Clinical Electrocardiography: A Simplified Approach, 7th Edition (2006)

Part II. CARDIAC RHYTHM DISTURBANCES

Chapter 21. Pacemakers and Implantable Cardioverter-Defibrillators

A brief introduction

This chapter provides a brief overview of an important aspect of clinical electrocardiography—electronic cardiac devices, including pacemakers and implantable cardioverter-defibrillator (ICD) devices. Particular emphasis is placed on introducing the different types of pacemakers, major indications for pacemaking, recognition of pacemaker malfunction, and the functions and uses of ICD devices.

PACEMAKERS

A pacemaker is a battery-powered device designed to stimulate the heart electrically. This device is used primarily when a patient's own heart rate is excessively slow (see Chapter 20 for discussion of bradycardias). A pacemaker has two major components: a battery that serves as the power source and wire electrodes that are attached to the heart chamber(s) being stimulated.

Pacemakers are either temporary or permanent (implanted). With temporary pacemakers, the pacing wire is connected to a battery outside the body. With long-term implanted pacemakers, the battery is inserted subcutaneously, usually under the chest wall. With both types, the pacemaker wire is usually threaded through a vein into the right ventricular cavity so that the pacemaker electrode can stimulate the endocardium of the right ventricle ( Fig. 21-1 ). Occasionally, an epicardial pacemaker wire is used. This wire is sewn directly into the epicardium of the left or right ventricle, and the battery is implanted under the skin of the abdomen. Atrial pacing can also be performed. Many patients benefit from a dual-chamber pacemaker therapy in which electrodes are placed in both the right atrium and right ventricle.

FIGURE 21-1  Implanted pacemaker generator (battery) with a wire electrode inserted through the left subclavian vein into the right ventricle.

As described later, pacemakers have two additional specialized uses: (1) treating certain types of tachycardias, and (2) improving ventricular function in selected patients with congestive heart failure as part of cardiac resynchronization therapy using biventricular pacing.

PACEMAKER ECG PATTERNS

When a ventricular pacemaker fires, it produces a sharp vertical deflection (pacemaker spike) followed by a QRS complex (representing depolarization of the ventricle). Can you predict what the ECG shows with a functioning right ventricular pacemaker? The ECG should show a left bundle branch block (LBBB) pattern (see Fig. 7-8 ). Recall that the pacemaker is initially stimulating the right ventricle and therefore left ventricular depolarization is delayed.

Typical pacemaker tracings are shown in Figures 7-8 and 21-2 . The vertical line preceding each QRS complex is the pacemaker spike. This sharp deflection is followed by a wide QRS complex with LBBB morphology (QS in lead V1 and wide R wave in lead V6). What pattern would you predict with an epicardial pacemaker stimulating the left ventricle? It would be a right bundle branch block pattern.

FIGURE 21-2  Pacemaker beats. The first P-QRS cycle is from a normal sinus beat. It is followed by four pacemaker beats. Notice the pacemaker spike (S) preceding each paced beat. Pacemaker beats are wide and resemble bundle branch block beats. Because this type of pacemaker senses and paces only in the right ventricle and is inhibited by the intrinsic QRS complexes, it is termed a VVI unit. (See Appendix at the end of this chapter.)

An atrial pacemaker produces a spike followed by a P wave ( Fig. 21-3 ).

FIGURE 21-3  With the pacemaker electrode placed in the right atrium, a pacemaker spike (A) is seen before each P wave. The QRS complex is normal because the ventricle is not being electronically paced.

Pacemaker patterns seen with biventricular pacing as part of cardiac resynchronization therapy are described later in this chapter.

PACEMAKER BATTERIES

A variety of battery units can be used to power implanted pacemakers. Early pacemaker batteries used mercury-zinc cells. Because of their relatively short life span, however, these units were supplanted by lithium batteries, which may last 5 or more years. As the power cell of a conventional pacemaker wears out, the pacemaker rate usually starts to slow.

VENTRICULAR PACING: FIXED-RATE AND DEMAND PACEMAKERS

The two modes of pacemaker function are fixed rate and demand. A fixed-rate pacemaker is one that fires at a specific preset rate, regardless of the patient's own heart rate. The earliest pacemakers were fixed-rate devices. Contemporary pacemakers are demand units. A demand pacemaker literally functions “on demand,” that is, only when the patient's heart rate falls below a preset value. Therefore a demand pacemaker incorporates two distinct features: (1) a sensing mechanism designed so that the pacemaker is inhibited when the patient's own heart rate is adequate, and (2) a pacing mechanism designed to trigger the pacemaker when no intrinsic QRS complexes occur within a predetermined period. By contrast, fixed-rate pacemakers lack a sensing mechanism.

Demand units can be temporarily converted to fixed-rate mode by placing a special magnet on the chest wall over the battery. The magnet test is routinely performed when the pacemaker rate is being checked. Present-day demand-type pacemakers are also “programmable.” This means that the pacing rate can be adjusted once a pacemaker is implanted. Adjustment of rate is accomplished by placing a special telemetry device on the chest wall to allow communication with the pacemaker.

Demand ventricular pacemakers usually are QRS (R wave) inhibited. They emit pulses only when the spontaneous heart rate falls below the escape rate of the pacemaker (e.g., 70 beats/min) ( Fig. 21-4 ). They do not emit pulses when the patient's spontaneous heart rate is faster than the escape rate of the pacemaker. Each time a QRS-inhibited pacemaker senses a spontaneous QRS complex, formation of a pacemaker pulse is inhibited. Therefore these pacemakers show pacemaker spikes only when the spontaneous heart rate is slower than the escape rate of the pacemaker. The spikes appear before each QRS complex.

FIGURE 21-4  A ventricular demand (QRS-inhibited) pacemaker emits an electronic pulse only when the intrinsic heart rate falls below the escape rate of the pacemaker.

The QRS-inhibited pacemaker also has a refractory period (e.g., 0.4 sec) that begins whenever the pacemaker senses a QRS complex or emits a pulse ( Fig. 21-5 ). During the refractory period, the pacemaker cannot sense another R wave. If spontaneous ventricular beats or ventricular premature complexes occur during the refractory period, however, they are not inhibited but appear on the ECG.

FIGURE 21-5  During the refractory period a ventricular demand pacemaker does not sense any electrical activity. The refractory period is followed by the alert period. If no QRS complex is sensed by the end of the alert period, the pacemaker emits an escape pulse.

The refractory period is followed by an alert period, during which the pacemaker can sense an R wave. If no QRS complex is sensed by the end of the alert period, the pacemaker emits another pulse (seeFig. 21-5 ). If a spontaneous QRS complex occurs, however, the pacemaker is recycled into another refractory period and then into another alert period.

DUAL-CHAMBER PACING

In dual-chamber pacemakers, electrodes are inserted into both the right atrium and right ventricle. With most models in use today, the circuitry permits sensing and pacing in both chambers. Thus the atrial lead is able to sense the patient's intrinsic P waves and stimulates the atrium when the atrial rate becomes too slow. The circuitry is designed to allow for a physiologic delay between atrial and ventricular stimulation. This atrioventricular (AV) delay (interval between the atrial and ventricular pacemaker spikes) is analogous to the PR interval seen in physiologic conduction.

With the type of dual-chamber pacemaker that allows for both atrial sensing and pacing and ventricular sensing and pacing, a variety of ECG patterns may be seen, depending on the patient's intrinsic electrical activity. A schematic of these pacemaker patterns appears in Figure 21-6 .

FIGURE 21-6  Dual-chamber (DDD) pacemakers sense and pace in both atria and ventricles. The pacemaker emits a stimulus (spike) whenever a native P wave or QRS complex is not sensed within some programmed time interval.

Dual-chamber pacing is helpful in maintaining physiologic timing between atrial and ventricular systole. When ventricular pacing alone is used, this physiologic timing is lost. In some patients, the loss of timed atrial contractions causes a marked reduction in cardiac output. Dual-chamber pacing produces a significant improvement in the cardiac performance of these individuals. In selected patients, dual-chamber pacing may allow a physiologic increase in ventricular rate during exercise. For example, consider the patient with complete heart block and underlying sinus rhythm whose ventricular rate with a ventricular pacemaker is constant (e.g., 72 beats/min) regardless of the atrial (P wave) rate. With a dual-chamber pacemaker, the ventricular rate can increase in tandem with the sinus rate during exercise, further increasing cardiac output. Atrial sensing or pacing is obviously of no use in patients with chronic atrial fibrillation or atrial flutter.

PROGRAMMABILITY

In the early days of cardiac pacing, the pacemaker rate was not adjustable once the unit had been inserted. A major advance was the introduction of programmable pacemakers, in which the pacemaker rate could be externally changed.

In addition to rate, many other parameters can be externally programmed in modern pacemakers. These parameters include the voltage of the pacemaker discharge, the sensitivity of the electrode to the intrinsic beats, the pacemaker refractory period, and the duration of the pacemaker spike.

INDICATIONS FOR CARDIAC PACING

Implanted (Permanent) Pacemakers

The major reason for implanting a pacemaker is the presence of a symptomatic bradyarrhythmia. In particular, electronic pacemakers may be indicated for numerous conditions, including syncope, light-headedness, weakness, or congestive failure associated with complete heart block, second-degree AV block, marked sinus bradycardia or sinus pauses (sick sinus syndrome), slow junctional rhythms, or atrial fibrillation or flutter with an excessively slow ventricular response.

Pacemaker functions have also been incorporated in new generations of implantable cardioverter-defibrillator (ICD) devices, as described in the section to follow.

Temporary Pacemakers

Temporary pacemakers may be transvenous or transcutaneous. With transvenous pacemakers, the battery is connected to a pacing electrode that has been threaded through a vein into the right ventricle. With transcutaneous temporary pacing, specially designed electrodes are pasted on the chest wall. Although this technique is not successful in all patients and may cause some discomfort, it may be useful in certain critical circumstances when transvenous pacing is not available (see Chapter 19 ).

Temporary pacemakers are often employed during cardiac emergencies (e.g., myocardial infarction [MI]) when an extremely slow heart rate occurs. For example, they may be used immediately after open heart surgery or during cardiac arrest (see Chapter 19 ) when the ECG shows asystole or a slow escape rhythm that does not respond to drug therapy. Occasionally, temporary pacemakers are needed in patients with digitalis or other drug toxicity that is causing profound bradycardia.

As noted, temporary or permanent pacemakers are usually employed when the heart rate is too slow. Sometimes, a pacemaker is implanted to treat a tachyarrhythmia (e.g., ventricular tachycardia). The use of temporary pacing to treat atrial flutter is mentioned in Chapter 15 . The use of overdrive pacemaking as part of ICD devices is discussed in this chapter.

PACEMAKER MALFUNCTION

Pacemaker malfunctions occur when either the sensing or pacing function is impaired. For example, when the pacemaker battery runs down, the pacing rate generally slows and failure to sense or pacemay also occur. Failure to sense can be diagnosed by observing pacemaker spikes despite the patient's own adequate rate ( Fig. 21-7 ). The two most common causes of failure to sense (without actual battery failure) are dislodgment of the pacemaker wire and excessive fibrosis around the tip of the pacing wire.

FIGURE 21-7  Notice that after the first two paced complexes, a series of sinus beats with a prolonged PR interval is seen. Failure of the pacemaker unit to sense these intrinsic QRS complexes leads to inappropriate pacemaker spikes (•), which sometimes fall on T waves. Three of these spikes do not capture the ventricle because they occur during the refractory period of the cardiac cycle.  (Adapted from Conover MB: Understanding Electrocardiography, 4th ed. St. Louis, Mosby, 1996.)

Pacemaker malfunction can also result from failure to pace. This problem is diagnosed by observing pacemaker spikes without subsequent QRS complexes (failure to “capture”) ( Fig. 21-8 ), or by finding no pacemaker spikes even though the patient has an excessively slow heart rate ( Fig. 21-9 ). Failure to pace can also be caused by dislodgment of the pacemaker wire or by fibrosis around the tip of the pacing wire. In such cases, pacemaker spikes occur without associated QRS complexes. In other cases (particularly with a broken electrode wire, a short circuit in the pacing circuit, electrical interference from the muscles of the chest wall, or battery failure), failure to pace occurs without any pacemaker spike.

FIGURE 21-8  Notice that beats 1, 3, and 4 show pacemaker spikes (s) and normally paced wide QRS complexes and T waves. The remaining beats show only pacemaker spikes without capture. (R represents the patient's slow spontaneous QRS complexes, which the pacemaker also fails to sense.)

FIGURE 21-9  The underlying rhythm is second-degree (2:1) AV block. Despite the very slow QRS, the pacemaker fails to function.

Pacemaker malfunction in patients with temporary pacemakers should always prompt an immediate search for loose connections between the battery and the pacing wire, a faulty battery, or a dislodged wire.

COMPLICATIONS OF PACEMAKER THERAPY

Pacemakers are not without potential harm. Therefore careful thought should be given before a temporary or particularly a permanent pacemaker is inserted. Infection may occur at the pacemaker site. The electrode may perforate the ventricular wall. The pacemaker itself may cause serious arrhythmias. For example, dual-chamber pacemakers may facilitate runs of supraventricular tachycardia (“endless loop” pacemaker-mediated arrhythmias). Occasionally, a pacemaker also paces the muscles of the chest wall or the diaphragm, resulting in patient discomfort.

Patients with ventricular demand-type pacemakers also lose the normal physiologic timing afforded by the sequential contraction of the atria and ventricles. In some cases, patients will develop symptoms (so-called pacemaker syndrome) due to this loss of physiologic timing. Complaints may include light-headedness, fainting, shortness of breath, and cough. Upgrading the pacemaker unit to a dual-chamber device with atrial and ventricular sensing and pacing will generally alleviate these symptoms. Right ventricular pacing may also reduce cardiac functions by causing asynchronous ventricular activation.

DIAGNOSIS OF MYOCARDIAL INFARCTION WITH PACEMAKERS

The ECG diagnosis of MI may be difficult or impossible when all the QRS complexes are paced. With a right ventricular electrode, the ECG shows a left bundle branch block (LBBB) configuration. As described in Chapter 8 , LBBB generally masks both the QRS and the ST-T changes of MI. Therefore, unless you see spontaneous QRS-T complexes, you may not be able to diagnose acute or prior MI based on the ECG alone.

Finally, pacemakers may also produce ECG changes simulating MI. After periods of ventricular pacing, the ECG may show deep T wave inversions in the nonpaced beats. These so-called postpacemaker (“memory”) T wave inversions can be mistaken for primary ischemic ST-T changes.

PACEMAKERS AND CARDIAC RESYNCHRONIZATION THERAPY IN CHRONIC HEART FAILURE

As noted, the major use of implanted pacemakers is to treat symptomatic bradycardias ( Chapter 20 ). A more recent and innovative use of electronic pacemakers is to help improve ventricular function in selected patients with heart failure. This therapy was designed specifically to increase the low cardiac output by coordinating the contraction pattern of the two ventricles. Therefore this approach, which employs simultaneous pacing of the right and left ventricles, is referred to as cardiac resynchronization therapy (CRT) or biventricular (BiV) pacing.

As the name implies, BiV pacemaker technology is based on positioning one pacemaker lead (electrode wire) in the right ventricle and a second one in a position to stimulate simultaneously the left ventricle. The pacing wire for the left ventricle is placed in a cardiac vein on the lateral surface of the heart. This site can be accessed via the coronary sinus, the heart's main venous blood vessel that delivers blood from the heart back to the right ventricle, as shown in Figure 21-10 . Except in patients with atrial fibrillation or flutter, an atrial pacing electrode is also placed to allow for atrial sensing and, if needed, atrial pacing. In this way, the unit can be programmed such that the BiV stimulus is delivered at an optimal interval after the P wave.

FIGURE 21-10  Biventricular (BiV) pacemaker. Note the pacemaker lead in the coronary sinus vein that allows pacing of the left ventricle simultaneously with the right ventricle. BiV pacing is used in selected patients with congestive heart failure with left ventricular conduction delays to help “resynchronize” cardiac activation and thereby improve cardiac function.

Currently, the major indication for CRT is for patients with severe chronic heart failure who: (1) are still symptomatic on conventional medical therapy, and (2) have a wide QRS complex due to complete LBBB (or a similar) pattern. The LBBB results in an asynchronous pattern of ventricular contraction. Pacing the right and left ventricles at the same time with this kind of intraventricular conduction delay may help restore a more coordinated sequence of cardiac activation and contraction.

CRT has proven to be useful in improving symptoms (e.g., fatigue, shortness of breath) and objective measures of ventricular performance in appropriately selected groups of patients. Further, such therapy may also decrease the number of hospitalizations and even improve survival in some patients with heart failure.

As described, the ECG during standard pacing of the right ventricle shows an LBBB type pattern. In contrast, with BiV during CRT, the ECG usually shows an RBBB type pattern ( Fig. 21-11 ).

FIGURE 21-11  Right ventricular and biventricular pacing. A, Patient with heart failure who had a standard dual chamber (right atrial and right ventricular) pacemaker. B, To improve cardiac function, the pacemaker was upgraded to a biventricular (BiV) device. Note that during right ventricular pacing (A), the ECG shows a left bundle branch block morphology. The preceding sinus P waves are sensed by the atrial lead. In contrast, during biventricular pacing (B), the QRS complexes show a right bundle branch block morphology. Also, the QRS duration is somewhat shorter during biventricular pacing, due to the cardiac resynchronization effects of pacing the ventricles in a nearly simultaneous fashion.

BiV pacing in patients with heart failure can be combined with implantable cardioverter-defibrillator (ICD) therapy, which is described in the next section.

 

IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR THERAPY

Sudden cardiac arrest, occurring unexpectedly, is most commonly due to the abrupt onset of ventricular fibrillation, often preceded by a run of ventricular tachycardia ( Chapter 19 ). Less common causes are asystole and pulseless electrical activity. A major challenge in contemporary cardiology is how to prevent or interrupt episodes of ventricular arrhythmias that will otherwise lead to sudden cardiac death in high-risk patients.

The three major approaches to this problem used currently are: (1) antiarrhythmic drug therapy; (2) radiofrequency catheter ablation, designed to destroy arrhythmogenic areas of the ventricles; and (3) implantable cardioverter-defibrillators (ICDs). The rapid development of ICD therapy over the past few decades has been propelled by the findings that antiarrhythmic drug therapy is often ineffective or even dangerous and that catheter ablation has major limitations.

ICD therapy, as the name implies, involves the internal placement of a device, resembling a pacemaker, capable of delivering electrical shocks to the heart to terminate (cardiovert or defibrillate) a life-threatening run of ventricular tachycardia or ventricular fibrillation. This approach is modeled on conventional external cardioversion/defibrillation devices used in advanced cardiopulmonary resuscitation (CPR), which deliver an electrical shock via paddles placed on the chest wall to treat these types of tachycardias.

ICD TECHNOLOGY

ICD devices resemble pacemakers and have two major components: a lead system and a pulse generator ( Fig. 21-12 ). The lead system is used to sense cardiac electrical activity in the ventricles (and sometimes atria) and also to deliver shocks produced by the pulse generator. The ICD generator (about the size of a small pager) is usually inserted in the area of the pectoral muscle under the left collarbone, with the attached leads advanced through veins into the right side of the heart, like a pacemaker.

FIGURE 21-12  An implanted cardioverter-defibrillator (ICD) device resembles a pacemaker with a pulse generator and a lead system. The device can sense potentially lethal ventricular arrhythmias and deliver appropriate electrical therapy, including defibrillatory shocks.

Contemporary ICD devices have many programmable features and have the capacity to deliver tiered (staged) therapy when they detect a tachyarrhythmia ( Fig. 21-13 ). For example, the device may be programmed to perform antitachycardia (overdrive) pacing if it detects a presumed episode of ventricular tachycardia. This type of pacing may convert the arrhythmia without the need for an electrical cardioversion shock. If the arrhythmia persists or degenerates into ventricular fibrillation, actual shocks are delivered at increasing intensities. Newer ICD models also function as pacemakers in case of bradycardia. The ICD units have a storage capability, allowing cardiac electrophysiologists to interrogate the device periodically and obtain a detailed record of any arrhythmias sensed and any antitachycardia pacing or shocks delivered.

FIGURE 21-13  Tiered arrhythmia therapy and implanted cardioverter-defibrillators (ICDs). These devices are capable of automatically delivering staged therapy in treating ventricular tachycardia (VT) or ventricular fibrillation (VF), including antitachycardia pacing (A)and cardioversion shocks (B) for VT, and defibrillation shocks (C) for VF.

INDICATIONS FOR ICD THERAPY

The indications for ICD therapy have been expanding over recent years, based on miniaturization of the device, ease of implantation, and compelling clinical data showing a high degree of efficacy and safety compared with drug therapy.

A major and compelling indication is in secondary prevention of recurrent sudden death risk in patients who have already been resuscitated from an episode of cardiac arrest with ventricular fibrillation or ventricular tachycardia not due to a transient or reversible cause. Examples of transient or reversible causes of cardiac arrest include electrolyte abnormalities such as hypokalemia, acute myocardial infarction, and the use of drugs such as epinephrine or cocaine.

ICD therapy is also recommended in primary prevention of sudden death in very high–risk patients who have spontaneous episodes of sustained ventricular tachycardia with underlying structural heart disease (e.g., prior infarction, cardiomyopathy) or in selected patients without evident structural heart disease. In addition, ICD therapy is used prophylactically in certain patients with syncope or chronic heart disease who have ventricular fibrillation or sustained ventricular tachycardia that is induced during an electrophysiologic study, as well as in selected patients with documented inherited or familial conditions with a high risk of a first episode of life-threatening ventricular tachyarrhythmia, especially long QT syndrome and hypertrophic cardiomyopathy.

Expanded indications for ICD placement for primary prevention of sudden cardiac death now also include selected patients with ischemic or nonischemic cardiomyopathy and other patients with coronary artery disease and a low left ventricular ejection fraction due to myocardial infarction, even in the absence of spontaneous or inducible ventricular tachyarrhythmia.

For detailed and updated guidelines to current and evolving indications for ICD therapy, and also pacemaker therapy, readers are referred to the websites of the American Heart Association, the American College of Cardiology, and the Heart Rhythm Society.

COMPLICATIONS OF ICD THERAPY

ICD devices, despite their utility, are not without risk. The implantation procedure carries a small risk of death and serious morbidity related to vascular or myocardial perforation, infection, and thrombosis. After implantation, patients may suffer from inappropriate and painful shocks delivered in response to electrical artifacts or non-life-threatening rhythms.

 

 

APPENDIX: THE THREE- AND FIVE-LETTER PACEMAKER CODE

A simple three-position pacemaker code is often used to describe a particular pacemaker's functions and mode of response. As shown in Table 21-1 , the letter in the first position indicates the chamber(s) being paced—the atrium (A), ventricle (V), or both (D). The letter in the second position indicates the chamber(s) where sensing occurs—again the atrium (A), ventricle (V), or both (D). Finally, the letter in the third position refers to the mode of response of the pacemaker-triggered (T), inhibited (I), or dual (D).

TABLE 21-1   -- Three-Position (Simplified) Pacemaker Code

Position

Category

Letters used

I

Chamber(s) paced

 

Ventricle

V

Atrium

A

Dual (atrium and ventricle)

D

None

O

II

Chamber(s) sensed

 

Ventricle

V

Atrium

A

Dual (atrium and ventricle)

D

None

O

III

Mode of response(s) to sensing

 

Triggered

T

Inhibited

I

Dual (triggered and inhibited)[*]

D

None

O

*

Dual mode of response refers to dual-chamber pacemakers in which atrial pacing may be inhibited by the patient's own P waves and a ventricular spike may be inhibited by the patient's P wave if atrioventricular block is present. Asingle-chamber (VVI) pacemaker and a dual-chamber (DDD) pacemaker are depicted schematically below.

Thus a VVI unit is identified as a single-chamber pacemaker that both paces (V) and senses (V) exclusively in the ventricle and is inhibited (I) by the patient's own QRS complexes.

The most versatile pacemakers are the DDD units. These are dual-chamber pacemakers that can pace the atrium or ventricle (D) and sense in the atrium or ventricle (D). In addition, the mode of response is dual (D). Consequently, atrial pacing can be inhibited by the patient's P waves, and a ventricular pacer spike is triggered by the patient's P waves if a native QRS complex does not appear within a preset time because of AV block.

The basic three-letter pacemaker code has been expanded to five letters, reflecting ongoing advances in pacemaker electronics. The fourth letter indicates the programming features of the pacemaker, including rate responsiveness (R). Contemporary rate-responsive pacemakers are designed with special sensors to detect muscle activity, breathing, or other variables that correlate with increased activity. The pacing rate automatically increases with exercise to accommodate the need for increased cardiac output.

Thus a pacemaker that paces and senses only in the right ventricle and has rate-responsive capabilities is designated VVI-R. The fifth letter (less frequently used) indicates whether there is multisite pacing in the atria or ventricles (e.g., biventricular pacing).

 

REVIEW

Electronic pacemakers are battery-powered devices used to stimulate the heart electrically, particularly when a patient's own heart rate is excessively slow. When the pacemaker wire is attached to the right ventricular endocardium, the ECG shows a left bundle branch block pattern because of delayed left ventricular stimulation. Each QRS complex is preceded by a pacemaker spike. Cardiac pacing can be done in a fixed-rate or demand mode. Demand pacemakers are inhibited when the heart rate is faster than the escape rate of the pacemaker.

A temporary pacemaker is a unit with an external battery. Temporary pacing wires can be inserted during cardiac emergencies (e.g., cardiac arrest caused by asystole or myocardial infarction [MI] complicated by high-degree heart block or sinus arrest). An implanted permanent pacemaker, in which the battery is inserted subcutaneously (usually in the chest wall) is indicated for patients with symptomatic second- or third-degree AV block or other major bradyarrhythmias (e.g., sinus arrest or slow junctional escape rhythm) leading to inadequate cardiac output.

Dual-chamber (atrial and ventricular) pacemakers were developed to maintain physiologic timing between atrial and ventricular contractions, thereby increasing cardiac output.

When the pacemaker battery starts to run down, the pacemaker rate slows. Dislodgment of the pacemaker wire or excessive fibrosis around the tip of the wire can cause failure to sense or failure to pace. Pacing failure in permanent units can also be caused by electrode fracture, short circuits, or electrical interference from skeletal muscles.

Pacemakers may obscure the ECG diagnosis of MI. Conversely, after electronic pacing of the ventricles, deep noninfarctional T wave inversions may appear in spontaneous QRS complexes (postpacemaker T wave pattern).

Biventricular pacing, designed to coordinate (resynchronize) the contraction of the left and right ventricles, is used primarily in selected patients with chronic heart failure.

Implantable cardioverter-defibrillator (ICD) therapy involves the internal placement of a device capable of delivering electrical shocks to the heart to interrupt a life-threatening run of ventricular tachycardia or ventricular fibrillation and thereby prevent syncope or sudden death. This therapy is used as secondary prevention in patients who have already been resuscitated from an episode of cardiac arrest due to ventricular fibrillation or ventricular tachycardia not due to a transient or reversible cause or in carefully selected patients at high risk for experiencing a sustained ventricular tachyarrhythmia (primary prevention).

 

QUESTIONS

 

1.   

Which of the following is the major indication for a permanent pacemaker?

 

a.   

History of multiple prior myocardial infarctions

 

b.   

Symptomatic bradyarrhythmia

 

c.   

Digitalis toxicity

 

d.   

Ventricular bigeminy

 

e.   

Paroxysmal supraventricular tachycardia

 

2.   

What does the following rhythm strip show?

 

 

a.   

Failure to sense

 

b.   

Failure to pace

 

c.   

Normal pacemaker function with a ventricular premature beat

 

d.   

Failure to sense and pace

 

3.   

What is shown in the following rhythm strip? 

 

 

4.   

Biventricular (BiV) pacing is used primarily in which of the following conditions?

 

a.   

Recurrent ventricular tachycardia

 

b.   

Chronic heart failure with left bundle branch block

 

c.   

Long QT syndromes

 

d.   

Acute myocardial infarction with cardiogenic shock

 

5.   

True or false: Implantable cardioverter-defibrillators (ICDs) are most often employed with acute MI.