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
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 |
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.
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).
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
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.
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).
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).
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).
Neurocardiogenic Syncope
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.
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