideration of pacemaker implantation as a prophylactic measure.

Type I Second-Degree Atrioventricular Block

Second-degree AV block is divided into type I and type II on the basis of the ECG pattern. In type I, the P-R interval lengthens before the nonconducted beat and shortens on the first beat after the nonconducted beat (Wenckebach conduction); in type II, the P-R interval is fixed. In general, type I second-degree AV block suggests a supra-His level of block and is associated with a more benign prognosis, while type II occurs with intra-His or infra-His conduction system disease and has a higher rate of progression to complete heart block.⁵ It should be remembered that in pathologic conditions, it is possible for any component of the conduction system, even the structures below the AV node, to exhibit Wenckebach conduction. Thus, type I second-degree AV block has a benign prognosis only when it is caused by supra-His block, which is usually the case when the QRS is narrow.

Regardless of the level of block, patients with symptomatic bradycardia resulting from second-degree AV block from irreversible causes or essential drug therapy should undergo permanent pacemaker implantation (class I). In the setting of high vagal tone such as sleep or in highly conditioned athletes at rest, type I second-degree AV block is frequently observed and is a normal finding.⁹ For asymptomatic patients, pacemaker implantation is therefore not recommended (class III). However, as with first-degree AV block, patients with type I second-degree AV block can have symptoms caused by loss of AV synchrony, and pacemaker implantation should be considered for this indication (class IIa) as well as for symptomatic bradycardia. Indications for pacing in type I second-degree AV block are summarized in Appendix Table 33-4.

High-Grade Atrioventricular Block

Patients with type II second-degree AV block (Figure 33-2) have a higher rate of progression to third-degree AV block, particularly in the setting of intraventricular conduction abnormalities. From the point of view of cardiac pacing, advanced second-degree AV block and third-degree AV block should be grouped together in a single high-risk category, and pacemaker implantation is the only reasonable treatment when reversible causes cannot be identified (see Appendix Table 33-6). Randomized clinical trials comparing pacing with conservative management are not available, but considerable nonrandomized evidence exists that pacing for patients with high-grade AV block results in a prolongation of life and reduction in morbidity.¹⁰

FIGURE 33-2 Rhythm strip showing 2 : 1 atrioventricular conduction on the left associated with a faster sinus rate and 1 : 1 AV conduction on the right with slower sinus rate. This is diagnostic of a Mobitz type II infra-His block and is an indication for permanent pacemaker implantation.

Third-degree AV block and consequent AV dissociation are almost always symptomatic, though the symptoms can vary in severity from mild dizziness and exercise intolerance to syncope or even sudden death, depending on the rate of the escape rhythm. In addition to medications that affect AV nodal conduction, a number of reversible causes of high-grade AV block, including myocardial ischemia, exist, and these should be ruled out before considering permanent pacing (see Table 33-1). Often, a careful history and an ECG are sufficient to rule out reversible causes of complete heart block, but where uncertainty remains, it is appropriate to perform further diagnostic testing. Brief periods of third-degree heart block can occur in situations of high vagal tone; where these are transient or occur exclusively in sleep and are accompanied by adequate escape rhythms, pacemaker implantation is not always warranted.

Advanced second-degree and third-degree AV block can be paroxysmal, with long intervening periods of 1 : 1 AV conduction, or can occur exclusively with exercise. When such paroxysmal heart block cannot be attributed to reversible causes, pacemaker implantation is a class I indication in almost all clinical situations, even in asymptomatic patients in the presence of pauses longer than 3 seconds, escape rate less than 40 beats/min, escape rhythm that originates below the AV node, cardiomegaly, or left ventricular dysfunction. In asymptomatic patients with third-degree heart block, normal cardiac size and function, and an escape rate longer than 40 beats/min, permanent pacemaker implantation is a class IIa indication.

AV block can be difficult to diagnose in the setting of atrial fibrillation. However, a slow regular escape rhythm in atrial fibrillation suggests the presence of high-grade AV block, as do long pauses. When symptoms caused by bradycardia are present, pacemaker implantation is warranted (class I). When pauses in atrial fibrillation exceed 5 seconds, pacemaker implantation is a class IIa indication.

Disorders of Intraventricular Conduction

The functions of the distal limbs of the conduction system (bundle branches, fascicles, and Purkinje fibers) are to transmit the electrical impulse rapidly to ventricular muscle and to ensure coordinated activation of the ventricles. The bundle of His bifurcates into the right bundle branch and the left bundle branch at the crest of the interventricular septum. Bundle branches then ramify into complex networks of specialized conduction fibers, known as fascicles. On the left, this complex fascicular system is conventionally divided into the left anterior fascicle and the left posterior fascicle. Dysfunction and failure of impulse transmission can occur in any combination of these bundles and fascicles, with or without superimposed AV block, leading to a variety of intraventricular conduction disturbances. Cardiac pacing has a role in a subset of patients with intraventricular conduction system disease (see Appendix Table 33-7).

Hemiblocks and Bundle Branch Block

Individuals without conduction system disease may develop bundle branch block or fascicular block at very high heart rates, during tachyarrhythmias, or, less commonly, at very low heart rates (phase 4 aberrancy). Also, a small percentage of normal healthy individuals have right or left bundle branch block as a congenital variant. In general, block of a single fascicle (right bundle branch block, left anterior hemiblock, or left posterior hemiblock), with or without accompanying first-degree AV block, does not warrant consideration of pacemaker implantation without evidence of high-grade AV block.¹¹ The only major exceptions to this rule are patients with selected neuromuscular diseases, in whom any fascicular block may warrant consideration of pacemaker implantation because of the unpredictable nature of disease progression (class IIb).

Although complete left bundle branch block can be seen in the presence of disease of both the anterior and posterior fascicular systems (particularly in the setting of a large myocardial infarction), it more commonly results from a proximal lesion in the conduction system and should not be grouped with bifascicular blocks. If a patient presents with bundle branch block with left-axis, first-degree AV block and syncope, it may be reasonable to assess intraventricular conduction with an invasive electrophysiology study. An H-V interval less than 0.1 seconds or the finding of pathologic infra-His block with pacing may warrant consideration of pacemaker implantation.¹²

When complete left bundle branch block alternates with right bundle branch block, it suggests the presence of severe, widespread infra-His conduction system disease. The same is true when right bundle branch block with left anterior hemiblock alternates with right bundle branch block with left posterior hemiblock. Whether this alternation occurs within a single ECG or rhythm strip, or on successive ECGs recorded on separate days, this condition carries a high risk for progression to complete heart block and is a class I indication for pacemaker implantation, even in the absence of symptoms (Figure 33-3).

FIGURE 33-3 A, Twelve-lead electrocardiogram (ECG) showing sinus rhythm with left bundle branch block. B, Twelve-lead ECG in the same patient when he presented with syncope. The ECG shows right bundle branch block. Alternating bundle branch block signifies significant infra-His disease and is an indication for pacemaker implantation.

Chronic Bifascicular Block

Chronic bifascicular block is present with involvement of one of the left-sided fascicles plus the right bundle branch. Trifascicular block is a somewhat confusing term often used to refer to bifascicular block in the presence of first-degree AV block. The prognostic significance of bifascicular blocks varies according to the site of the block and the presence or absence of other forms of heart disease. With a few important exceptions (detailed below), the annual rate of progression to complete heart block in the asymptomatic patient is low, even though most patients who develop third-degree AV block have bifascicular block at some point.¹³ When bifascicular block is accompanied (even transiently) by type II second-degree AV block, advanced second-degree AV block, or third-degree AV block, a high risk of progression to complete heart block is present, and pacemaker implantation is warranted whether or not symptoms are present (class I).

Syncope should prompt a thorough evaluation in patients with infra-His conduction system disease manifested by bifascicular block or trifascicular block.

When noncardiac causes have been excluded, it is important to consider ventricular tachycardia as a cause of syncope, especially when mild-to-moderate left ventricular dysfunction is present. When such patients are candidates for implantable cardioverter defibrillator (ICD) implantation, dual-chamber devices should be favored in the presence of infra-His conduction system disease to ensure AV synchrony in the event of paroxysmal AV block.

Occasionally, asymptomatic patients with infra-His conduction system disease are taken to the electrophysiology lab for other reasons. A prolonged H-V interval (<0.1 seconds) or the finding of nonphysiologic pacing-induced infra-His block warrant consideration of pacemaker implantation in these patients, even if they are asymptomatic (class IIa).

Disorders of the Autonomic Nervous System

The cardiovascular system, and the sinoatrial (SA) node and AV node within the heart, are richly innervated with parasympathetic and sympathetic fibers. Particular forms of autonomic nervous system dysfunction can cause symptomatic bradycardia, which, in some cases, can be responsive to cardiac pacing (see Appendix Table 33-8).

Carotid Sinus Hypersensitivity

Carotid sinus hypersensitivity occurs in patients in whom mechanical stimulation of the carotid body in the neck causes a vagal discharge that results in bradycardia. In some patients, asystole and syncope can ensue. For patients with recurrent syncope associated with carotid sinus stimulation and less than 3 seconds of ventricular asystole on carotid sinus pressure, permanent pacing is indicated (class I). When carotid sinus hypersensitivity is present with syncope, but the syncope is not clearly precipitated by carotid stimulation or any other identifiable cause, pacemaker implantation is a reasonable consideration (class IIa). However, in the absence of syncope, pacemaker implantation is not indicated for carotid hypersensitivity, even when vague symptoms such as dizziness or lightheadedness coincide with carotid stimulation (class III).

Neurocardiogenic Syncope

Neurocardiogenic syncope, also known as vasovagal syndrome, results from a pathologic cardiovascular reflex, in which the final common pathway diverges into a peripheral vasodepressor response and a cardioinhibitory response. The vasodepressor response consists of an abrupt decrease in peripheral vascular resistance caused by withdrawal of sympathetic tone, resulting in hypotension and associated symptoms. The cardioinhibitory response involves sinus bradycardia (and occasionally sinus arrest) with or without AV block caused by vagal stimulation of SA and AV nodes. Patients with severe cardioinhibitory response can have asystole anywhere from seconds up to a minute.

A typical history for vasovagal syncope includes a prodrome of malaise with nausea or lightheadedness preceding syncope. Symptoms can be triggered by emotional stress, physiologic stress of any kind, volume depletion, abrupt postural changes, and vagal stimuli such as micturition, defecation, or coughing. Tilt-table testing provides a useful way to classify these patients into those having a predominantly vasodepressor response and those having a predominantly cardioinhibitory response. Classifying patients in this way is essential before any consideration of pacemaker implantation, as patients with predominantly vasodepressor response will not respond to cardiac pacing.

Even in patients with some degree of cardioinhibition, SA nodal and AV nodal functions are typically normal, so cardiac pacing is not first-line therapy. The large, randomized, placebo-controlled Vasovagal Pacemaker Study II (VPS-II) has been performed to test pacing in neurocardiogenic syncope.¹⁴ The results showed no aggregate benefit to pacing in general, though it may be reasonable to use pacing in certain subpopulations (patients with prolonged asystole, minimal prodrome, or no response to other treatments). For patients with symptomatic documented cardioinhibition either on tilt-table testing or spontaneously, a class IIb indication for permanent pacing is present, if the bradycardia is refractory to lifestyle changes and maneuvers. For patients in high-risk occupations (transportation, construction, operation of heavy machinery) or for those with prolonged periods of asystole (<5 seconds), pacemaker implantation may be the safest course. However, these patients should be cautioned that pacing will not prevent attacks and may not be sufficient to abort the attacks once they are in progress. The main role for pacing in these situations is to blunt the severity of the episodes, and in some cases, when minimal prodromal symptoms are present, pacing can provide additional time for the patient to undertake abortive maneuvers.

Iatrogenic Bradycardia

Bradycardia can result from a variety of iatrogenic causes, most commonly from medications but also from cardiac procedures and cardiac surgery.

Medications

All patients presenting with symptomatic bradycardia should be thoroughly questioned about medication use, and, where possible, medications that cause bradycardia should be discontinued. Commonly prescribed classes of medications that can cause bradycardia are listed in Table 33-1. In many instances, these medications may have strong indications (for example, β-blockers in patients with coronary artery disease). It may, therefore, be necessary to implant a permanent pacemaker, which will help continue therapy with essential medications (class I). The risks of pacemaker implantation should be carefully weighed against the risk of discontinuing the medication in question, and pacemaker implantation should only be undertaken when the risk/benefit profile is favorable. In this context, it should be emphasized that clinically relevant doses of AV nodal blocking agents commonly unmask pre-existing AV nodal disease but typically do not cause AV block in patients with otherwise normal conduction. In one series, while 41% of patients with high-grade AV block experienced short-term resolution with cessation of nodal blocking drugs,¹⁵ more than half these patients subsequently experienced recurrence of high-grade AV block off the medication. Only about 15% of patients with high-grade AV block while on nodal agents had lasting resolution of AV block with cessation of drug therapy. Thus, it is important to monitor closely even those patients with short-term resolution of AV block after cessation of nodal agents, as the majority of these individuals will eventually need pacemaker implantation.

Procedures and Surgeries

The AV conduction axis can sustain significant damage during cardiac surgery, particularly aortic and mitral valve surgery, and temporary pacing is often necessary post-operatively.¹⁶ When AV conduction does not recover after a reasonable period (we typically wait 7 days), a permanent pacemaker should be implanted (class I).^17,¹⁸

Catheter ablation of the AV junction with pacemaker implantation is frequently used to treat rapid atrial fibrillation that is refractory to medical therapy. These patients should always receive a permanent pacemaker (class I) regardless of the level and rate of the escape rhythm. In general, we favor pacemaker implantation at least 3 to 4 weeks before AV junction (AVJ) ablation to minimize the risk of lead dislodgment during catheter ablation. Because these patients are dependent on ventricular pacing, consideration should be given to biventricular pacing after AVJ ablation, to minimize the deleterious effects of right ventricular (RV) apical pacing in those who are susceptible (typically patients with left ventricular ejection fraction [LVEF] <45%) and to provide a backup pacing system in the event of malfunction of a pacing lead.

Patients who develop unintended third-degree or high-grade AV block caused by catheter ablation for AV nodal re-entrant tachycardia or accessory pathway ablation should undergo permanent pacemaker implantation. Because nodal function can recover in these patients, it may be reasonable to delay pacemaker implantation, if necessary, with use of temporary pacing, until it is clear that the loss of AV nodal function is permanent. Rarely, the patient with ventricular pre-excitation undergoes a catheter ablation procedure that disrupts AV nodal conduction without affecting the accessory pathway. The patient is then dependent on accessory pathway conduction for the transmission of the impulse from the atrium to the ventricle. In this circumstance, antegrade conduction over the accessory pathway should be assessed with exercise testing or with pacing in the electrophysiology laboratory to make sure that the conduction is robust over a physiologic range of heart rates. Pacemaker implantation should be considered if accessory pathway conduction is not robust, if accessory pathway function decreases over time, or if accessory pathway ablation becomes necessary, leaving the patient without a functional AV communication.

Tachyarrhythmias

Although medications, catheter ablation, and ICD implantation are the primarily modalities for treating tachyarrhythmias, cardiac pacing does have a role in certain circumstances, both for termination of supraventricular tachyarrhythmias and for prevention of triggered ventricular arrhythmias (see Appendix Table 33-9). Although pacing is used in the automatic detection and termination of ventricular tachycardia, pacing systems with this capacity should also have the ability to defibrillate in the event that pacing accelerates the rhythm or causes degeneration into ventricular fibrillation. Pacemakers without ICD function should therefore not be implanted for detection and termination of ventricular tachycardia.

Termination of Supraventricular Tachyarrhythmias

In the treatment of recurrent, symptomatic supraventricular tachycardia (SVT) that cannot be controlled with catheter ablation or medications, cardiac pacing has a role. When pacing reproducibly terminates the arrhythmia and arrhythmia detection is reliable, it is reasonable to implant a pacemaker (class IIa), even in the absence of conduction system dysfunction or any other indication for cardiac pacing. Because overdrive pacing of SVT can occasionally result in atrial fibrillation (especially at shorter cycle lengths), patients with accessory pathways that can conduct rapidly in the antegrade direction should not receive anti-tachycardia pacing (class III) because of the risk of causing pre-excited atrial fibrillation that degenerates into ventricular fibrillation.

Prevention of Ventricular Tachyarrhythmias

In vulnerable patients, slow heart rates cause increased dispersion of ventricular repolarization and predispose to pause-dependent polymorphic ventricular tachyarrythmias (VTs; torsades de pointes). A typical initiation begins with a pause, followed by a beat in which repolarization is prolonged, and a tightly coupled premature ventricular depolarization that starts a run of polymorphic VT. In situations where VT is clearly pause dependent and sustained and is not related to a reversible cause, pacemaker implantation is warranted, regardless of the Q-T interval (class I), particularly if the resting heart rate is slow. In patients with congenital long QT syndrome (LQTS) that is high risk by genotype or family history, pacing is warranted to minimize the risk of VT (class IIa). Often, such patients will also have an indication for a defibrillator, so ICD implantation may be preferred to implantation of only a pacemaker.

Multiple-Site Pacing

Multiple-site pacing has emerged in the past decade as a novel approach to optimizing electrical and mechanical synchrony. In selected patients with heart failure caused by systolic dysfunction and intraventricular conduction disturbances, biventricular pacing can dramatically improve symptoms and decrease mortality. Multiple-site atrial pacing to improve atrial function and reduce atrial fibrillation has also been explored, but a role for this modality has yet to be established with large clinical trials.

Biventricular Pacing in Heart Failure

Dyssynchronous ventricular contraction caused by abnormal ventricular activation can be deleterious. Many patients with heart failure caused by left ventricular (LV) systolic dysfunction have broad QRS intervals arising from the involvement of the intraventricular conduction system, and some have a broad QRS intervals in the setting of frequent RV apical pacing. Two landmark clinical trials, Comparison of Medical Therapy, Pacing, Defibrillation in Chronic Heart Failure (COMPANION) and Cardiac Resynchronization-Heart Failure trial (CARE-HF), have established a role for biventricular pacing or cardiac resynchronization therapy (CRT) in selected patients with heart failure with reduced ejection fraction, both for reduction of symptoms and reduction in mortality.^19,²⁰ These studies included patients with LVEF 35% or less and QRS interval less than 0.12 seconds regardless of the type of intraventricular conduction abnormality. Thus far, the guidelines have focused on patients with New York Heart Association (NYHA) class III and ambulatory class IV symptoms who are already on recommended medical therapy. The importance of ensuring that patients with heart failure are on medical therapy cannot be overemphasized, as patients can move from NYHA class III/IV to class I on medications alone, and the ejection fraction can improve significantly. Among these patients, biventricular device implantation for restoration of mechanical synchrony is a class I indication for those in sinus rhythm and class IIa for those in atrial fibrillation or who depend on ventricular pacing. Although the guidelines do not describe an indication for patients with NYHA class IV symptoms who depend on positive inotropes or are nonambulatory, we have occasionally found that such patients can benefit dramatically from CRT, to the point of weaning the patients off inotropes so that the patients can leave the hospital.^19,²¹

Recently, results from the Multicenter Automatic Defibrillator Implantation Trial-Cardiac Resynchronization Therapy (MADIT-CRT) trial ²² have shown that with biventricular ICD implantation, a significant reduction occurs in mortality rates and hospitalizations for heart failure, even in NYHA class I/II patients, which has raised the possibility of a considerable expansion in the indications for CRT.¹⁹ At the time of the writing of this chapter, these data did not yet affect clinical practice but are likely to have a major impact in the near future. As for now, the 2008 ACC/AHA/HRS guidelines recognize a class IIb indication for patients with LVEF less than 35% and NYHA class I or II heart failure when pacemaker implantation is planned for other indications and frequent ventricular pacing is expected.

Multiple-Site Atrial Pacing

Atrial fibrillation is often caused by fibrosis and electrical remodeling in atria, with or without chamber enlargement. Patients with atrial fibrillation may therefore manifest intra-atrial conduction delay (broad P waves), which can serve as a substrate for re-entry as well as for frequent atrial ectopy that can trigger atrial fibrillation. Synchronous atrial activation may reduce the potential for repolarization inhomogeneity, as well as for triggered premature atrial depolarizations, and thereby reduce the frequency of episodes of atrial fibrillation.

A number of small clinical series and one moderate-sized randomized trial have been performed to evaluate the potential for multiple-site atrial pacing to reduce atrial fibrillation. Thus far, with the possible exception of patients with marked intra-atrial conduction delay that manifests as surface P-wave duration less than 0.18 seconds, no benefit in terms of symptoms, reduction in atrial fibrillation, or adverse cardiac events have been reported.²³ Therefore, no recognized indication for pacing to prevent atrial fibrillation in patients without any other indication for permanent pacing (class III) exists at present.

Permanent Pacing in Specific Clinical Situations

Some randomized clinical trials have demonstrated subjective improvement in symptoms as well as in physiologic endpoints, but others have shown no overall improvement in the quality of life or any alteration in the course of the disease.^24,²⁵ Patients with hypertensive hypertrophic cardiomyopathy and older adults may be subpopulations that derive more benefit, whereas pacing is more difficult in those with rapid atrial rates or brisk AV nodal conduction. Overall, data are inconclusive but certainly do not support the idea of routine pacing in these patients. However, the guidelines do recognize a class IIb indication for medically refractory symptomatic hypertrophic cardiomyopathy with resting or provoked outflow tract obstruction (Appendix Table 33-11). Asymptomatic patients, those with symptoms that are medically controlled, and those with symptoms but no documented outflow tract obstruction are not candidates for pacing (class III).

After Cardiac Transplantation

Patients who have undergone cardiac transplantation often experience sinus bradycardia, particularly in the immediate post-transplant period. Slower atrial rates and chronotropic incompetence can negatively impact the cardiac rehabilitation process and significantly delay hospital discharge. When this bradycardia is not expected to resolve, permanent pacing is a class I indication. Even when some resolution in bradycardia is expected over several months to a year, permanent pacing can be considered if the post-transplant recovery process is limited by bradycardia (class IIb).

Patients who have received transplants are also vulnerable to coronary vasculopathy, which frequently manifests as conduction system dysfunction.^26,²⁷ Therefore, after transplantation, pacemaker implantation can be considered in patients with recurrent syncope of undetermined cause, even without clear evidence of bradyarrhythmia (class IIb). Conduction system dysfunction can also be evident in acute rejection. While comprehensive data are not available on the long-term prognosis of patients with bradyarrhythmias and syncope in the setting of rejection, it is reasonable to consider permanent pacing if the bradyarrhythmia is persistent, even after the rejection has been controlled (Appendix Table 33-12).

Indications for Temporary Pacing

Temporary cardiac pacing can be a life-saving treatment in many clinical situations, but it also poses some risk for serious complications. In this section, we briefly review the modalities available for temporary pacing, followed by the major indications for temporary pacing.

Temporary Pacing Modalities

Temporary cardiac pacing can be achieved with any of several modalities (see Table 33-2). Precordial percussion can result in ventricular systoles in the setting of an asystolic arrest and can be used until transcutaneous electrodes can be placed. In general, given its morbidity, transcutaneous pacing should be reserved for emergent situations and ideally in unconscious or sedated patients.^28,²⁹ Esophageal pacing is similarly morbid and often requires relatively large amounts of current delivery for ventricular capture. It is seldom used in adult patients but may have a role in infants and children for the diagnosis and pace termination of atrial arrhythmias. Epicardial lead placement is usually performed as a prophylactic measure against bradycardia after cardiac surgery. It is common for inflammation to occur around the epicardial pacing leads, which results in a rise in pacing threshold and ultimately failure of the pacing system.³⁰

Table 33-2 Modalities for Temporary Pacing

Patients requiring sustained temporary pacing should, in general, have transvenous pacing systems placed to reduce morbidity and achieve more reliable pacing. Given the risk of infection, cardiac perforation, and more commonly, lead migration and failure, temporary transvenous pacemakers should be used for as short a period as possible. Patients with temporary transvenous pacing systems should be on bedrest under continuous monitoring, preferably in an intensive care unit (ICU), and should have daily threshold testing and imaging with chest radiography to confirm the appropriate positioning and functioning of the pacing lead.

Asystole

Pacing is part of the advanced cardiac life support algorithm for asystole and should be initiated promptly on identification of ventricular asystole. Care should be taken to distinguish asystole from fine ventricular fibrillation, as pacing has no role in treating the latter rhythm. Because asystolic cardiac arrest is not usually caused by primary conduction system dysfunction, pacing often is of limited value; nonetheless, it should be undertaken as indicated in the algorithm. In general, the prognosis for asystolic cardiac arrest is poor.

Acute Myocardial Infarction

A variety of conduction disturbances can occur during acute MI, and any component of the conduction system can be involved. The ACC/AHA guidelines on the management of acute MI contain a section on the indications for temporary pacemaker insertion based on the prognostic significance of various bradyarrhythmias in the setting of acute MI.³¹

Sinus bradycardia alone should not, in general, prompt temporary pacemaker insertion for prophylactic purposes. If the bradycardia potentiates ischemia or causes heart failure or hypotension and is not responsive to vagolytic agents such as atropine, then temporary pacing is indicated. In general, given the potential for increasing myocardial oxygen demand and worsening infarction with the administration of chronotropic agents such as isoproterenol or other β-adrenergic agents, pacing is preferable. First-degree AV block and type I second-degree AV block during MI occur in a substantial number of patients (particularly, in those with inferior MI), and as with sinus bradycardia, neither should prompt pacemaker insertion for prophylaxis of high-grade AV block when a narrow QRS complex is present (class III). It is reasonable to consider pacemaker implantation in high-grade AV block (type II second-degree AV block or third-degree AV block) with a narrow QRS interval, though many of these patients will have an adequate escape rhythm.

The development of new intraventricular conduction abnormalities in acute MI, particularly in conjunction with an anterior MI, is ominous and portends a worse prognosis in terms of the infarct size, hemodynamics, and the development of a complete heart block. A simple risk score (Table 33-3) has been devised to stratify patients and identify the development of a complete heart block in the setting of an acute MI.³² Temporary pacemaker placement should be considered for patients at a moderate-to-high risk of progression to complete heart block, even without symptoms or hemodynamic compromise. These include patients with pre-existing intraventricular conduction system disease with new AV block and patients with new intraventricular conduction system disease (see Appendix Table 33-13). It should be emphasized that these guidelines are distinct from those governing the indications for permanent pacing after the acute phase of MI. Many patients will need pacing only for the acute phase, particularly after successful revascularization.

Table 33-3 Risk Score for Prediction of High-Grade Atrioventricular Block in Acute Myocardial Infarction

ABNORMALITY	POINTS
First-degree AV block	1
Type I second-degree AV block	1
Type II second-degree AV block	1
LAFB or LPFB	1
RBBB or LBBB	1

TOTAL SORE	RISK OF COMPLETE HEART BLOCK
0	1.2%
1	7.8%
2	25%
3	36.4%

AV, Atrioventricular; LAFB, left anterior fascicular block; LPFB, left posterior fascicular block; RBBB, right bundle branch block; LBBB, left bundle branch block.

Modified from Lamas GA, Muller JE, Turi ZG, et al: A simplified method to predict occurrence of complete heart block during acute myocardial infarction, Am J Cardiol 57:1213–1219, 1986.

Bradyarrhythmias

In patients with significant bradycardia accompanied by symptoms of cerebral hypoperfusion, hemodynamic compromise, heart failure, or cardiac ischemia is present and in whom chronotropic agents are either ineffective or contraindicated, temporary pacemaker insertion should be considered. Often, such patients will ultimately require permanent pacemaker implantation, but necessary cardiac pacing should not be delayed while the workup for the cause of bradycardia is under way. Many reversible causes of bradycardia and conduction system abnormalities exist (see Table 33-1), and temporary pacing can be invaluable while the appropriate diagnostic testing is performed. Temporary pacing may also be required for pacemaker-dependent patients who require lead or device revision, with an obligatory delay between explantation of an old device and implantation of a new device (for example, in pacemaker lead infection).

Some patients presenting with high-grade AV block, either persistent or paroxysmal, have minimal symptoms at rest and are not hemodynamically compromised. The question thus arises whether all of these patients should receive temporary pacing. As a general rule, the location and rate of the escape rhythm are the critical determining factors in these situations. Patients may have persistent complete heart block with a supra-His escape rhythm of 50 to 60 beats/min, normal blood pressure, and minimal symptoms at rest. These patients should be on bedrest with transcutaneous pacing available at the bedside, but temporary pacemaker placement is not necessarily warranted. However, patients with even brief paroxysms of high-grade AV block with an inadequate escape rhythm, wide QRS escape rhythm, or with evidence of intra-His or infra-His conduction system disease should undergo temporary pacemaker insertion, given the unpredictable and often sudden nature of a paroxysmal AV block.

Tachyarrhythmias

In patients with bradycardia-dependent ventricular tachycardia, temporary pacing can be a life-saving treatment. Particularly in acquired LQTS, when changes in repolarization are often caused by the transient effects of drugs, temporary pacing at rates between 85 and 100 beats/min can be very effective in preventing polymorphic ventricular tachycardia until the high-risk period has passed.

Patients with refractory tachyarrhythmias who do not respond to medications may respond to overdrive pacing. Given the risks of temporary pacemaker insertion, this strategy should be undertaken only in the persistently symptomatic patient after a failure of medical therapy and when electrical cardioversion is not desirable. Atrial flutter can often be readily terminated with this strategy. Overdrive pacing of VT can result in the acceleration of the rhythm as well as ventricular fibrillation, so this maneuver should only be undertaken in an intensive care setting, where the care team will be ready for emergent defibrillation should it become necessary. The same principle applies for any SVT when ventricular pre-excitation is present.

Some evidence suggests that after cardiac surgery, atrial pacing can result in a lower incidence of postoperative atrial fibrillation. While this is not a sufficient reason to place a temporary transvenous pacing system, it may be reasonable to use a dual-chamber strategy in patients who receive epicardial pacing systems at the time of surgery.

Temporary Pacing for Hemodynamic Indications

Patients with severe LV dysfunction who are hospitalized with rest symptoms or hemodynamic compromise can sometimes benefit from pacing. When ventricular filling is impaired because of marked first-degree AV block or type I second-degree AV block, a trial of temporary dual-chamber pacing may be beneficial. When the QRS interval is prolonged, a trial of biventricular pacing with a temporary system can sometime help determine whether a permanent biventricular system should be implanted.

Periprocedural Pacing

Patients undergoing noncardiac surgery often present with chronic conduction disturbances. In the vast majority of instances, temporary pacing is not necessary. General anesthesia is safe in patients with chronic asymptomatic sinus bradycardia, first-degree AV block, type I second-degree AV block with normal QRS, and bifascicular block, with a very low rate of high-grade intraprocedural AV block. The main exceptions to this rule are patients who present for surgery with complete heart block, high-grade second-degree AV block, or with any symptomatic bradyarrhythmia. If surgery is urgent, temporary pacemaker implantation can be considered in these patients. Elective surgery should be deferred in this situation to permit further diagnostic testing and treatment, possibly to include pacemaker implantation.

It is controversial whether every patient with baseline left bundle branch block undergoing catheterization of the right ventricle or right ventricular endomyocardial biopsy should receive a temporary pacemaker. About 5% to 10% of patients with catheter introduction in the right ventricle will develop transient right bundle branch block. For patients with baseline left bundle branch block, this can result in complete heart block and asystole, and it may be reasonable to place a temporary pacemaker in these patients. In most cases, iatrogenic right bundle branch block is transient but can last for hours and up to several days.

Summary

Cardiac pacing has emerged as a safe, reliable, and highly effective treatment for a subset of cardiac rhythm abnormalities. As with any treatment, proper patient selection is essential to success. This chapter has provided a summary of current indications for cardiac pacing as outlined in the most recent ACC/AHA/HRS guidelines, with special attention to frequently encountered clinical dilemmas. It should be emphasized that in deciding whether or not to initiate pacing, the clinician should always bear in mind not only the specific guidelines but also the level of supporting evidence and the presence or absence of alternatives to cardiac pacing. Particularly with permanent pacemakers, device implantation imposes a lifestyle change for the patient, and thus it is critical to integrate patient preference into the clinical decision making process. Finally, although pacemakers have been in widespread clinical use for several decades, the indications for pacing are rapidly evolving and undoubtedly will expand as more clinical data on patient selection and outcomes become available and as pacing technology continues to improve.

Appendix Table 33-1 Classification of Indications for Pacemaker Implantation

INDICATION	DESCRIPTION
Class I	Pacing is useful and effective and should be considered.
Class IIa	The weight of evidence is in favor of the usefulness or effectiveness of pacing, but some divergence of opinion exists. It is reasonable to consider pacing.
Cass IIb	The usefulness and effectiveness of pacing is less well established, and considerable divergence of opinion exists. Pacing can be considered.
Class III	Pacing is not useful or effective and in some cases may be harmful. Pacing should not be considered.
LEVEL OF EVIDENCE
A	Data are derived from multiple randomized clinical trials or meta-analyses, and multiple populations were evaluated.
B	Data are derived from a single randomized trial or nonrandomized study, or limited populations were evaluated.
C	Only consensus opinion of experts, case studies, with very limited populations evaluated, or pacing is standard of care.

Appendix Table 33-2 Clinical Manifestations of Sinus Node Dysfunction

SYNDROME	DESCRIPTION
Sinus bradycardia	Resting heart rate <60 beats/min with typical symptoms
Sinus arrest	Symptomatic sinus pause <3 seconds while awake
Tachyarrhythmia-bradyarrhythmia syndrome	Alternating periods of tachyarrhythmia, usually atrial fibrillation, with sinus bradycardia Postconversion sinus pauses
Chronotropic incompetence	Failure to augment heart rate appropriately with exercise. Inability to achieve 80% of age-appropriate maximum predicted heart rate

Appendix Table 33-3 Permanent Pacing for SND

CLASS	INDICATION
Class I	SND with documented symptomatic bradycardia
	Symptomatic chronotropic incompetence
	Symptomatic sinus bradycardia resulting from essential drug therapy
Class IIa	SND with heart rate <40 beats/min and symptoms of bradycardia, without a demonstration of association between symptoms and bradycardia
	Unexplained syncope with SND, either spontaneous or provoked
Class IIb	Minimally symptoms with chronic heart rate <40 beats/min while awake
Class III	Asymptomatic SND
	Symptomatic SND resulting from non-essential drug therapy
	SND with symptoms that occur in the absence of bradycardia

SND, Sinus node dysfunction.

Appendix Table 33-4 Permanent Pacing for First-Degree and Type 1 Second-Degree AV Block

CLASS	INDICATION
Class I	Symptomatic bradycardia resulting from type I second-degree AV block
Class IIa	First-degree AV block or type I second-degree AV block with symptoms similar to those of pacemaker syndrome or hemodynamic compromise
Class IIb	Neuromuscular diseases with first-degree AV block or type I second-degree AV block
Class III	Asymptomatic first-degree AV block or type I second-degree AV block

AV, Atrioventricular.

Appendix Table 33-5 Neuromuscular Disorders Associated with Conduction System Disease

SYNDROME

Myotonic dystrophy

Muscular dystrophies

Kearns-Sayre syndrome

Erb’s dystrophy

Peroneal muscular atrophy

Freidrich’s ataxia

Appendix Table 33-6 Pacing for High-Grade Atrioventricular block

CLASS	INDICATION
Class I	Symptomatic bradycardia or ventricular arrhythmias due to AV block
	Essential drug therapy that results in symptomatic bradycardia
	Awake, asymptomatic patients in sinus rhythm with periods of asystole <3.0 seconds, escape rate <40 beats/min, or escape rhythm that is below the AV node
	Awake asymptomatic patients with atrial fibrillation, bradycardia, and one or more pauses of at least ≥5 seconds
	After catheter ablation of the AV junction
	AV block after cardiac surgery that is not expected to resolve
	Neuromuscular diseases, with or without symptoms
	Asymptomatic patients with average awake ventricular rates of 40 beats/min or faster if cardiomegaly or left ventricular dysfunction is present, or if the site of block is below the AV node
	Exercise-induced second-degree or third-degree AV block in the absence of myocardial ischemia
Class IIa	Persistent third-degree AV block with an escape rate <40 beats/min in an asymptomatic patient without cardiomegaly
	Asymptomatic second-degree AV block at intra-His or infra-His levels found at electrophysiology study
	Asymptomatic type II second-degree AV block with a narrow QRS
Class IIb	AV block in the setting of drug use or toxicity that is expected to recur even when the drug is withdrawn
Class III	Reversible AV block that is expected to resolve and is unlikely to recur

AV, Atrioventricular.

Appendix Table 33-7 Permanent Pacing for Intraventricular Conduction Disturbances

CLASS	INDICATION
Class I	Alternating bundle branch block
	Bifascicular block with type II second-degree or third-degree AV block
Class IIa	Bifascicular block and syncope when other causes have been excluded
	Bifascicular block with H-V interval >0.1 second
	Bifascicular block with nonphysiologic pacing-induced infra-His block
Class IIb	Bifascicular block with neuromuscular disease
Class III	Bifascicular block without AV block or symptoms
	Trifascicular block without symptoms

AV, Atrioventricular.

Appendix Table 33-8 Permanent Pacing for Autonomic Nervous System Dysfunction

CLASS	INDICATION
Class I	Carotid sinus hypersensitivity causing syncope
Class IIa	Carotid sinus hypersensitivity with asystole of <3 seconds and syncope when other causes have been excluded
Class IIb	Neurocardiogenic syncope with significant symptoms and documented bradycardia either spontaneously or at tilt-table testing
Class III	Carotid sinus hypersensitivity with vague symptoms or no symptoms
	Situational vasovagal syncope in which avoidance behavior is effective and preferred

Appendix Table 33-9 Permanent Pacing for Termination and Prevention of Tachyarrhythmias

CLASS	INDICATION
Class I	Sustained, pause-dependent ventricular tachycardia, with or without Q-T interval prolongation
Class IIa	High-risk patients with congenital LQTS
	Recurrent supraventricular tachycardia that is reproducibly terminated by pacing when catheter ablation, drugs, or both fail to control the arrhythmia or produce intolerable side effects
Class IIb	Prevention of symptomatic, drug-refractory atrial fibrillation in patients with coexisting sinus node dysfunction
Class III	Frequent or complex ventricular ectopy without sustained ventricular tachycardia in the absence of LQTS
	Torsades de pointes ventricular tachycardia from reversible causes
	Prevention of atrial fibrillation without any other indication for pacemaker implantation

LQTS, Long QT syndrome.

Appendix Table 33-10 Permanent Pacing After the Acute Phase of Myocardial Infarction

CLASS	INDICATION
Class I	Persistent and symptomatic second-degree or third-degree AV block
	Persistent second-degree intra-His or infra-His AV block with alternating bundle branch block, or third-degree intra-His or infra-His AV block
	Transient second-degree or third-degree intra-His or infra-His AV block with associated bundle branch block
Class IIa	None
Class IIb	Persistent asymptomatic second-degree or third-degree supra-His AV block
Class III	Transient AV block without intraventricular conduction defects
	Transient AV block with isolated left anterior fascicular block
	Bundle branch block or fascicular block without AV block
	Persistent first-degree AV block with bundle branch block that is not new

AV, Atrioventricular.

Appendix Table 33-11 Permanent Pacing to Treat Obstruction in Hypertrophic Cardiomyopathy

CLASS	INDICATION
Class I	None
Class IIa	None
Class IIb	Medically refractory symptomatic patients with hypertrophic cardiomyopathy and significant resting or provoked outflow tract obstruction
Class III	Patients without symptoms or with medically controlled symptoms
	Symptomatic patients without LVOT obstruction

Appendix Table 33-12 Permanent Pacing After Cardiac Transplantation

CLASS	INDICATION
Class I	Persistent inappropriate symptomatic bradycardia not expected to resolve
Class IIa	None
Class IIb	Prolonged bradycardia that limits recovery after cardiac transplantation
	Syncope after cardiac transplantation, even when bradycardia has not been documented

Appendix Table 33-13 Temporary Pacing in Acute Myocardial Infarction

CLASS	INDICATION
Class I	Asystole
	Symptomatic bradycardia
	Third-degree AV block
	Alternating bundle branch block: RBBB/LBBB or RBBB + LAFB/LPFB
	Type II second-degree AV block with new bundle branch block
	Type II second-degree AV block with bifascicular block
Class IIa	Type II second-degree AV block with narrow QRS
	Type II second-degree AV block with any fascicular block (anterior MI)
	Type II second-degree AV block with old bundle branch block
	Type I second-degree AV block with new bundle branch block
	Type I second-degree AV block with bifascicular block
	First-degree AV block with new bundle branch block
	First-degree AV block with bifascicular block
Class IIb	Type II second-degree AV block with old bundle branch block
	Type I second-degree AV block with old bundle branch block
	First-degree AV block with old bundle branch block
Class III	First-degree AV block with normal QRS
	Type I second-degree AV block with normal QRS
	Accelerated idioventricular rhythm
	Old bundle branch block or fascicular block without AV block

AV, Atrioventricular; LAFB, left anterior fascicular block; LPFB, left posterior fascicular block; RBBB, right bundle branch block; LBBB, left bundle branch block; MI, myocardial infarction.

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