Sample Chapter

January 2008

Section 1

Worldwide, more than 500,000 permanent cardiac pacemakers are implanted each year. As the population ages and as indications for pacemakers expand, the number of implants continues to increase. Advances in technology have played an important role in the evolution of pacemaker therapy: currently available pacemakers are smaller and more reliable than older models and contain a multitude of sophisticated programmable features.

The role of cardiac pacing is to augment or replace the heart's intrinsic electrical system. Pacing has generally been performed in patients who have bradycardia or are thought to be at risk for bradycardia. More recently, pacing has also been used to restore electrical and contractile synchrony in patients with congestive heart failure.

The heart's conduction system consists of specialized structures capable of automaticity and rapid electrical impulse conduction. It provides appropriate timing and synchrony needed to maintain appropriate cardiac output.

Sinoatrial Node

In normal circumstances, the sinoatrial (SA) node (also referred to as the sinus node) is the origin of impulse generation and dictates the intrinsic heart rate. The SA node is located in the superior aspect of the right atrium. It is composed of specialized tissue that normally demonstrates the fastest rate of spontaneous depolarization (automaticity) of any of the cardiac tissues.

Atrioventricular Node

The atrioventricular (AV) node is the junction between the atria and the ventricular conduction system. This node is a dense and complex structure that plays three important roles. First, it demonstrates spontaneous depolarization and is capable of acting as an auxiliary pacemaker. Second, it delays propagation of the impulse between the atria and the ventricles, thereby allowing normal atrioventricular synchrony. Third, it acts as a filter, limiting the number of impulses that can be propagated from the atria to the ventricles and protecting the heart from rapid ventricular rates in the setting of abnormally fast atrial rates, such as atrial fibrillation.

His-Purkinje System

The His-Purkinje system originates at the inferior border of the AV node. From this point, the bundle of His courses down the interventricular septum, where it diverges into the left and right bundle branches, which arborize into the Purkinje fiber network. The bundle of His and the bundle branches provide rapid and synchronous depolarization of the ventricles. The Purkinje fibers serve as the interface between the specialized conduction system and the local ventricular myocardium.

Modulation of Heart Rate

The basal heart rate is maintained by the balance between sympathetic and parasympathetic tone. Changes in the heart rate are mediated by the autonomic nervous system and circulating catecholamines. During exercise, there is a normal physiologic acceleration of the heart rate that results from increased demand for cardiac output. This acceleration is mediated by both increased sympathetic tone and reduced parasympathetic tone. Inability to increase the heart rate in response to increased demand for cardiac output can result in a number of symptoms, including fatigue, poor exercise tolerance, and exertional dyspnea.

Disruption or imbalance of sympathetic and parasympathetic inputs to the SA node or the AV node can cause profound abnormalities in the heart rate, resulting in inappropriate increases or decreases that give rise to significant symptoms. SA node dysfunction may be caused by intrinsic abnormalities of the conduction system or by imbalances in autonomic tone.

General Considerations

The cardiac conduction system can be affected by any of a wide variety of pathologic states, ranging from benign abnormalities to conditions that can lead to severe symptoms and substantial morbidity and mortality. In certain subgroups of the heart failure population, electrical conduction abnormalities are associated with significant contractile dysfunction, exacerbating heart failure symptoms and worsening functional status.

Guidelines for permanent pacemaker implantation were established by a joint task force of the American College of Cardiology and the American Heart Association and were first published in 1984. These guidelines were subsequently revised in 1991, 1998, and 2002.¹ The North American Society of Pacing and Electrophysiology (NASPE), now known as the Heart Rhythm Society, was also involved in the 2002 revision. New revisions to the published guidelines, which will include indications for biventricular pacing and resynchronization therapy, are expected in 2008.

Current recommendations for pacemaker implantation are summarized [see Table 1]. The recommendations are divided into the following three broad categories on the basis of the consensus of experts in the field:

• Class I: conditions for which there is evidence or general agreement that a given procedure or treatment is beneficial, useful, and effective.

• Class II: conditions for which there is conflicting evidence or a divergence of opinion about the usefulness or efficacy of a procedure or treatment.

  IIa: conditions for which the weight of the evidence or expert opinion is in favor of usefulness/efficacy.

  IIb: conditions for which usefulness or efficacy is less well established by evidence or opinion.

• Class III: conditions for which there is evidence or general agreement that a procedure or treatment is not useful or effective and, in some cases, may be harmful.

Guidelines for Specific Pacemaker Indications

SA Node Dysfunction

SA node dysfunction encompasses a number of different arrhythmias, including sinus bradycardia, sinus arrest, sinoatrial block, and the bradycardia-tachycardia syndrome. The bradycardia-tachycardia syndrome is characterized by atrial tachyarrhythmias (usually atrial fibrillation) alternating with periods of bradycardia or sinus pauses. Another form of SA node dysfunction, termed chronotropic incompetence, is the inability to normally increase the sinus rate during exercise, with resulting exercise intolerance.

SA node dysfunction must be differentiated from the physiologic sinus bradycardia seen in trained athletes. During sleep, sinus rates as low as 30 beats/min and type I second-degree AV block are commonly seen in normal persons and do not constitute an indication for pacing.

Pacing is indicated when SA node dysfunction causes significant (< 40 beats/min) or symptomatic bradycardia, chronotropic incompetence, frequent long pauses, or syncope. Pacing is also indicated when SA node dysfunction is found on electrophysiologic testing performed to assess otherwise unexplained syncope.

Acquired Atrioventricular Block

AV block is defined as delayed or failed conduction from the atria to the ventricles. It is usually categorized as occurring either at or below the level of the AV node. First-degree AV block describes conduction delay from the sinus impulse to the ventricles and is defined as prolongation of the PR interval without a dropped QRS complex. Usually, first-degree AV block occurs at the level of the AV node, though it may also occur in the His-Purkinje system. Pacing is indicated only in marked first degree AV block with a PR interval greater than 0.3 seconds in patients with congestive heart failure who may benefit hemodynamically from restoration of normal AV synchrony.

Second-degree AV block is present when some, but not all, P waves are conducted to the ventricles. It can be further subdivided into Mobitz type I (Wenckebach) and Mobitz type II. In type I second-degree AV block, there is a progressive prolongation of the PR interval preceding a nonconducted P wave. The anatomic site of the block is usually the AV node, and the QRS complex is usually narrow. In type II second-degree AV block, there is a fixed PR interval preceding the dropped QRS complex. Type II block is often accompanied by bundle branch block, and its anatomic location is usually below the AV node in the His-Purkinje system.

When every other P wave is conducted, 2:1 AV block is present; 2:1 block cannot be classified as either type I or type II block, because there are not consecutive PR intervals preceding the nonconducted P wave. When 2:1 block is accompanied by bundle branch block, the site of the block is likely to be below the AV node in the His-Purkinje system. On the other hand, when 2:1 block is associated with a narrow QRS complex, or when Mobitz type I (Wenckebach) AV block is also seen in the same patient, then the site of the 2:1 block is likely to be in the AV node.

High-degree (or advanced) type II AV block is defined as block of two or more consecutive P waves. Complete heart block, or third-degree block, denotes a complete absence of conduction from the atria to the ventricles. In advanced or complete heart block, there is often an escape rhythm that can originate from the area of the AV node (which generally results in a narrow QRS with typical escape rate 50 to 60 beats/min) or from one of the ventricles (wide QRS with typical escape rate 30 to 40 beats/min). A hallmark of complete heart block with escape rhythm is a regular ventricular rate.

The anatomic location of AV block has important prognostic and therapeutic implications. Typically, a block occurring at the level of the AV node—such as first-degree block, type I second-degree block, and 2:1 block at the level of the AV node—does not lead to abrupt complete heart block, though gradual progression is common. A block occurring below the level of the AV node, on the other hand, can often progress quickly to complete heart block. In addition, high-degree or complete heart block at the level of the AV node is more likely to be ameliorated by an escape rhythm, whereas block at the level of the His-Purkinje system has a greater risk of resulting in complete ventricular asystole.

Pacing is indicated in second-degree AV block, regardless of type, when associated with symptomatic bradycardia. Type II second-degree AV block is also an indication for pacing when associated with a wide QRS complex, regardless of symptoms, because it likely indicates His-Purkinje system disease.

In cases of third-degree or high-degree AV block, pacing is indicated when the block is associated with symptomatic bradycardia; periods of asystole longer than 3 seconds; or an escape rhythm slower than 40 beats/min while the patient is awake, especially in patients with left ventricular systolic dysfunction. Pacemaker implantation is indicated for most patients with third-degree or high-degree AV block that does not have a reversible cause. One exception is transient third-degree block occurring during sleep or in other situations of high vagal tone that can be avoided; such patients generally do not have an indication for pacing.

Chronic Bifascicular and Trifascicular Block

The conduction system below the AV node is composed of three fascicles: the right bundle branch, the left anterior fascicle, and the left posterior fascicle. The left anterior and left posterior fascicles are divisions of the left bundle branch. Bifascicular block denotes either left bundle branch block (LBBB) or blockage of the right bundle branch plus either the left anterior or posterior fascicle. Trifascicular block is present when alternating bundle branch block is seen or when right bundle branch block occurs in conjunction with alternating left anterior and left posterior hemiblock. Trifascicular block may also be present when bifascicular block is accompanied by first-degree AV block, if the first-degree block represents conduction delay in the only fascicle that continues to conduct impulses. More commonly, however, this electrocardiographic pattern is the result of bifascicular block combined with conduction delay at the AV node.

Pacing is generally indicated in chronic bifascicular and trifascicular block when associated with alternating bundle branch block, severe His-Purkinje system disease confirmed by electrophysiologic testing, intermittent type II second-degree or third-degree AV block, or unexplained syncope.

Acute Myocardial Infarction

Conduction abnormalities are common in the setting of acute myocardial infarction. Pathophysiologic mechanisms include ischemia, necrosis, autonomic influences, and the neurohumoral response to injury. Temporary transvenous pacing is occasionally required during the acute phase of an infarction. The need for temporary pacing does not necessarily imply a need for permanent pacing, because many of the conduction abnormalities are transient and resolve after revascularization or upon recovery from the acute phase of the infarction.

Patients with acute inferior infarction can manifest a variety of abnormalities, including SA node dysfunction, first-degree AV block, type I second-degree block, and third-degree block at the level of the AV node. It is uncommon for any of these conduction disturbances to persist after the acute phase of the infarction. These patients often require temporary pacing if they manifest hemodynamic instability, but they rarely require permanent pacing.

Patients with anterior infarction can manifest bundle branch block, bifascicular block, trifascicular block, type II second-degree block, or complete heart block. These patients are much more likely to require permanent pacing than those with inferior infarction are. Although conduction abnormalities are associated with higher mortality in the setting of anterior infarction, the increased mortality is a consequence of the larger infarct size and is not directly related to the conduction abnormality.

Pacing is indicated when symptomatic second- or third-degree AV block persists after the acute phase of a myocardial infarction. Pacing is also indicated in case of even transient advanced second- or third-degree AV block when associated with bundle branch block.

Cardiac Surgery

Heart block or sinus node dysfunction can develop after coronary artery bypass graft surgery, cardiac valve replacement or repair, or surgical repair or palliation of congenital heart defects. Surgical procedures for the treatment of atrial fibrillation can also be associated with heart block or sinus node dysfunction. Most commonly, bradyarrhythmias will resolve after a period of temporary pacing with epicardial or transvenous pacing wires. Not infrequently, however, the postoperative bradyarrhythmia does not resolve, and permanent pacing is required. Patients undergoing aortic valve replacement are more likely to require permanent pacemakers than patients undergoing mitral valve replacement or repair.

Pacing for Neurocardiogenic Syncope and Hypersensitive Carotid Syndrome

Neurocardiogenic syncope results from hypotension secondary to bradyarrhythmias, vasodilation, or both, as a consequence of abrupt imbalance of autonomic input to the heart and the vascular system. Classic neurocardiogenic syncope involves sinus tachycardia followed by bradycardia, vasodilation, and syncope. Some patients have primarily a vasodepressive (vasodilation) syndrome, whereas others have a syndrome with a significant cardioinhibitory component (bradycardia). Thus, bradycardia is not always a contributing component in neurocardiogenic syncope. Head-up tilt testing is often useful for diagnosing the presence and type of neurocardiogenic syncope.

The hypersensitive carotid syndrome is characterized by a similar abnormal response of the autonomic nervous system, in which baroreceptors in the carotid sinus trigger a vasodepressive or cardioinhibitory response. A hyperactive carotid sinus response is defined as a sinus pause longer than 3 seconds or a substantial symptomatic decrease in systolic blood pressure.

Pacing is indicated when the cardioinhibitory response—confirmed by carotid sinus stimulation or tilt table testing—leads to significant symptomatic bradycardia or syncope, and when other measures (e.g., avoidance therapy, medications) are ineffective or not preferred.

Cardiac Resynchronization Therapy

Severe cardiomyopathies, either ischemic or nonischemic, are associated with progressive dilatation of the left ventricle and functional mitral valve regurgitation. There is often associated disease of the cardiac conduction system, most commonly manifested as LBBB, although right bundle branch block and nonspecific intraventicular conduction delay can also accompany cardiomyopathy. Examination of cardiac contraction in these patients often reveals dyssynchrony at multiple levels. In the setting of LBBB, atrioventricular dyssynchrony denotes delay of left ventricular contraction relative to left atrial contraction, whereas interventricular dyssynchrony is manifested by right ventricular contraction preceding left ventricular contraction. The third level of dyssynchrony is intraventricular; in the setting of LBBB, this consists of delayed contraction of the lateral wall of the left ventricle relative to that of the interventricular septum.

Biventricular pacing, otherwise known as cardiac resynchronization therapy (CRT), utilizes simultaneous or near simultaneous pacing through a transvenous right ventricular lead and a left ventricular lead implanted epicardially or through the coronary sinus. CRT allows for simultaneous activation of septal and lateral walls of the left ventricle and restores atrioventricular, interventricular, and intraventricular synchrony. Several studies have reported significant improvement in functional status, mitral regurgitation, left ventricular ejection fraction, and survival in patients treated with CRT.^2,3 Candidates for CRT devices are currently required to have New York Heart Association (NYHA) functional class III symptoms despite adequate treatment of heart failure, a left ventricular ejection fraction of less than 35%, and evidence of intraventricular conduction delay, usually in a left bundle branch pattern.

Other Pacemaker Indications

Besides those already mentioned, there are several indications for which pacemakers are implanted that warrant brief mention, including treatment of hypertrophic cardiomyopathy and prevention or suppression of tachyarrhythmias.

In addition, pacing is indicated in patients with any degree of AV block or fascicular block from a neuromuscular disorder, including myotonic dystrophy, Kearns-Sayre syndrome, and limb girdle and peroneal muscular atrophy. The main reason is the unpredictable rate of progression to significant conduction system disease.

A basic pacemaker system is made up of three main components: the pulse generator, the pacemaker lead(s), and the programmer.

Pulse Generator

Figure 1. Five Pacemaker Generators\

Over the past 35 years, pulse generators have evolved from large, bulky devices into small, sophisticated systems [see Figure 1]. All pulse generators contain hardware, software, and a battery; however, the systems currently available can differ from one another with respect to a number of factors, including number of cardiac chambers paced, biventricular pacing capability, presence and type of activity sensor, size, battery life, and cost. All of these factors are taken into account in selecting a specific generator for a specific patient.

Generators are usually described as being either single chamber or dual chamber. Single-chamber systems have one lead, which is usually placed in the right ventricle (though it may, on occasion, be placed in the atrium). Dual-chamber systems have two leads, one of which is implanted in the right atrium and the other in the right ventricle. The biventricular pacemaker devices currently used in patients with heart failure have a third lead that is usually placed in a branch of the coronary sinus to provide left ventricular pacing. Dual-chamber systems can be programmed to single-chamber modes of operation.

At present, most generators use lithium iodine batteries that have a typical life span of 5 to 10 years for standard single or dual chamber pacemakers, and 3 to 6 years for biventricular pacemakers. These batteries are not rechargeable or replaceable; accordingly, when the battery reaches the end of its life, a new generator must be implanted.

Pacemaker Leads

Figure 2. Four Pacemaker Leads

Pacemaker leads are the electrical conduits from the generator to the myocardium. Most leads are implanted transvenously. There are still occasional applications for epicardial leads, but these are generally limited to patients with mechanical tricuspid valves, certain congenital heart abnormalities, or other conditions that preclude transvenous leads. Like pulse generators, leads have gone through a complex evolution since they were first developed. Various types are currently used [see Figure 2]; the major differences among them relate to type of insulation, fixation mechanism, and polarity.

Most pacemaker leads are insulated with either silicone or polyurethane. Each of these insulators has its strengths and weaknesses. For instance, silicone is more inert but is subject to thinning or abrasion, whereas polyurethane is more resistant to mechanical stress but can be chemically reactive in the body's environment. Recently, a copolymer of silicone and polyurethane that may combine the strengths of each has been developed.

Leads can be attached to the myocardium via either passive or active fixation. Passive fixation leads usually have tines at the distal tip to help maintain stability. Active fixation leads have a corkscrew helix mechanism at the distal end, which inserts into the myocardium. Both fixation mechanisms are reliable, and lead dislodgment is uncommon with either one.

Leads can be either unipolar or bipolar. Unipolar leads have a single conductor and a single electrode; the pacing circuit involves the single electrode and the metal housing of the generator. Bipolar leads have two conductors and two electrodes; the pacing circuit is between the two electrodes. Advantages of unipolar leads include decreased diameter and reduced susceptibility to lead fracture. Advantages of bipolar leads include reduced risk of inappropriate sensing of myopotentials, greater resistance to electromagnetic interference (EMI), less likelihood of pectoral muscle stimulation, and better compatibility with implanted defibrillators. At present, bipolar leads are more commonly used, but unipolar leads are still employed on occasion.

Although leads are becoming more reliable, they still represent the weakest link in the pacemaker system. A minimally acceptable benchmark for mechanical failure of leads is less than 5% over 5 years.

Pacemaker Programmer

The programming computer allows telemetric communication with the implanted pulse generator and serves as the interface between the health care provider and the pacemaker. Because there is no standardization among pacemaker manufacturers, each company's device requires its own programmer.

Programmers are equipped with a wand that provides external telemetry through the skin, thus allowing direct communication with the pacemaker generator and access to the software contained within it. The pacemaker programmer is used to perform a multitude of functions, including assessing battery status, modifying pacemaker settings, and providing access to diagnostic information the pacemaker has stored (e.g., heart rate trends and tachyarrhythmia documentation).

Pacemaker Magnets

Pacemaker generators are designed to respond to the placement of a strong magnet over the device. The response of most pacemakers is to pace at a set “magnet rate” in an asynchronous mode. Magnets also can be used to perform any of a number of functions designated by the manufacturer, including checking battery status, threshold testing, and obtaining event snapshots (in much the same way as an event monitor). Magnets should be available in the hospital and clinic, as well as on code carts for immediate access.

Although such use is beyond the scope of this chapter, it is worth mentioning that magnets can also temporarily turn off defibrillation therapy in implantable cardioverter-defibrillators.

Detailed description of specific programming techniques and indications is beyond the scope of this chapter; however, familiarity with the basic functions and nomenclature is critical for understanding how pacemakers function.

Basic Functions

A pacemaker has three basic functions: pacing, sensing, and action. Its other, more complicated functions are based on these three. Pacing is the delivery of an electrical impulse to the myocardium to elicit depolarization. Sensing is the ability to “see” intrinsic depolarization (i.e., the local intrinsic electrical signal that passes by the tip of the lead). Action is the response of the pacemaker to a sensed event—namely, either inhibition or triggering of a paced event.

Codes

The basic functions—pacing, sensing, and action—are determined by basic pacemaker programming. In 1974, the American Heart Association and the American College of Cardiology proposed a three-letter code for describing the basic functions of pacemakers. Under the guidance of NASPE and the British Pacing and Electrophysiology Group (BPEG), this code evolved into the five-position code currently in use [see Table 2].⁴ The first position denotes the chamber or chambers paced; the second denotes the chamber or chambers sensed; the third denotes the action or actions performed; the fourth denotes rate response; and the fifth denotes multiple-site pacing. The simplest mode of pacing is VVI, otherwise known as ventricular demand pacing or ventricular inhibited pacing. The most commonly used mode in dual-chamber pacing is DDD.

Timing Cycles

Figure 3. Four Forms of DDD Pacing

A pacemaker is governed by timing cycles, which are a hierarchy of clocks that regulate how the pacemaker functions. The most basic timing cycle is the lower rate, which reflects how long the pacemaker will wait after a paced or sensed beat before initiating pacing. For instance, if the pacemaker is set to VVI mode at a lower rate of 60 beats/min, then as long as the interval between intrinsic beats is less then 1,000 msec, the pacemaker will reset the lower rate clock with each sensed QRS complex, and pacing will not occur. If, however, the intrinsic heart rate falls below 60 beats/min, the pacemaker's lower-rate clock will time out before an intrinsic beat is sensed, and pacing will occur. After a paced beat, the lower-rate clock is reset and the cycle repeats. In a modern dual-chamber pacemaker, there are a number of additional timing cycles that regulate how the pacemaker responds to these paced and sensed events [see Figure 3].

Selection of a pacing system and its program mode should be tailored to the pacing indication. A single-chamber pacemaker can be implanted with a lead in the atrium or ventricle. Single-chamber ventricular pacing is most appropriate in the setting of chronic atrial fibrillation, in which case a lead in the atrium would have no utility. Single-chamber ventricular pacemakers can also be used in patients with sinus rhythm in whom the need for pacing is thought to be very intermittent. In patients with sinus rhythm in whom a substantial amount of pacing is anticipated, single-chamber ventricular pacemakers should be avoided, for three reasons: they may cause so-called pacemaker syndrome (i.e., symptoms related to AV dyssynchrony during ventricular pacing); they are associated with a higher likelihood of developing atrial fibrillation; and recent evidence indicates that excessive right ventricular pacing should be avoided if possible (see below).

Single-chamber atrial pacemakers can be used in patients with sinus node dysfunction and normal AV conduction. However, single-chamber atrial pacemakers are not widely used in the United States because of the possibility, often unpredictable, of the development of problems with AV conduction, resulting either from progression of conduction system disease or from necessary drug therapy.

Dual-chamber pacing prevents pacemaker syndrome by preserving atrioventricular synchrony. Compared with single-chamber ventricular pacing, dual-chamber pacing has been shown to decrease the incidence of atrial fibrillation and heart failure hospitalization, especially in patients with sinus node dysfunction.⁵ However, excessive amounts of right ventricular pacing from dual-chamber pacemakers are associated with increased likelihood of atrial fibrillation and heart failure hospitalization.⁶ This is thought to be a consequence of the abnormal and dyssynchronous activation of both ventricles during right ventricular pacing. Therefore, it is important to program dual-chamber pacemakers to minimize right ventricular pacing. Newer pacemaker modes allow for minimizing ventricular pacing and have been shown to reduce the incidence of atrial fibrillation.⁷

Conversely, in patients with biventricular or resynchronization devices, ventricular pacing is desirable to optimally restore synchrony. In such patients, pacemakers should be programmed to maximize ventricular pacing, generally by setting a short AV pacing delay.

Most pacemakers are implanted by cardiologists, and most implantation procedures are performed in the cardiac catheterization laboratory.⁸

Preprocedural Considerations

There are several issues that should be considered after the need to implant a pacemaker has been established. In particular, the patient's underlying health must be assessed and any comorbid conditions evaluated.

In select patients, the issue of reversal and reinitiation of oral anticoagulation must be addressed before implantation. In the past, patients receiving warfarin generally had their international normalized ratios (INRs) normalized before the procedure. Furthermore, patients with a strong indication for anticoagulation (e.g., patients with a mechanical heart valve) required prolonged hospitalization for reinitiation of oral anticoagulation after the procedure. In the past few years, however, favorable results have been reported with routine pacemaker implantation in patients undergoing therapeutic anticoagulation with warfarin. These results suggest that preprocedural reversal of anticoagulation may not be necessary.^9,10

Pacemakers can interfere with or preclude certain imaging procedures, such as mammography and magnetic resonance imaging. In the case of elective pacemaker implants in women, a baseline mammogram should be considered beforehand.¹¹ Any MRI procedures that may be indicated should also be performed before implantation.

Local anesthesia is typically employed in conjunction with parenteral sedation. In certain circumstances (e.g., in pediatric patients or other patients who would tolerate the procedure poorly under local anesthesia), an anesthetist should be involved, but such circumstances are relatively uncommon. Antibiotic prophylaxis is recommended, and a variety of antibiotic regiments have been advocated.¹²

Pacemaker Pocket Placement

The pulse generator pocket is usually placed on the upper left aspect of the chest, just medial to the angle of the deltopectoral groove and 2 to 3 cm below the clavicle. In the case of left-handed patients or in certain other specific situations (e.g., when left subclavian vein occlusion is present or the patient has undergone a left mastectomy), the pacemaker may be located on the right side. It is important to locate the generator medially enough that it does not interfere with normal shoulder function. The pocket is formed deep to the subcutaneous tissue and above the plane of the pectoral fascia. Occasionally, if the patient is extremely thin or if cosmetic considerations are a priority, the generator may be placed either below the pectoral muscle or via a retromammary approach.

Vascular Access

Vascular access is most frequently gained by placing a venous sheath using the Seldinger technique. The subclavian vein remains the most common venous access site; however, the axillary vein is becoming an increasingly popular site. Venous access may also be obtained via the cephalic vein or the internal jugular vein. Leads may be tunneled subcutaneously from a remote entry site (e.g., the internal jugular vein) to the site of the generator pocket. Occasionally, thoracotomy and the use of epicardial lead systems are still necessary.

Risks

Overall, transvenous pacemaker implantation is both safe and well tolerated. The risk of major adverse events (e.g., death, myocardial infarction, stroke, and the need for emergency thoracotomy) is approximately 0.1%. Other complications encountered include pneuomothorax, vascular injury, cardiac perforation, tamponade, local bleeding, pocket hematoma, infection, and venous thrombosis. There is also a small risk that one or more leads may become dislodged and require repositioning in a second procedure.

Postprocedural Care

At most institutions, it is standard practice to admit patients for overnight observation after routine pacemaker implantation. Routine exchange of the pacemaker generator because of battery depletion is often performed as a same-day outpatient procedure. Longer hospitalizations may be required in certain specific situations, as when anticoagulation must be reversed and reinitiated or when a major comorbid condition must be treated.

After implantation of new devices or leads, the ipsilateral arm is placed in a sling or a soft restraint for 12 to 24 hours. Non-narcotic analgesics are usually sufficient for pain control, but occasionally, oral narcotics are indicated. Patients are monitored via continuous telemetry. We routinely obtain a portable chest x-ray and a 12-lead electrocardiogram immediately after implantation.

Figure 4. Appearance of Dual-chamber Pacemaker on X-Ray

The day after the procedure, the pacemaker is interrogated and the final settings confirmed. Posteroanterior and lateral chest x-rays are obtained both to verify the positioning of the leads and to rule out the possibility of a slowly accumulating pneumothorax [see Figure 4].

Before discharge, the patient receives instruction about the pacemaker and is given a temporary pacemaker card that lists the manufacturer, the specific generator and lead(s) used, and complete serial-number information. Later, the manufacturer mails the patient a permanent identification card, which the patient is asked to keep on hand at all times.

Postdischarge Instructions and Restrictions

Postoperative care focuses on averting hematoma and preventing lead dislodgment. Patients are prohibited from showering for the first 48 to 72 hours. After this period, they may shower, but for the first week, they are advised to cover the implantation site with plastic wrap to protect it from contamination. When 24 hours have passed after implantation, minimal range-of-motion restrictions are placed on the ipsilateral arm and shoulder. Patients are asked to refrain from raising the arm above shoulder level and to perform only limited heavy lifting for the first few weeks. After this period, patients may return to normal activity levels without having to be concerned about displacing the leads or the generator system.

Usually, a follow-up visit is scheduled 7 to 10 days after implantation. During this visit, a wound check is performed to ensure proper healing and to remove the skin suture if it is nonresorbable. As a rule, the pacemaker pocket heals completely within 2 to 4 weeks.

Long-Term Follow-Up

Pacemaker patients need routine follow-up care, including interrogation of the pacemaker. Follow-up care can be provided during office visits, via transtelephonic monitoring (TTM), or both. Several documents containing guidelines for follow-up have been published.^1,13,14 We recommend that patients either be seen in the office or undergo TTM every 3 to 6 months. As the battery approaches the end of its life, more frequent visits may be required.

Pacemaker complications are infrequent but can lead to serious situations. To minimize adverse consequences, it is important to identify problems early in their course, initiate appropriate workup and treatment, and refer when necessary [see Table 3]. Generally, pacemaker complications can be classified according to whether they primarily affect the pocket, the generator, or the leads.

Generator Pocket Complications

Pocket hematomas can occur in any patient but are especially likely to occur in those receiving anticoagulants, especially heparin. These hematomas are usually self-limited, and intervention is rarely necessary. Acute management includes direct manual compression, sandbag compression, pressure dressings, or a combination thereof. Needle aspiration and opening the pocket to drain the hematoma are discouraged because of the risk of introducing infection. Reoperation is generally limited to situations in which there is impending compromise of the incision, uncontrollable bleeding, uncontrollable pain, or suspected infection. Other possible pocket problems include erosion of the underlying hardware through the skin, infection, pocket pain, migration of the pulse generator, and misplacement of the generator (so that it interferes with shoulder movement).

Erosion of the underlying hardware through the skin can be quite serious, in that it usually leads to infection of the system. In normal circumstances, the underlying hardware, including the leads, can be felt during palpation of the pacemaker pocket, especially if the patient is thin. In extreme cases, the outlines of the generator and the leads can be clearly seen through the skin. It is important to be able to distinguish between normal palpability or visibility and impending pacemaker pocket erosion. Normally, the skin overlying the pacemaker is freely mobile, without discoloration or tenderness to palpation. Fixation, erythema, thinning, atrophy, and scaling of the skin over the underlying hardware are signs of impending erosion. It is crucial to identify early signs of erosion before the hardware breaks the skin. If the skin is intact, surgical revision of the pocket is often all that is needed to protect the hardware from contamination and infection. Once the hardware has been exposed, however, it must be assumed that the device is infected; treatment often requires a much more complex procedure that includes removal of all the hardware.^15,16

Device migration is unusual but can cause significant discomfort. In some cases, surgical revision of the pocket is required to restore an appropriate position.

Chronic pacemaker pocket pain is infrequent. There is normally some postoperative discomfort while the site heals and the capsule of scar tissue develops. Chronic pain may indicate that the device is not properly located in relation to the shoulder joint and the clavicle or may be an early sign of subacute infection.

Generator Complications

Normal battery depletion aside, pacemaker generators are generally very reliable, and true allergy to pacemaker materials is very rare. Manufacturers issue advisories including safety alerts and recalls when they become aware of a device malfunction. These have increased in frequency over the past several years.¹⁷ When an advisory is issued, the physician's responsibility involves identifying affected patients and making specific recommendations to these patients. Appropriate action may involve increased frequency of follow-up, noninvasive downloading of additional software instructions to the implanted pacemaker, or generator replacement. Advisories generate substantial patient anxiety, increased outpatient appointments, and use of other hospital resources, with significant financial implications.

Lead Complications

Pacemaker lead complications include dislodgment, infection, conductor fracture, and insulation failure. Conductor fractures can occur throughout the body of the lead, but the most common location is the area where the lead passes between the first rib and the clavicle (the so-called subclavian crush syndrome). Insulation failure occurs most commonly in the portions of lead within the subcutaneous pacemaker pocket. Conductor fractures or insulation breaks may be subclinical or may give rise to symptoms related to failure to pace or sense appropriately. Extracardiac stimulation and changes in measured parameters of lead function may be noted. Some lead fractures may be evident on chest x-ray; however, only the lead conductor, and not the insulation, is radiopaque. Even with a conductor fracture, the x-ray often shows no abnormality

An uncommon lead complication is the so-called twiddler's syndrome, which refers to patients who, whether intentionally or subconsciously, continually manipulate the generator within the pocket, eventually causing lead damage or dislodgment.

Pacemaker Infections

Bacterial infections can affect any part of the pacemaker system, and the consequences can be devastating. The most common pathogens are staphylococci, especially Staphylococcus epidermidis. Once a pacemaker infection is established, it is difficult to eradicate with antibiotics; thus, infected pacemaker systems usually must be removed in their entirety. Patients with pacemakers in place who acquire S. aureus bacteremia are at significant risk for a secondary device infection.¹⁶ If infection of an implanted cardiac device is suspected, prompt referral to an experienced center is critical.

To function appropriately, pacemakers must be able to sense a clean signal from the myocardium. A number of potential sources can interfere with such signals and thereby affect pacemaker function.^18,19 The most significant of these is electromagnetic interference (EMI) from devices in the patient's environment. The most common detrimental effect of EMI is inhibition of pacing: the pacemaker senses the EMI and interprets it as cardiac activity. In a pacemaker-dependent patient, this misinterpretation can lead to asystole. Other detrimental effects include reversion to an asynchronous pacing mode, reversion to a backup pacing mode, inappropriate activation of other features, and damage to the pacemaker circuitry. Modern pacemakers with bipolar leads are less susceptible to EMI; in addition, they often contain filters and other features designed to protect the patient from device malfunction.

Sources of EMI

Figure 5. Determination of Reprogramming Prior to Electrosurgery

Sources of EMI can be divided into household sources, industrial sources, and medical sources [see Table 4]. In general, household appliances such as microwave ovens, hairdryers, and television remote controls are safe for pacemaker recipients to use. Medical sources of EMI are common in both noninvasive and invasive procedures. MRI scans are generally contraindicated in pacemaker patients; they should be performed only in life-threatening situations and with close monitoring (see below). Surgical procedures involving electocautery are important sources of EMI and often necessitate pacemaker reprogramming before and after the procedure. As a rule, only patients who are pacemaker dependent require reprogramming. The location of the procedure in relation to the pacemaker generator is also an important consideration in deciding whether reprogramming is indicated. On the basis of case reports and our own clinical experience, we have developed an approach to determine who needs pacemaker reprogramming before surgery [see Figure 5].

Pacemakers and MRI Scans

MRI scanners utilize large magnetic fields that can affect pacemaker function in four different ways: (1) overheating of the generator, causing permanent damage to its electronic components, (2) heating of the leads, leading to tissue injury and affecting pacemaker performance, (3) generating a pacing current, which could possibly induce arrhythmias, and (4) causing unwanted programming change. For these reasons, the Food and Drug Administration and device manufacturers recommend against the use of MRI in patients with implanted pacemakers.

Several small studies have shown successful diagnostic MRI imaging in selected patients with pacemakers.^20,21 Some hospitals and physicians have protocols for cautiously performing MRI imaging in selected pacemaker patients. Therefore, if MRI scanning is thought to be absolutely necessary in a critically ill patient, and if the benefit of the MRI is thought to outweigh its risks in such a patient, consideration could be made to refer the patient to a hospital program that is performing MRI in selected pacemaker patients.

If MRI scanning is the only alternative for a pacemaker recipient, care should be taken not to perform the test within 6 weeks of device implantation or when old leads are left abandoned. Pacemaker-dependent patients should have their device programmed in asynchronous mode with magnet mode turned off. Care should be taken to monitor the patient's heart rhythm during the scan, and a cardiac electrophysiologist should be available on site.

With the growth of MRI, including that used for cardiac imaging, MRI-compatible pacemaker generators and leads are currently being developed.

Pacemaker technology is advancing on many fronts.^22,23 Devices are becoming smaller and more sophisticated. Improvements in pacemaker software are allowing closer replication of normal physiologic cardiac function. New automatic features (e.g., automatic mode switching in response to atrial fibrillation, automatic capture verification, and automatic sensing) are leading to greater reliability and simplified follow-up. Cardiac resynchronization therapy has become established in selected heart failure patients; in many cases, such therapy leads to dramatic subjective and objective improvement. Pacemaker and implantable cardioverter-defibrillator technologies are converging. New information technology is allowing improved collection, storage, and analysis of pacemaker patient data. Internet-based patient management systems have been developed that include automatic wireless interrogation performed at the patient's home. Preliminary work on experimental pacemakers not requiring pacing leads has been reported.²⁴

Roger A. Freedman, M.D., has received grants for clinical research from Boston Scientific Corporation, Medtronic Inc., and St. Jude Medical, Inc. He has served as a consultant to Boston Scientific Corporation, Medtronic Inc., St. Jude Medical, Inc., and Sorin Corp. His department has received program support from Boston Scientific Corporation, Medtronic Inc., and St. Jude Medical, Inc.

Jonathan Lowy, M.D., has received research grants from Boston Scientific Corporation and Medtronic, Inc., and has served as a consultant to Boston Scientific Corporation, Medtronic Inc., and St. Jude Medical.

Nazem W. Akoum, M.D., F.A.C.P., has no commercial relationships with manufacturers of products or providers of services discussed in this chapter.