ACP medicine, 3rd Edition

Cardiovascular Medicine

Pacemaker Therapy

Jonathan Lowy M.D.1

Roger A. Freedman M.D.2

1Director of Electrophysiology, St. John's Hospital, Bellingham, Washington

2Professor of Medicine, University of Utah School of Medicine

Roger A. Freedman, M.D., has received grants for clinical research from Guidant Corporation, Medtronic Inc., and St. Jude Medical, Inc., has served as a consultant to Guidant Corporation and St. Jude Medical, Inc., has received program support from Guidant Corporation and Medtronic Inc., and has served as a speaker for Guidant Corporation.

Jonathan Lowy, M.D., has received grants for clinical research from Guidant Corporation.

May 2004

Worldwide, more than 250,000 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.

Normal Cardiac Electrical System

The primary role of cardiac pacing is to augment or replace the heart's intrinsic electrical system. This specialized system consists of structures capable of automaticity and conduction and provides the timing and synchrony needed to maintain appropriate cardiac output.


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 demonstrates the fastest rate of spontaneous depolarization (automaticity) of any of the cardiac tissues.


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.


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 and terminates in 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.


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. 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.

Indications for Permanent Pacing


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.

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 1984.1 These guidelines were subsequently revised in 1991,2 1998,3 and 2002.4 The North American Society of Pacing and Electrophysiology (NASPE) was also involved in the 2002 revision [see Table 1]. Current recommendations are divided into the following three broad categories on the basis of (1) the strength of the available data and (2) 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.

Table 1 Guidelines for Permanent Pacemaker Implantation


Indications for Pacing

Class I

Class IIa

Class IIb

Class III

Acquired AV block

Third-degreee AV block or advanced second-degree AV block associated with any of the following:
   Symptomatic bradycardia
   Medical conditions requiring medications that result in symptomatic bradycardia (e.g., beta blockers, calcium channel blockers, antiarrhythmic agents)
   Asymptomatic asystole ≥ 3 sec or escape rate < 40 beats/min in awake patient
   Ablation of AV junction
   Postoperative AV block not expected to resolve after cardiac surgery
   Neuromuscular disease, including myotonic muscular dystrophy, Kearns-Sayre syndrome, Erb dystrophy, and peroneal muscular atrophy, with or without symptoms of bradycardia
Second-degree AV block, regardless of type, with documented associated bradycardia

Asymptomatic third-degree AV block with average ventricular rate ≥ 40 beats/min when awake
Asymptomatic type II second-degreeAV block with narrow QRS complex
Asymptomatic type I second-degree AV block found during electrophysiologic study performed for another reason
First- or second-degree AV block with symptoms similar to those of pacemaker syndrome

Marked first-degree
   AV delay > 30 msec in
   patients with left ventricular
   and congestive symptoms
   of heart failure
Neuromuscular disease,
   including myotonic
   muscular dystrophy,
   Kearns-Sayre syndrome,
   Erb dystrophy,
   and peroneal muscular
   atrophy, with or
   without symptoms of
   bradycardia, with any
   degree of AV block,
   with or without

Asymptomatic first-degree
   AV block
Asymptomatic type I
   (Wenckebach) second-degree AV block
   Any AV block that is expected
   to resolve and does not

Chronic bifascicular
   and trifascicular

Intermittent third-degree AV block
Type II second-degree AV block
Alternating bundle-branch block

Syncope in which other causes
   (specifically, ventricular
   tachycardia) have been
   excluded but that has not
   been demonstrated to be
   due to AV block
Asymptomatic patients in
   whom electrophysiologic
   study reveals prolonged
   HV interval
Electrophysiologic study
   finding of nonphysiologic
   block below His bundle

Neuromuscular diseases
   with any degree
   of fascicular block,
   with or without
   symptoms, in which
   there is unpredictable

Fascicular block without
   AV block or symptoms
Fascicular block with first-degree
   AV block without


Persistent second-degree AV block in His-Purkinje
   system with bifascicular block
   or third-degree AV block within or below
   His-Purkinje system after acute MI
Persistent and symptomatic second- or
   third-degree AV block
Transient advanced second- or third-degree
   infranodal AV block and associated
   bundle-branch block; electrophysiologic
   study may be indicated to identify
   level of block


Persistent second- or
   third-degree block at
   level of AV node

Transient AV block in absence
   of intraventricular
   conduction delay
Transient AV block in presence
   of isolated left anterior
   fascicular block
Acquired left anterior
     hemiblock in absence of
     AV block
Persistent first-degree AV
     block in presence of old
     bundle-branch block

SA node

SA node dysfunction with documented
   symptomatic bradycardia
Symptomatic SA node dysfunction resulting
   in bradycardia that occurs as
   consequence of essential drug therapy
   to which there is no acceptable
Symptomatic chronotropic incompetence

SA node dysfunction occurring
   either spontaneously or as a
   result of drug therapy with
   heart rate < 40 beats/min
   where there is clear association
   between symptoms but
   where actual presence of
   bradycardia during symptoms
   has not been documented
Syncope of unexplained origin
   in which major abnormalities
   of SA node are elicited during
   electrophysiologic studies

Patients with minimal
   symptoms with resting
   heart rates < 40
   beats/min while

Asymptomatic patients, including
   those on drug
   therapy with resting heart
   rates < 40 beats/min
Patients with symptoms of
   bradycardia in which SA
   node dysfunction is clearly
   not associated with
SA node dysfunction with
   symptomatic bradycardia
   caused by unnecessary
     drug therapy

   syncope and
   carotid sinus

Recurrent syncope caused by carotid
   sinus massage that results in ventricular
   asystole ≥ 3 sec (must occur
   in absence of any medication that
   depresses SA node or AV conduction)

Recurrent syncope without
   another cause and cardioinhibitory
   response to carotid
   sinus massage
Symptomatic and recurrent
   neurocardiogenic syncope
   associated with documented


Hyperactive cardioinhibitory
   response to carotid
   sinus massage in absence
   of symptoms or in presence
   of vague symptoms
Recurrent symptoms in
   absence of documented
   cardioinhibitory response
Situational vasovagal syncope
   in which avoiding
   behavior or environmental
   factors is effective


Acquired Atrioventricular Block

AV block is defined as delayed or failed conduction from the atria to the ventricles.5,6,7,8,9 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.

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. High-degree (or advanced) type II AV block is defined as blockage 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.

The anatomic location of AV block has important prognostic 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 typically 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 often ameliorated by junctional escape rhythms, whereas escape rhythms are much less reliable when the block is at the level of the His-Purkinje system.

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 blockage of the right bundle and either the left anterior or the left 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.10 Trifascicular block may also be present when bifascicular block is accompanied by first-degree AV block. More commonly, however, this electrocardiogram pattern is the result of bifascicular block combined with conduction delay at the AV node.

Acute Myocardial Infarction

Conduction abnormalities are common in the setting of acute myocardial infarction.11,12,13,14,15 Pathophysiologic mechanisms include ischemia, necrosis, autonomic influences, and the neurohumoral response to injury. Temporary transvenous pacing is often required during the acute phase of an infarction. The need for temporary pacing does not, however, predict the need for permanent pacing, given that 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.

SA Node Dysfunction

SA node dysfunction is a loose term that includes a number of different arrhythmias, including sinus bradycardia, sinus arrest, sinoatrial block, and the bradycardia-tachycardia syndrome.16,17,18,19,20 The bradycardia-tachycardia syndrome is characterized by atrial tachyarrhythmias (usually atrial fibrillation) alternating with periods of bradycardia or sinus pauses. 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.

Pacing for Neurocardiogenic Syncope and Hypersensitive Carotid Syndrome

Neurocardiogenic syncope is syncope secondary to vasodilatation or bradyarrhythmias resulting from abrupt imbalance of autonomic input to the heart and the vascular system.21,22,23,24,25 Classic neurocardiogenic syncope involves sinus tachycardia followed by bradycardia, vasodilatation, and syncope. Some patients have primarily a vasodepressive (vasodilatation) 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.

Other Pacemaker Indications

Besides those already mentioned, there are several indications for which pacemakers are implanted that warrant mention, including treatment of hypertrophic cardiomyopathy, prevention or suppression of tachyarrhythmias, and resynchronization therapy for congestive heart failure. Cardiac resynchronization therapy is an exciting new development in the treatment of heart failure but lies outside the scope of this chapter.

Pacemaker Systems

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


Over the past 30 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 chambers, 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.


Figure 1. Pacemaker Generators

Shown are five different pacemaker generators. The first three are older single-chamber devices from (a) 1972, (b) 1977, and (c) 1983. The last two are modern dual-chamber devices from (d) 1994 and (e) 2000.

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 currently use lithium iodine batteries that have a typical life span of 5 to 10 years. 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 are the 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 have to do with type of insulation, fixation mechanism, and polarity.


Figure 2. Pacemaker Leads

Shown are four different pacemaker leads. The first (a) is a passive-fixation lead with soft tines at the tip (arrow); it is also a preformed J lead used for atrial pacing. The second (b) is an active-fixation lead with a fixed helix. The third (c) and fourth (d) are active-fixation leads with a retractable helix; the fourth has the helix mechanism exposed.

Most pacemaker leads are insulated with either silicone or polyurethane. In the past, there were significant differences between the two materials with respect to durability and handling. Today, however, the differences are minimal, and the choice of material is usually operator dependent.

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.

Finally, leads can be either unipolar or bipolar. Unipolar leads have a single conductor and a single electrode; the unipolar 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.

Currently available lead systems are very reliable: failure rates at 5 years are typically 5% or lower.


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 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 life, 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.

Pacemaker Programming

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.


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.


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].26 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.

Table 2 NASPE-BPEG Generic Five-Position Code for Antibradycardia Pacing








Parameter measured

Chamber(s) paced

Chamber(s) sensed

Response or action

Rate modulation

Multisite pacing

Possible values

O = None
A = Atrium
V = Ventricle
D = Dual (A + V)

O = None
A = Atrium
V = Ventricle
D = Dual (A + V)

O = None
I = Inhibited
T = Triggered
D = Dual (I + T)

O = None
R = Rate response on

O = None
A = Atrium
V = Ventricle
D = Dual (A + V)

NASPE—North American Society of Pacing and Electrophysiology  BPEG—British Pacing and Electrophysiology Group


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. 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, how ever, 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].


Figure 3. Forms of DDD Pacing

Illustrated are different forms of DDD pacing. In the first two beats (labeled “Inhibited”), the pacemaker senses both the intrinsic P wave and the QRS complex; the result is inhibition of pacing. In the next two beats (labeled “Atrial”), there is a pacing spike preceding each P wave; the result is atrial pacing. The intrinsic QRS complex is then sensed, and ventricular pacing is inhibited. In the third set of beats (labeled “Sequential”), there are pacing spikes preceding both the P wave and the QRS complex. Both chambers are paced. The paced QRS morphology is noticeably different from the intrinsic complexes seen in the previous examples. In the final set of beats (labeled “Tracking”), an intrinsic P wave is followed by a paced QRS. The intrinsic atrial beat is sensed and triggers ventricular pacing.

Patients with chronic atrial fibrillation and slow ventricular response are generally treated with single-chamber ventricular pacemakers. Such devices are also occasionally used in patients with isolated SA node dysfunction.

Pacemaker Implantation

Most pacemakers are implanted by cardiologists, and most implantation procedures are performed in the cardiac catheterization laboratory.27


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, all patients receiving warfarin had their international normalized ratios (INRs) normalized before the procedure. Furthermore, patients with a strong indication for anticoagulation (e.g., 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.28,29

Pacemakers can interfere with or preclude certain imaging procedures, such as mammography and magnetic resonance imaging. In the case of elective pacemaker implants, a baseline mammogram should be performed beforehand.30 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 commonly employed, but not in a uniform manner. There are no strict guidelines, and antibiotic regimens vary greatly.31


The pulse generator pocket is usually placed on the upper left aspect of the chest, just medial to the angle of the deltopectoral grove 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 acclusion 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 is most frequently gained by means of 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. In addition, 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.


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 sometimes 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 have to be repositioned in a second procedure.


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. Nonnarcotic 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 ECG immediately after implantation.

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].


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

Shown is the typical appearance of a dual-chamber pacemaker on posteroanterior (left) and lateral (right) chest x-rays. The RV lead is at the apex, and the RA lead is in the right atrial appendage.

Before discharge, the patient receives instruction about the pacemaker teaching 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.


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.


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. Guidelines for follow-up have been published by NASPE,32 as well as by the Canadian Working Group in Cardiac Pacing.33 We recommend that patients either be seen in the office or undergo TTM every 3 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.

Table 3 Common Findings Related to Pacemaker Problems


Potential Causes


When to Refer

Oozing at incision site

Local bleeding

External compression; avoid needle
     aspiration or surgical drainage if
Withhold anticoagulation

Impending wound dehiscence,
     uncontrolled pain
Signs of infection

Palpable hardware, including
     header or leads

Benign unless findings consistent with impending erosion

No treatment
Cushion with gauze or dressing to avoid irritation from clothing
Pocket revision

Signs of impending erosion
Pain requiring consideration of
     pocket revision

Adhesion of skin
Thinning or atrophy of skin
Scaling of skin

Impending generator or lead erosion

Pocket revision

If hardware becomes exposed,
     extraction may be required

Exposed hardware

Erosion with infection

Blood cultures
Blood count
Hardware extraction


Pocket erythema
Pocket swelling
Purulent discharge

Local inflammatory reaction
Local trauma

Blood cultures
Chest x-ray
Blood counts


Pocket pain

Superficial implant
Generator migration
Pacemaker allergy
Superficial irritation from bra strap or clothing

Chest x-ray
Examination of generator pocket for signs of migration or infection

Signs of infection
Continued pain despite mild analgesics

Fever, chills, or other signs of systemic infection or bacteremia, even without signs of pocket infection

Systemic infection, including bacteremia,
     bloodstream infection, or

Blood cultures
Chest x-ray
Blood counts


Ipsilateral arm swelling
Arm heaviness
Superior vena cava syndrome

Venous thrombosis

Doppler ultrasonography
Arm elevation


Pectoral muscle twitching
Diaphragmatic stimulation

Lead fracture
Unipolar pacing
Autocapture feature
Phrenic nerve stimulation

Chest x-ray
Pacemaker interrogation



Pocket hematomas can occur in any patient but are especially likely to occur in those receiving anticoagulants. 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, 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 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, the device must be assumed to be infected, and treatment usually involves a much more complex procedure that includes removal of all the hardware.34

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 also 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.


On the whole, pacemaker generators are highly reliable: normal battery depletion aside, failure is unusual. True allergy to pacemaker materials does occur but is rare.


Pacemaker lead complications include dislodgment, fracture, and infection. 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; fracture at this site leads to the so-called subclavian crush syndrome. Lead fractures may be asymptomatic 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 conductors are radiopaque, and thus, simple disruption of the outer insulation will not be visible.

A common 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.


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.35 If infection of an implanted cardiac device is suspected, prompt referral to an experienced center is critical.

External Interference with Pacemaker Function

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.36,37 The most significant of these is EMI, which can have several detrimental effects on pacing systems. 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 have catastrophic consequences. 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 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.38,39,40 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.41,42 Surgical procedures involving electocauterization are important sources of EMI and often necessitate pacemaker reprogramming before and after the procedure.43 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 we use to determine who needs pacemaker reprogramming before surgery [see Figure 5].

Table 4 Sources of Electromagnetic Interference That Can Affect Pacemakers



Safe with Pacemaker

Specific Recommendations

Medical sources



Rarely done; restricted to life-threatening situations with close monitoring

CT scanning


Pacemaker may interfere with images of thorax



Activity sensors should be disabled
Pacemaker-dependent patients should be programmed to asynchronous mode
Shocks should be synchronized to R wave
Contraindicated in patients with abdominal implants

External direct current cardioversion


Avoid placing patches or paddles directly over pacemaker
Have transcutaneous pacing available
Use lowest possible energy and biphasic waveform when possible
Interrogate pacemaker after procedure



Test at highest output for pacemaker inhibition before discharge

Peripheral nerve stimulation


Nerve conduction studies below the elbow or knee are safe

Transcutaneous electric nerve stimulation (TENS)


May require increasing sensing threshold
Avoid placing TENS electrodes parallel to pacing vector

Radiation therapy


Avoid direct irradiation; maximize shielding
If total dose is expected to exceed 10 Gy, device may have to be relocated out of field
Reprogram to asynchronous mode if patient is pacemaker dependent
Initiate continuous monitoring if patient is pacemaker dependent
Check device function after each session and for first few weeks after therapy

Diagnostic ultrasonography, including echocardiography


No precautions needed

Surgical electrocautery


[see Figure 5]

Household and industrial sources

Microwave ovens, TV remote-control devices, cordless telephones, other household appliances


All devices considered safe; controlled studies lacking

Slot machines


May cause interaction and spurious shocks with ICDs

Walk-through metal detectors


Do not dwell in scanner; device will probably set off alarm
Patients should be advised to carry pacemaker ID card as proof

Handheld security wand


Patient should instruct person conducting search not to put wand directly over pacemaker generator

Cellular telephones


Keep phone at least 10 cm from pacemaker; do not keep phone in shirt pocket above pacemaker; try to use contralateral ear when using phone

Electronic article surveillance devices


Do not dwell in scanner

Industrial sources, including large electric motors, magnets, and high-voltage power


Depends on source and proximity of pacemaker, site visit may be needed to determine safety

Arc-welding equipment


Cannot be used because of magnetic field of cable

ICD—implantable cardioverter-defibrillator


Figure 5. Method of Determining Reprogramming Prior to Electrosurgery

Algorithm outlines our method of determining which pacemaker patients need reprogramming to an asynchronous mode before procedures involving electrosurgery.

The Future

Pacemaker technology is advancing on many fronts.44,45 Devices are becoming smaller and more sophisticated. Improvements in pacemaker software are allowing closer imitation 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. New indications for pacing (including cardiac resynchronization therapy for heart failure and treatment of sleep apnea) are evolving. 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 are being developed that will include automatic wireless interrogation performed at the patient's home.


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Editors: Dale, David C.; Federman, Daniel D.