Jose L. Baez-Escudero, MD and Miguel Valderrábano, MD

1. What are the components of a pacing system?

    Pacing systems consist of a pulse generator and pacing leads, which can be placed in either the atria or the ventricles. Pacemakers provide an electrical stimulus to cause cardiac depolarization during periods when intrinsic cardiac electrical activity is inappropriately slow or absent. The battery most commonly used in permanent pacers has a life span of 5 to 9 years.

2. What is the accepted pacing nomenclature for the different pacing modalities?

    The North American Society of Pacing and Electrophysiology and the British Pacing and Electrophysiology Group have developed a code to describe various pacing modes. It usually consists of three letters, but some systems use four or five:

A pacemaker in VVI mode denotes that it paces and senses the ventricle and is inhibited by a sensed ventricular event. The DDD mode denotes that both chambers are capable of being sensed and paced.

3. What is the most important clinical feature that establishes the need for cardiac pacing?

    The most important clinical feature consists of symptoms clearly associated with bradycardia. Symptomatic bradycardia is the cardinal feature in the placement of a permanent pacemaker in acquired atrioventricular (AV) block in adults. Reversible causes, such as drug toxicity (digoxin, beta-adrenergic blocking agents [β-blockers], and calcium channel blockers), electrolyte abnormalities, Lyme disease, transient increases in vagal tone, and sleep apnea syndrome, should be sought, and the offending agents should be discontinued. The clinical manifestations of symptomatic bradycardia include fatigue, lightheadedness, dizziness, presyncope, syncope, manifestations of cerebral ischemia, dyspnea on exertion, decreased exercise tolerance, and congestive heart failure.

4. What are the three types of acquired AV block?

    There are three degrees of AV block: first, second, and third (complete). This classification is based on both the electrocardiogram (ECG) and the anatomic location of the conduction disturbance.

    First-degree block refers to a stable prolongation of the PR interval to more than 200 ms and represents delay in conduction at the level of the AV node. There are no class I indications for pacing in isolated asymptomatic first-degree block.

    Second-degree block is divided into two types. Mobitz type I (Wenckebach) exhibits progressive prolongation of the PR interval before an atrial impulse fails to stimulate the ventricle. Anatomically, this form of block occurs above the bundle of His in the AV node. Type II exhibits no prolongation of the PR interval before a dropped beat and anatomically occurs at the level of the bundle of His. This rhythm may be associated with a wide QRS complex.

    Third-degree or complete block defines the absence of AV conduction and refers to complete dissociation of the atrial and ventricular rhythms, with a ventricular rate less than the atrial rate. The width and rate of the ventricular escape rhythm help to identify an anatomic location for the block: narrow QRS is associated with minimal slowing of the rate, generally at the AV node, and wide QRS is associated with considerable slowing of rate at or below the bundle of His. Permanent pacemaker implantation is indicated for third-degree and advanced second-degree AV block at any anatomic level associated with bradycardia with symptoms (including heart failure) or ventricular arrhythmias presumed to be due to AV block.

5. What is the anatomic location of bifascicular or trifascicular block?

    Bifascicular block is located below the AV node and involves a combination of block at the level of the right bundle with block within one of the fascicles of the left bundle (left anterior or left posterior fascicle).

    Trifascicular block refers to the presence of a prolonged PR interval in addition to a bifascicular block. Based on the surface ECG, it is impossible to tell whether the prolonged PR interval is due to delay at the AV node (suprahisian) or in the remaining conducting fascicle (infrahisian, hence the term trifascicular block). Pacing is indicated when bifascicular or trifascicular block is associated with the following:

6. When is pacing indicated for asymptomatic bradycardia?

    There are few indications for pacing in patients with bradycardia who are truly asymptomatic:

Potential (class II) indications for pacing in asymptomatic patients include the following:

When bradycardia, even if extreme, is present only during sleep, pacing is not indicated.

7. What is sick sinus syndrome?

    Sinus node dysfunction (SND), also referred to as sick sinus syndrome, is a common cause of bradycardia. Its prevalence has been estimated to be as high as 1 in 600 patients over the age of 65 years, and the syndrome accounts for approximately 50% of pacemaker implantations in the United States. SND may be due to replacement of nodal tissue with fibrous tissue at the sinus node itself, or it may be due to extrinsic causes (e.g., drugs, electrolyte imbalance, hypothermia, hypothyroidism, increased intracranial pressure, or excessive vagal tone). Abnormal automaticity and conduction in the atrium predispose patients to atrial fibrillation and flutter, and the bradycardia-tachycardia syndrome is a common manifestation of sinus node dysfunction. Therapy to control the ventricular rate during tachycardia by blocking AV conduction with β-blockers, calcium-channel blockers, or digitalis may not be possible, because it may further depress the sinus node. Permanent pacemaker implantation is indicated for SND with documented symptomatic bradycardia, including frequent sinus pauses that produce symptoms. It is also indicated for symptomatic chronotropic incompetence and for symptomatic sinus bradycardia that results from required drug therapy for medical conditions (e.g., rate control for atrial tachyarrhythmias, chronic stable angina, or systolic heart failure).

8. Is pacing indicated for neurocardiogenic syncope?

    Neurocardiogenic syncope occurs when triggering of a neural reflex results in a usually self-limited episode of systemic hypotension characterized by both bradycardia and peripheral vasodilation. Many of these patients have a prominent vasodepressor component to their syndrome, and implantation of a pacemaker may not completely relieve symptoms. Hence, the role of pacing in patients with neurocardiac syncope and confirmed bradycardia is controversial. When bradycardia occurs only in specific situations, patient education, pharmacologic trials, and prevention strategies are indicated before pacing in most patients.

9. What are the indications for pacing after myocardial infarction (MI)?

    Indications in this setting do not require the presence of symptoms. The indications, in large part, are to treat the intraventricular conduction defects that result from infarction. Pacing is indicated in the setting of acute MI for the following:

Pacing in the setting of an acute MI may be temporary rather than long-term or permanent.

10. What are potential complications associated with pacemaker implantation?

    Complications in the hands of experienced operators are rare (approximately 1% to 2%) and include bleeding, infection, pneumothorax, hemothorax, cardiac arrhythmias, cardiac perforation causing tamponade, diaphragmatic (phrenic) nerve pacing, pocket hematoma, coronary sinus trauma, and prolonged radiation exposure. Late complications include erosion of the pacer through the skin (requires pacer replacement, lead extraction, and systemic antibiotics), and lead malfunction (e.g., lead fracture, break in lead insulation, or dislodgement).

11. What is pacemaker syndrome?

    Historically, pacemaker syndrome refers to progressive worsening of symptoms, particularly congestive heart failure, after single-chamber ventricular pacing. This was due to asynchronous ventricular pacing, leading to inappropriately timed atrial contractions, including those occurring during ventricular systole. Dual-chamber pacing and appropriate pacing mode selection prevent the occurrence of pacemaker syndrome. Pseudo–pacemaker syndrome occurs when a patient without a pacemaker has PR prolongation so severe that the P waves are closer to the preceding R waves than to the following ones, leading to atrial contractions during the preceding ventricular systole.

12. What is twiddler’s syndrome?

    Twiddler’s syndrome is a rare complication of pacemaker implantation caused by repetitive and often unintentional twisting of the generator in the pacemaker pocket, producing lead dislodgement or fracture and subsequent pacemaker failure. It is most commonly observed in patients with behavioral disorders.

13. What is pacemaker-mediated tachycardia?

    Pacemaker-mediated tachycardia (PMT) is a form of reentrant tachycardia that can occur in patients who have a dual-chamber pacemaker. If the AV node retrogradely conducts a ventricular-paced beat or a premature ventricular contraction (PVC) back to the atrium and depolarizes the atrium before the next atrial-paced beat, this atrial activation will be sensed by the pacemaker atrial lead and interpreted as an intrinsic atrial depolarization. Consecutively, the pacemaker will then pace the ventricle after the programmed AV delay and perpetuate the cycle of ventricular pacing → retrograde ventriculoatrial (VA) conduction → atrial sensing → ventricular pacing (the pacemaker forms the antegrade limb of the circuit, and the AV node is the retrograde limb). Consider PMT in patients with a dual-chamber pacemaker who experience palpitations, rapid heart rates, lightheadedness, syncope, or chest discomfort. It is corrected by programming the pacemaker with a postventricular atrial refractory period (PVARP) so that atrial events occurring shortly after ventricular events are ignored by the pacemaker.

14. What is cardiac resynchronization therapy?

    Cardiac resynchronization therapy (CRT) refers to simultaneous pacing of both ventricles (biventricular [Bi-V] pacing). The rationale for CRT is based on the observation that the presence of a bundle branch block or other intraventricular conduction delay can worsen systolic heart failure by causing ventricular dyssynchrony, thereby reducing the efficiency of contraction. Pacing of the left ventricle (LV) is achieved either by placing a transvenous lead in the lateral venous system of the heart through the coronary sinus (preferred approach; Fig. 37-1) or by placement of an epicardial LV lead (requires a limited thoracotomy and general anesthesia). The rationale for CRT is that ventricular dyssynchrony can further impair the pump function of a failing ventricle. Potential mechanisms of benefit include improved contractile function (improvement in ejection fraction [EF], increase in cardiac index and blood pressure, decrease in pulmonary capillary wedge pressure) and reverse ventricular remodeling (reductions in LV end-systolic and end-diastolic dimensions, severity of mitral regurgitation, and LV mass).

15. When is CRT indicated?

    CRT is indicated in patients with advanced heart failure (usually New York Heart Association [NYHA] class III or IV), severe systolic dysfunction (LV ejection fraction 35% or less), and intraventricular conduction delay (QRS more than 120 ms), who are in sinus rhythm and have been on optimal medical therapy. CRT can be achieved with a device designed only for pacing or can be combined with a defibrillator (many patients who are candidates for an implantable cardioverter-defibrillator [ICD] are also candidates for CRT). CRT has been shown not only to improve quality of life and decrease heart failure symptoms (improvement in NYHA class by one class or increased 6-minute walk distance) but also to reduce mortality and improve survival.

16. Do all patients with dyssynchrony respond to CRT?

    Not all patients who undergo CRT have a clinical response to it. In general, responders have lower mortality, fewer heart failure events, and fewer symptoms than nonresponders. The incidence of nonresponders is about 25% and is similar among patients with ischemic and nonischemic cardiomyopathy.

17. What are some additional benefits seen in responders to CRT?

    CRT allows patients to tolerate more aggressive medical therapy and neurohormonal blockade, particularly with β-blockers. It also improves diastolic function. CRT reduces frequency of ventricular arrhythmias and ICD therapies among patients previously treated with an ICD who were upgraded to a CRT device. It may also reduce frequency and duration of atrial tachyarrhythmias, including atrial fibrillation.

18. Is a CRT defibrillator (CRT-D) useful in minimally symptomatic patients with heart failure?

    Until recently, it was unknown if CRT would benefit patients with NYHA class I-II heart failure symptoms. Many patients with NYHA class I-II symptoms meet criteria for placement of an ICD as primary prevention. Many of these patients eventually progress to NYHA class III-IV symptoms over time. Two recently completed trials—Multicenter Automatic Defibrillator Implantation Trial with Cardiac Resynchronization Therapy (MADIT-CRT) and Resynchronization Reverses Remodeling in Systolic Left Ventricular Dysfunction (REVERSE)—evaluated the effect of CRT on patients with minimal or mild congestive heart failure (CHF) symptoms (NYHA class I-II). The larger MADIT-CRT trial randomized more than 1800 patients with EF less than 30%, QRS wider than 130 ms, and NYHA class I-II, to CRT-D or to standard ICD alone. Patients in the CRT-D group had a significant reduction in the combined endpoint of death or heart failure hospitalization (25% for the ICD group vs. 17% for the CRT-D group; P = 0.001). Based on these results, the U.S. Food and Drug Administration approved a new indication for CRT-D for ischemic cardiomyopathy patients with NYHA class I or greater heart failure or for non-ischemic cardiomyopathy with NYHA class II or greater, including all patients with EF less than 30%, QRS wider than 130 ms, and left bundle branch block. The requirement of left bundle branch block was based on subgroup analysis. This new indication expands the use of CRT-D to patients with less symptomatic heart failure.

19. Can ventricular pacing be deleterious?

    In patients with LV dysfunction, right ventricular pacing alone can lead to intraventricular dyssynchrony, precipitate heart failure, and lead to overall worse outcomes. In such patients, consideration should be given to CRT.

20. Can CRT help patients with CHF and narrow QRS?

    Initial single-center, nonrandomized case series reported improvement in LV function in patients with CHF and narrow QRS who received CRT. The theory was that the QRS duration on ECG may not accurately detect electrical dyssynchrony that may benefit from CRT. This theory was primarily driven by the perception of ventricular dyssynchrony as measured by echocardiographic tissue velocity parameters. The Resynchronization Therapy in Normal QRS (RethinQ) trial randomized patients with NYHA class III symptoms, EF less than 35%, narrow QRS (<130 ms), and echocardiographic evidence of dyssynchrony, to receive an ICD alone or CRT-D. There was no significant difference in the primary endpoint of improvement in peak oxygen consumption at 6 months. At this time, there is no conclusive evidence to support the use of CRT in patients with a narrow QRS duration of less than 120 ms.

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