Single-lead (or single-chamber) pacemakers (see Fig. 21-1), as their name indicates, are used to stimulate only one chamber (right atrium or right ventricle). Atrial single-lead pacemakers (with the lead positioned in the right atrium) can be used to treat isolated sinus node dysfunction with normal AV conduction (Fig. 21-2). In the United States, single-lead atrial pacemakers are rarely used. Even patients with isolated sinus node dysfunction usually receive dual-chamber devices because AV conduction abnormalities often develop later as the patient ages.

Figure 21-2 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 and the atrioventricular (AV) conduction system is functional.

Ventricular single-lead pacemakers (with the lead positioned in the right ventricle) are primarily used to generate the heartbeat in patients with chronic atrial fibrillation with an excessively slow ventricular response. The atrial fibrillation precludes effective atrial stimulation so that there is no reason to insert an atrial lead (Fig. 21-3).

Figure 21-3 The ventricular (QRS) rhythm is completely regular because of ventricular pacing. However, the underlying rhythm is atrial fibrillation. Fibrillatory waves are small in amplitude in most leads and best seen in lead V₁. Most computer ECG interpretations will read this as “ventricular pacing” without noting atrial fibrillation. Unless the reader specifies “atrial fibrillation” in the report, this important diagnosis, which carries risk of stroke, will go unnoticed. Furthermore, on physical examination, the clinician may be “tricked” into thinking the regular rhythm is sinus.

In dual-chamber pacemakers, electrodes are inserted into both the right atrium and right ventricle (Figs. 21-4 and 21-5). The circuitry is designed to allow for a physiologic delay (normal synchrony) between atrial and ventricular stimulation. This AV delay (interval between the atrial and ventricular pacemaker spikes) is analogous to the PR interval under physiologic conditions.

Figure 21-4 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.

Figure 21-5 Paced beat morphology in dual-chamber pacemaking. Both atrial and ventricular pacing spikes are present. The atrial (a) pacing spike is followed by a P wave with very low amplitude. The ventricular (V) pacing spike is followed by a wide QRS complex with T wave pointing in the opposite direction (discordant). The QRS after the pacing spike resembles a left bundle branch block (LBBB), with a leftward axis, consistent with pacing from the right ventricular apex.

ECG Morphology of Paced Beats

Paced beats start with a pacing spike—a sharp vertical deflection from the pacemaker stimulus. If the pacing threshold is low, the amplitude of pacing spikes can be very small and they can be easily missed.

A paced P wave demonstrates a pacing spike followed by a P wave (see Fig. 21-2).

A paced QRS beat also starts with a pacing spike, followed by a wide QRS complex (see Figs. 21-3 and 21-6). The wide QRS is due to the fact that activation of the ventricles starts at the tip of the lead and spreads to the other ventricle through slowly conducting myocardium, similar to what occurs with ventricular premature beats (VPBs) or ventricular escape beats. The QRS morphology depends on the lead (electrode) position. The most commonly used ventricular electrode site is the right ventricular apex. Pacing at this location produces a wide QRS (usually resembling an LBBB pattern; see Chapter 7) with a leftward axis (QRS deflections are predominantly negative in leads II, III, and aVF and positive in leads I and aVL).

As with VPBs, the T waves in paced beats normally are discordant—directed opposite to the main QRS direction (see Figs. 21-3 and 21-5). Concordant T wave (i.e., pointing in the same direction as the paced QRS) during ventricular pacing may indicate acute myocardial ischemia (see following discussion).

Ventricular paced beats, similar to VPBs, can also sometimes conduct in a retrograde manner to the atria, producing near simultaneous atrial and ventricular depolarization and contraction (Fig. 21-6). When this occurs repeatedly, atrial contraction against the closed AV valves produces recurrent, sudden increases in jugular (and pulmonary) vein pressures, which may be seen as “cannon” A waves in the neck examination. Of note for clinicians, these abrupt pressure changes, in turn, may activate a vagal reflex and cause severe symptoms (palpitations, pulsation in the neck, dizziness, and blood pressure drop), often referred to as the pacemaker syndrome. Therefore, patients in sinus rhythm with AV block are usually implanted with dual-chamber pacemakers so that ventricular pacing will occur after atrial pacing, maintaining physiologic AV timing (synchrony).

Figure 21-6 Note the negative P wave (arrows) after the paced beats due to activation of the atria from bottom to top following the paced ventricular beats.

Electronic Pacemaker Programming: Shorthand Code

Historically, pacemaker programming has been described by a standard three- or four-letter code, usually followed by a number indicating the lower rate limit. Although many new pacing enhancements have been introduced since the inception of this code, it is still widely used (Table 21-1).

TABLE 21-1 Standard Four-Letter Pacemaker Code

Single-Chamber Pacemaker Programming

As noted, modern pacemakers are programmed in the on-demand mode providing pacing support only when needed. In the case of a single-chamber pacemaker this function is accomplished by specifying the lower rate limit (for example 60 beats/min). The pacemaker constantly monitors the patient’s heart rate in the implanted chamber on a beat to beat basis. Any time the rate drops below the lower rate limit (in the case of 60/min, the critical pause after a spontaneous QRS complex will be >1 sec), the pacemaker will deliver a pacing stimulus (Fig. 21-7). This corresponds to the code: VVI 60.

Figure 21-7 VVI pacing cycle (10 beats). Sensing of intrinsic activity in the ventricles inhibits pacemaker output. Once the pause after the last QRS complex reaches 1 sec, the pacemaker produces a pacing spike resulting in a paced beat (wide QRS). Beats 2 and 8 are fusion beats (coinciding conducted and paced beats). Note also that the normally conducted beats (narrow QRS complexes) have inverted T waves, probably due to “cardiac memory” associated with intermittent pacing, not to ischemia.

To simulate the heart rate increase that normally occurs with exertion, pacemakers can now also be programmed in a rate-responsive or adaptive mode. The purpose of this mode is to increase the lower rate limit dynamically, depending on the level of physical activity as detected by a sensor incorporated in the generator unit. For example, one of your patients may have rate-responsive ventricular single-chamber pacemaker programming, referred to as VVIR 60-110, in which the R indicates “rate-responsive” and the second number (110 in this case) represents the upper pacing limit, which is the maximum rate that the device will pace the ventricles in response to its activity sensor.

Dual-Chamber Pacemaker Programming

Dual-chamber pacemakers have two leads (one in the right atrium, one in the right ventricle), each capable of sensing intrinsic electrical activity to determine the need for pacing in each chamber. For “on-demand” dual-chamber pacemakers—the most common types—atrial pacing is determined by the lower rate limit while ventricular pacing is determined by the separately programmed maximum AV delay.

Depending on the atrial rate and the status of intrinsic AV conduction, dual-chamber pacemakers can produce four different combinations of pacing/sensing ECG patterns (Figs. 21-4, 21-7 and 21-8):

Figure 21-8 DDD pacing. Four different pacing/sensing combinations can be present depending on the sinus rate and atrioventricular (AV) conduction. See also Figure 21-4.

This programming corresponds to the code in Table 21-1.

DDD pacing and sensing occur in both chambers (the first and second D). The response to sensing is also dual (D): inhibition if intrinsic activity in the chamber is sensed (A sense, V sense) or triggering V pacing when there is sensing in the A but no AV conduction at maximum AV delay (A sense, V pace). As with single-chamber pacemakers, dual-chamber devices can be programmed in a rate-responsive mode.

DDD and DDDR are the most commonly used pacing modes in dual-chamber pacemakers. Dual-chamber pacemakers can be reprogrammed in a single-chamber mode as well.

On-demand programming has significant advantages, including prolonging battery life and avoiding unnecessary pacing especially in the ventricle. Its downside is the possibility to mistake external electrical signals for the patient’s own electrical activity. This would result in pacemaker inhibition and inappropriate withholding of pacing. Situations like this can occur, for example, with the use of electrosurgical equipment or exposure to strong electromagnetic fields, such as created by magnetic resonance imaging (MRI) machines. In these cases pacemakers can be reprogrammed in asynchronous mode (DOO or VOO) and will provide pacing at the lower rate limit regardless of ambient electrical activity. DOO mode is used in MRI-compatible pacemakers for the duration of the scan.

Clinicians should be familiar with two additional programming features in dual-chamber pacemakers designed to optimize device function during atrial arrhythmias: maximal tracking rate and automatic mode switching.

1. The maximal tracking rate is the highest ventricular pacing rate allowed in response to atrial sensing and is usually set at 110 to 150 beats/min. It is designed to prevent excessively rapid ventricular pacing during supraventricular arrhythmias. (Note the distinction between the maximum activity-related rate, the highest rate the pacemaker will fire during exercise as part of its rate-responsiveness, and the maximal tracking rate, the absolute highest the pacemaker will fire in response to atrial sensing.)

2. Automatic mode switching changes the pacing mode from DDD to VVIR in response to sensing high atrial rates suggestive of atrial flutter or fibrillation to regularize and slow ventricular pacing rhythm during these arrhythmias.

Managing Adverse Effects of Right Ventricular Pacing

Right ventricular pacing produces wide QRS similar to that seen in LBBB and delayed activation/contraction of the left ventricular lateral wall (ventricular dyssynchrony). Current data suggest that pacing-induced ventricular dyssynchrony over time can lead to worsening of left ventricular function and development of chronic heart failure especially in patients with impaired baseline ventricular fraction.

Many modern dual-chamber pacemakers have sophisticated algorithms aimed to minimize the amount of right ventricular pacing by automatically adjusting the maximum AV delay to take full physiologic AV conduction. This protective function can result in very long PR or “AR” intervals (in case of A-paced rhythms) with conducted QRS complexes and does not necessarily imply pacemaker malfunction. Some of these algorithms even allow single nonconducted P waves (second-degree AV block). Once the P wave blocks, V pacing is initiated.

Biventricular Pacemakers: Cardiac Resynchronization Therapy

This positive effect is accomplished by biventricular pacing. In addition to the usual right ventricular pacing lead, another electrode is placed to stimulate the left ventricle. Usually this second lead is advanced transvenously through a branch of the coronary sinus on the posterolateral wall of the left ventricle (Fig. 21-9) because this is the latest activated area with intrinsic LBBB or with right ventricular pacing.

Figure 21-9 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.

Both ventricles are then paced simultaneously, producing fusion-type QRS complexes (Figs. 21-10 and 21-11) that represent a “hybrid” between those seen with pure right and left ventricular pacing. The QRS morphology can be quite variable depending on the position of the left ventricular electrode, but usually the QRS has prominent R waves in leads V₁-V₂ (RBBB-type morphology due to posterior left ventricular wall activation from back to front) as well as Q waves in leads I and aVL (left ventricular electrode activating the heart from left to right). The QRS duration during biventricular pacing is usually shorter than with right ventricular pacing or with an intrinsic LBBB.

Figure 21-10 Effect of biventricular pacing on QRS width and shape. A, Baseline ECG shows typical left bundle branch block (LBBB) pattern with QRS duration of 160 msec. B, Right ventricular apical pacing. QRS duration has increased to 182 msec. C, Biventricular pacing. Note change in QRS morphology with prominent Q waves in leads I and aVL, and R waves in leads V₁ and V₂ as the result of left ventricular activation. Of note, QRS duration has decreased to 136 msec due to resynchronization effects.

Figure 21-11 Right ventricular and biventricular (BiV) 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 device. Note that during right ventricular pacing (A), the ECG shows a left bundle branch block (LBBB) morphology. The preceding sinus P waves are sensed by the atrial lead. In contrast, during biventricular pacing (BiV), the QRS complexes show a right bundle branch block (RBBB) morphology. Also, the QRS duration is somewhat shorter during BiV pacing, due to the cardiac resynchronization effects of pacing the ventricles in a nearly simultaneous fashion.

ECG Diagnosis Related to Paced Rhythms

Ventricular paced rhythms regularize ventricular rate and distort QRS and T wave shapes in a manner similar to LBBB. This makes further analysis of QRS, ST segment, and T wave virtually impossible. However, there are several ECG patterns that should not be missed even in paced rhythms or in ECGs obtained after ventricular pacing.

Implantable Cardioverter-Defibrillators

Key Point

Implantable cardioverter-defibrillators are electronic devices designed to terminate life-threatening ventricular arrhythmias by delivering bursts of antitachycardia pacing (ATP) or internal direct current shocks if needed.

Modern ICD systems resemble pacemakers in appearance, but with slightly larger generators and thicker right ventricular leads (Fig. 21-13). They are both implanted in a similar fashion. ICDs differ from the usual external defibrillation paddles or patches because in ICDs electrical current passes between one or two special coils on the ventricular lead and the generator.

Figure 21-13 An implanteable 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.

All current ICDs are capable of pacing and can be single-chamber, dual-chamber, or biventricular.

Arrhythmia detection is based primarily on the heart rate and can be programmed in up to several different heart rate zones (for example, slow VT, fast VT, and VF zones at 160, 180, 200 beats/min). Arrhythmia treatments then can be set up separately in each of the zones (Fig. 21-14) as part of automatic “tiered” (ramped) therapy.

Figure 21-14 Tiered (staged) arrhythmia therapy and implanteable 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) or cardioversion shocks (B) for VT and defibrillation shocks (C) for VF.

ICDs provide two programmable modalities of treatment for ventricular tachyarrhythmias: antitachycardia pacing (ATP) and direct current (DC) shocks. ATP works by pacing the heart faster than the rate of VT. This allows penetration of the signal into the reentrant arrhythmia circuit, “breaking” the reentrant loop and restoring normal rhythm. ATP terminates approximately 50% of ventricular arrhythmias, avoiding the need for ICD shocks. Unlike shock delivery, ATP is completely painless and usually goes unnoticed by the patient.

If ATP fails to convert the arrhythmia, then up to six consecutive synchronized or unsynchronized shocks can be delivered by the device (see Fig. 12-14). Modern ICD batteries have the capacity to deliver over 100 shocks and usually last 5 to 7 years.

Because tachyarrhythmia detection is based on the heart rate, a risk of inappropriate therapies exists for supraventricular tachyarrhythmias with rapid ventricular responses (for example, atrial fibrillation). ICDs use sophisticated algorithms to discriminate VT from supraventricular tachycardias (SVTs). However, limited information about arrhythmia mechanism and distinction is obtainable from a single ventricular lead, so that unwanted shocks due to SVT occur in approximately 15% of patients.

Recognizing Pacemaker and ICD Malfunction

Pacemakers are very reliable devices and pacemaker malfunctions are rare, especially after the acute postimplant phase. The commonly encountered problems are: failure to capture, failure to sense, and failure to pace.

Failure to capture is characterized by appropriately timed pacing spikes that are not followed by electrical activity of the heart (Fig. 21-15). The most common causes are lead dislodgment, leakage in the pacing circuit, inappropriately set pacing outputs, and rise in pacing threshold due to ischemia, fibrosis, or electrolyte abnormalities (e.g., hyperkalemia).

Figure 21-15 Notice that beats 1, 3, and 4 show pacemaker spikes and normally paced wide QRS complexes and T waves. The remaining beats show only pacemaker spikes without capture. (The pacemaker also fails to sense the patient’s slow spontaneous QRS complexes.)

Failure to sense (see Fig. 21-15) is characterized by excessive and inappropriately timed pacing activity. It can be due to lead dislodgment, inappropriately set sensitivity, or changes in intrinsic signal amplitude due to ischemia, electrolyte abnormalities, or fibrosis.

Failure to pace (Fig. 21-16) is usually due to the pacemaker inhibition by noncardiac electrical signals, such as from skeletal muscle, the diaphragm, external electromagnetic sources (electrocautery, lithotripsy, MRI machines), or electrical interference (“noise”) created by fractured pacemaker leads.