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.