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.
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.
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.
|TYPE OF CAUSE||SPECIFIC CAUSE|
|Autonomic nervous system||Neurocardiogenic syncope|
|Drugs and medications||β-Adrenergic blockers|
|Calcium channel blockers|
|Class IA antiarrhythmic drugs|
|Class IC antiarrhythmic drugs|
|Class III antiarrhythmic drugs|
|Neurologic||Elevated intracranial pressure|
|Spinal cord injury|
|Pulmonary||Obstructive sleep apnea|
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.
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 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.
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.
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.
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).
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 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).
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).
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 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, 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.