Clinical Presentation

Syncope and presyncope are the most dramatic symptoms of conduction disturbances; palpitations, dyspnea, angina, and fatigue are seen as well. Many patients are asymptomatic. A significant number of patients develop bradydysrhythmias after an acute myocardial infarction (AMI) (Table 80-1).³

TABLE 80-1 Incidence of Bradydysrhythmias in Acute Myocardial Infarction

Diagnostic Evaluation

A high-quality ECG is paramount for the appropriate evaluation of P waves and various intervals. Routine monitoring in the ICU is usually accomplished with a single or three-lead display at the bedside. The lead chosen should clearly delineate the P waves and QRS complexes. Complex arrhythmias may require Lewis leads, intraatrial leads, or esophageal ECG monitoring. Calipers significantly aid in the diagnosis of AV blocks and are helpful to “march out” P waves and intervals. Holter or continuous loop monitoring can also be an important tool in the evaluation of AV block.⁴ These monitors allow one to evaluate the cardiac conduction system during a patient’s activities of daily living. A monitoring period of at least 24 hours is recommended so that both daytime and nighttime activities are included.

Sinus Bradycardia

Sinus bradycardia is defined as a sinus rhythm with a heart rate less than 60 beats per minute. Sinus bradycardia is divided into two categories: appropriate and inappropriate. Appropriate bradycardia is seen in young, healthy individuals and endurance athletes; the heart rate increases appropriately with exercise. Pathologic sinus bradycardia does not increase appropriately with exercise. Medications are the most common cause of inappropriate sinus bradycardia; autonomic influences, electrolyte abnormalities, and intrinsic structural disorders are others. In older individuals, sinus bradycardia can result from a decrease in the sinus node firing rate, which is a normal part of the aging process. Ischemia may also increase vagal tone and result in a slower heart rate.

Sinus Arrest

Sinus arrest occurs when the pacemaker cells in the SA node fail to depolarize. Pauses of less than 3 seconds may be seen in up to 11% of normal individuals and should not cause concern.⁵ There is a higher incidence of sinus pause in athletes. Pauses longer than 3 seconds are usually considered pathologic and should be evaluated.

SA exit block and sinus arrest appear similar on ECGs, but they should be distinguished if possible. The duration of the pause in exit block is a multiple of the P-P interval. High-grade exit block cannot be distinguished from sinus arrest. The treatment is the same for both conditions.⁶

Noninvasive testing includes ECG, carotid sinus massage, and a tilt table test. Carotid sinus massage is useful to diagnose carotid sinus hypersensitivity. Risks of carotid sinus massage include transient ischemic attack and stroke, and the test should not be performed on patients with carotid bruits. The tilt table test is helpful to determine whether syncopal episodes are due to autonomic dysfunction. Invasive diagnostic testing of the SA node can also be performed, although this is rarely necessary.

The treatment of sinus node dysfunction can be temporary or permanent. Atropine or an isoproterenol drip can be used in the ICU as a bridge to permanent pacemaker placement. Temporary pacing is indicated for patients who fail to respond to medical therapy.

Carotid Sinus Hypersensitivity

Carotid sinus hypersensitivity is diagnosed when ventricular asystole greater than 3 seconds’ duration (usually due to a sinus pause or arrest) or a drop in systolic blood pressure greater than 50 mm Hg occurs in response to carotid massage. If symptoms occur, a 30 mm Hg drop in systolic blood pressure defines a positive response. Treatment is permanent pacing in symptomatic patients only.⁷

Postsurgical Bradydysrhythmias

Bradyarrhythmias are common after cardiac surgery. Valve surgery and septal myectomy can cause significant damage to the conduction system. Prolonged ischemia during heart transplantation may also result in sinus node or conduction system damage. The decision to place a permanent pacer should not be made until 5 to 7 days postoperatively, however, because the bradyarrhythmia may be temporary. Medication administered during surgery or reversible ischemia is often implicated. Pacing is required in 3.2% to 8.5% of patients with valve surgery and approximately 10% of patients with transplants.⁸

First-Degree Atrioventricular Block

First-degree AV block is characterized by a prolonged PR interval greater than 0.20 second in adults and 0.18 second in children who are not taking medications that can prolong the PR interval (Figure 80-1). All the P waves are conducted to the ventricles, and the PR interval is typically fixed. Potential causes of first-degree AV block include delayed conduction through the atria from the SA node to the AV node, a delay in AV node conduction, or prolonged infranodal conduction.

Figure 80-1 Electrocardiogram from patient with first-degree atrioventricular block. PR interval is approximately 0.29 second. All P waves are being conducted to ventricles. PR interval is constant.

Conduction delays from the SA node to the AV node are typically due to structural causes such as right atrial enlargement or an ostium primum atrial septal defect. A delay in AV node impulse conduction is the most common cause of first-degree AV block. Patients with delayed conduction in the AV node often have a PR interval greater than 0.30 second. Infranodal causes of first-degree AV block are rare and are typically associated with a wide QRS complex due to disease in the fascicles or the bundle of His. First-degree AV block can also occur when each of these conduction times is at the upper limit of normal and summate to produce an overall prolongation of the PR interval.⁷

First-degree AV block is typically benign and asymptomatic. It can be seen in 0.5% of young adults without heart disease. In older people, first-degree block is most often the result of idiopathic degenerative disease. A prolonged PR interval is often an incidental finding when an ECG is ordered for other reasons. It rarely warrants further workup or treatment.

Second-Degree Atrioventricular Block Type I

Second-degree AV block type I, or a Wenckebach (or Mobitz type I) rhythm, is defined by a progressive prolongation of the PR interval with each successive beat, with eventual failure of a P wave to conduct to the ventricles (Figure 80-2). This results in a dropped beat and failure of the ventricles to depolarize. The P waves occur at regular intervals. As the PR interval lengthens, the RR interval becomes shorter, which eventually results in decremental conduction. There is a reciprocal relationship between the RP interval and the PR interval.

Figure 80-2 Electrocardiogram rhythm strip from patient with second-degree atrioventricular block type I. Note progressive prolongation of PR interval until a failure of conduction occurs. Also note reciprocal RP shortening. Pattern of conduction is 3 : 2.

The pathophysiology of second-degree AV block type I is similar to that of first-degree AV block, except that intraatrial block is usually not a cause. For all practical purposes, second-degree AV block type I is caused by a block in AV node conduction. The QRS complex is generally narrow.

QRS complexes are typically grouped in twos, threes, fours, and so on. Group beating is characteristic of Wenckebach rhythms. The rhythm is described by recording the number of P waves and QRS complexes involved in the pattern of block (e.g., 4 : 3 or 3 : 2). During a dropped beat, a P wave is observed with no corresponding QRS complex. Second-degree AV block type I is a stable rhythm and has a much better prognosis than does a Mobitz type II rhythm. If the Wenckebach rhythm is due to medication, resolution of the block can be monitored with an ECG. Once the medication is discontinued, a shortening of the PR interval and a lengthening of the RP interval, with a corresponding improvement in AV node conduction, may be observed.

Second-Degree Atrioventricular Block Type II

Second-degree AV block type II (or Mobitz type II block) is characterized by a sudden nonconducted P wave without a change in the PR interval. A P wave with no corresponding QRS complex is observed on the ECG (Figure 80-3). This is an inherently unstable rhythm, and serious pathology may be present. In contrast to the Mobitz type I rhythm, type II is described as a high degree of AV block, with P wave–to–QRS ratios of 3 : 1 and 4 : 1. A Mobitz type II rhythm is almost always due to an infranodal conduction disturbance. The conducted QRS complexes are often wide, and a bundle branch block pattern is often observed. Second-degree AV block can result from anterior wall MI. Type II second-degree AV block can progress to complete heart block.

Figure 80-3 Electrocardiogram demonstrating second-degree atrioventricular block type II. PR interval is constant before and after blocked P waves. QRS complex is widened.

2 : 1 Atrioventricular Block

When conduction of every other P wave is blocked, 2 : 1 AV block is present. The PR interval of the conducted beat remains fixed. QRS complexes are regular and occur at half the atrial rate. 2 : 1 AV block can be caused by a Mobitz I (usually with a narrow QRS complex) or Mobitz II (with a wide QRS complex) rhythm, and the two entities are difficult to distinguish.

Third-Degree Atrioventricular Block

Third-degree AV block is characterized by complete AV dissociation. There is no conduction of the atrial signal through to the ventricle, so the atrial and ventricular systems operate independently. On ECGs, the P waves “march through” and are not associated with ventricular contraction. The PR intervals are irregular. The ventricular complexes may be junctional (narrow QRS complex; rate 40-60) or ventricular (wide QRS complex, rate <40). Depending on the escape heart rate, patients may present with tachypnea, dyspnea on exertion, fatigue, cyanosis, or syncope (Figure 80-4).

Figure 80-4 Complete heart block. PR intervals are irregular because ventricles and atria represent two independent sources of depolarization.

Third-degree block can be divided into congenital and acquired causes. Sixty percent of patients with congenital heart block are female. Patients with congenital third-degree block often have an escape rhythm with an adequate rate.⁹ Acquired third-degree block occurs most frequently in the seventh decade of life and usually requires permanent pacing; these patients are often male. Specific causes include medications, ischemia, progression from Mobitz type II rhythm, and infarction. Acute MI results in third-degree heart block in 14% of patients with inferior wall infarcts and 2% of patients with anterior infarcts. Third-degree block is usually observed within 24 hours after an MI. Third-degree block as a complication of inferior MI is usually temporary and may require only temporary pacing. Complete heart block as a result of anterior MI usually requires a permanent pacer.

Treatment involves correction of underlying disorders and immediate transcutaneous or transvenous pacing in unstable patients. If the primary cause cannot be medically managed, permanent pacing is required.

Diagnostic Pitfalls

Determining the degree of AV node block is usually straightforward if an adequate ECG has been obtained. There are circumstances, however, in which one may be misled to an incorrect diagnosis.

Third-degree block is occasionally misdiagnosed as second-degree block type II if there appears to be a constant PR interval. This may occur for short periods on an isolated rhythm strip. The clinician must therefore examine a strip for an appropriate length of time to make the correct diagnosis. Vagal maneuvers can also be attempted and may identify a second-degree AV block that is really a third-degree AV block.

With isorhythmic AV dissociation, the P waves and QRS complexes occur at a similar rate. The P waves may never “march out” long enough to determine whether they are all conducting. Interventions such as vagal maneuvers to change the PQRS relationship may aid in diagnosis.

When second-degree AV block is fixed (2 : 1, 3 : 1, 4 : 1), some P waves may be concealed during the repolarization phase of the ECG. This may occur in acute MI or with ischemia. Vagal maneuvers and examination of multiple leads may be necessary to correctly identify the AV block.

When complete AV dissociation occurs with accelerated junctional or ventricular rhythms, it is possible that some of the atrial impulses would be conducted if the heart rate were slower. It is best to designate these rhythms as complex AV dissociation.

Therapy

Medical therapy for AV block consists of atropine, adrenergic agents, Digibind (if appropriate), and pacing. Atropine decreases vagal tone and is useful for hypervagotonia but not AV node ischemia. It is more useful in inferior wall MI than anterior wall MI. Atropine will not improve third-degree AV block or a Mobitz type II block if the pathology is below the AV node, and it is ineffective in heart transplant patients. Atropine should be used with caution in patients with Mobitz type II rhythms, because a paradoxical decrease in heart rate can occur.

Digibind should be used in symptomatic patients with digoxin-induced AV block. The number of vials of Digibind required is approximately equal to the patient’s weight (in kilograms) times the digoxin serum level (in ng/mL) divided by 100.

Failure to Sense (Undersensing)

Undersensing occurs when the pacemaker generates output regardless of the patient’s underlying rhythm (Figure 80-5). A spike is seen at an interval earlier than the lower rate-limiting interval. Pacemaker output then competes with the patient’s own intrinsic rhythm. Although ventricular pacing can present a problem when the threshold for ventricular capture has been altered (e.g., by ischemia), and atrial pacing can produce atrial fibrillation, these are rarely urgent problems.¹⁵

Figure 80-5 Failure to sense. Atrial and ventricular pacing spikes are seen around the intrinsic QRS complexes. Pacemaker activity does not lead to capture.

Specific causes of failure to sense are listed in Table 80-3. Blanking is not a true cause; rather, it is an instance of functional undersensing in dual-chamber pacemakers. To prevent a pacemaker-induced tachycardia, a 12- to 125-millisecond period of inactivity is programmed into the ventricular component after an atrial complex. If an intrinsic QRS complex occurs during this period, it will not be sensed. Scar tissue does not conduct impulses as easily as normal myocardium does, so sensing may not occur. Most pulse generators begin asynchronous pacing at a critical point at the end of their life and will not sense intrinsic activity. Defibrillation can damage the unit; placing the defibrillator pad in an anteroposterior position may help. The unit should be observed closely after shocks are delivered.

TABLE 80-3 Causes of Undersensing

Failure to Pace (Generate Output)

This complication is noted when a pacemaker spike is not seen after the lower rate-limiting interval has been exceeded (except when hysteresis has been programmed; Figure 80-6). Oversensing occurs when stimuli are erroneously sensed as pacemaker output. As a result, the expected proper output is inhibited; this can be continuous or intermittent. Failure to pace can be a devastating complication for a pacemaker-dependent patient. It is important to determine whether output is truly occurring or not. A 12-lead ECG should be done, because spikes may be too small to be seen in a specific lead. Several causes are possible (Table 80-4).

Figure 80-6 Failure to pace. An unduly long interval passes after the third QRS complex before another beat occurs. Pacemaker should have fired before this intrinsic beat.

TABLE 80-4 Causes of Failure to Pace

Cross-talk is not a true malfunction of the pacemaker, but it can lead to an inhibition of activity. In a dual-chamber system, the output of one chamber is sensed as the output of the other, and no pacemaker spike is generated; this occurs more often in unipolar leads. This problem is corrected by programming a blanking period. For a brief period after the atrial output (12 to 25 milliseconds), the ventricular component is inhibited from firing. A second protection against cross-talk is to program the unit to fire depending on when in the AV interval the stimulus is detected. If it occurs immediately after the blanking period, a “safety” spike is generated because it is assumed that it is impossible to differentiate cross-talk from a native QRS complex.

Failure to Capture

This complication occurs when a pacemaker fires as expected but fails to depolarize the myocardium. A pacer spike is seen on the ECG, but no QRS complex immediately follows it (Figure 80-7). This can be dangerous for a pacemaker-dependent patient and may require temporary pacing until the problem is fixed. Most cases are due to problems with the lead/tissue interface, although isolated problems in the leads or the myocardium can also occur (Table 80-5).^13,16

Figure 80-7 Failure to capture. After first QRS complex, a small pacemaker spike occurs that does not result in depolarization of ventricle. A nonconducted P wave follows, and then a pacemaker spike with capture occurs.

TABLE 80-5 Causes of Failure to Capture

When a lead is placed into the myocardium, tissue fibrosis occurs over the first 4 to 6 weeks. Because scar tissue does not conduct as well as normal myocardium, the output voltage may need to be increased. Twiddler’s syndrome is seen when a patient fidgets with the generator and ends up pulling the leads from their attachments to the myocardium. It is confirmed by chest x-ray. The pacemaker is replaced and fixed tightly to the underlying fascia. Perforation of the ventricle typically occurs shortly after the leads are placed and is confirmed by a chest x-ray showing the tip of the lead outside the heart. It is suggested by a change in pacing to a right bundle branch pattern, failure to capture, contraction of the diaphragm or intercostal muscles with pacing, or development of a pericardial friction rub. Provided the patient is not anticoagulated, the perforation is usually well tolerated.¹⁴ Echocardiography can assess for the presence of pericardial effusion or tamponade. Repositioning of the lead is typically performed in the operating room after any coagulopathy has been reversed.

An increased threshold for capture can also be caused by myocardial ischemia, metabolic abnormalities, or certain drugs. Definitive treatment involves correcting the underlying disorder.

When assessing for failure to capture, a distinction must be made between pseudofusion and fusion beats. A pseudofusion beat occurs when the pacemaker fires at the same time that an intrinsic beat occurs. The pacemaker output does not depolarize the myocardium, and instead, the pacemaker spike simply deforms the native QRS complex. It is an example of failure to capture. A fusion beat occurs when both the native complex and the pacemaker spike depolarize the myocardium, resulting in a QRS complex that is a hybrid of the two.

Other Problems

Pacemaker-mediated tachycardia, also called endless loop or pacemaker reentrant tachycardia, is a complication of dual-chamber units. A premature atrial contraction or premature ventricular contraction that travels in a retrograde manner into the atria is sensed by the atrial component of the pacemaker, which induces the ventricular component to fire. The resulting ventricular depolarization reenters the atria, and the cycle continues. An upper rate limit is programmed into the pacemaker, so the tachycardia will not exceed this rate. A tachycardia paced by atrial and ventricular spikes is seen. Application of a magnet terminates the dysrhythmia; adenosine may not reliably block it.¹⁷ A blanking period must be programmed.

Pacemaker syndrome is seen when only the ventricle is paced. Patients present with lethargy, syncope, dizziness, weakness, fatigue, palpitations, or congestive heart failure. It occurs because of an inability to raise the heart rate with exercise and because of the loss of AV synchrony. Dual chamber pacing is required to correct this.

The diagnosis of MI in a patient with a functioning pacemaker is difficult. Criteria similar to those in patients with left bundle branch block have been proposed, but sensitivity and specificity are lower.¹⁵

Advanced Cardiac Life Support protocols are not contraindicated by the presence of a pacemaker. Defibrillator pads should be kept as far away from the pulse generator as possible to minimize any damage to the unit.

Examination by magnetic resonance imaging has been considered contraindicated because of the interaction between the strong magnetic field and the pulse generator. Increased pacing rates, decreased rates, and pacing at the magnet rate have all been seen. However, programming the pacemaker to an asynchronous mode (AOO, VOO, or DOO) and close monitoring of the patient, along with the use of lower magnetic fields, may allow safe imaging.¹⁸