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

Chapter 17. Atrioventricular (AV) Heart Block

Heart block is the general term for atrioventricular (AV) conduction disturbances. Normally, the AV junction (AV node and His bundle area) acts as a bridge between the atria and ventricles. As mentioned in Chapter 2 , the PR interval is primarily a measure of the lag in AV conduction between initial stimulation of the atria and initial stimulation of the ventricles. The normal PR interval in adults is between 0.12 and 0.2 second.

Heart block occurs when transmission through the AV junction is impaired either transiently or permanently ( Table 17-1 ). The mildest form is called first-degree heart block. The term first-degree AV block is actually a misnomer, however, because the impulse is not blocked but delayed. Therefore a preferable term is prolonged PR interval. With first-degree heart block, the PR interval is uniformly prolonged beyond 0.2 second. Second-degree heart block is an intermediate grade of AV conduction disturbance in which impulse transmission between the atria and ventricles fails intermittently. The most extreme form is third-degree or complete heart block. In this case, the AV junction does not conduct any stimuli between the atria and ventricles. The present chapter describes these three degrees of heart block, along with the related topic AV dissociation.

TABLE 17-1   -- Classification of AV Heart Blocks

PROLONGED PR INTERVAL (FIRST-DEGREE AV BLOCK)

With first-degree heart block, the PR interval is prolonged beyond 0.2 second and is relatively constant from beat to beat ( Fig. 17-1 ). A moderately prolonged PR interval does not produce symptoms or significant change in cardiac function. The PR interval may become prolonged for many reasons. Most factors that produce PR prolongation can also produce second- and third-degree block. For example, digitalis, which has a vagal effect on the AV junction, can produce any degree of heart block. Other drugs such as amiodarone, beta blockers, and calcium channel blockers (e.g., verapamil and diltiazem) can also severely depress AV conduction.

Patients with ischemic heart disease may have heart block of any degree. This finding may occur with chronic myocardial ischemia over a long time or with acute myocardial infarction (MI). Varying degrees of heart block are particularly common with inferior wall infarction because the right coronary artery, which generally supplies the inferior wall of the heart, also usually supplies the AV node. In addition, acute inferior MI is often associated with increased vagal tone. Heart block during inferior wall infarction tends to be transient.

Hyperkalemia may cause prolonged AV conduction. Other signs of hyperkalemia include peaking of the T waves and widening of the QRS complexes (see Chapter 10 ). Prolonged PR intervals may also occur with acute rheumatic fever. Not uncommonly, mild PR interval prolongation is seen as a normal variant, especially with physiologic sinus bradycardia during rest or sleep.

SECOND-DEGREE AV BLOCK

Second-degree AV block is somewhat more complicated because it has two major types: Mobitz type I block (also called Wenckebach block) and Mobitz type II block.

MOBITZ TYPE I (WENCKEBACH) AV BLOCK

With Mobitz type I or Wenckebach pattern, each stimulus from the atria to the ventricles appears to have a more difficult time passing through the AV junction. Finally the stimulus is not conducted at all. This blocked beat is followed by relative recovery of the AV junction, and the whole cycle starts again.

The characteristic ECG picture of Wenckebach block is progressive lengthening of the PR interval from beat to beat until a beat is “dropped.” The dropped beat is a P wave that is not followed by a QRS complex, indicating failure of the AV junction to conduct the stimulus from the atria to the ventricles. Importantly, the PR interval after the nonconducted P wave is shorter than the PR interval of the beat just before the nonconducted P wave. Figure 17-2 diagrammatically depicts the Wenckebach phenomenon, and Figure 17-3 shows an actual example of this pattern. The number of P waves occurring before a QRS complex is “dropped” may vary. In many cases, just two or three conducted P waves are seen. In other cases, longer cycles are seen.

What characterizes the classic Wenckebach pattern is (1) the sequence of a progressive lengthening of the PR interval followed by a nonconducted P wave, and then (2) shortening of the PR interval in the beat immediately after the nonconducted one. (Not all cases of type I AV block, however, show the classic pattern of progressive PR prolongation before the nonconducted beat. In some cases, for example, the PR interval may not prolong noticeably. Even in such atypical cases, however, the PR interval after the nonconducted beat will always be shorter than the PR interval before it.)

As you can see from the examples, the Wenckebach cycle also produces a distinct clustering of QRS complexes separated by a pause that results from the dropped beat. Any time you encounter an ECG with this type of group beating, you should suspect a Wenckebach block and look for the diagnostic pattern of lengthening PR intervals.

Clinically, patients with the Wenckebach type of AV block are usually without symptoms unless the ventricular rate is very slow. The pulse rate is irregular.

Common causes of Wenckebach block include drugs such as beta blockers, calcium channel blockers (diltiazem and verapamil), and digoxin. Wenckebach block is not uncommon with acute inferior wall MI. In such cases, it is usually transient and generally does not require any treatment except observation. Occasionally, these patients may progress into complete heart block. Of note, a physiologic increase in vagal tone may cause Wenckebach AV block in endurance athletes at rest or in young individuals during sleep.

MOBITZ TYPE II SECOND-DEGREE AV BLOCK

Mobitz type II AV block is a rarer and more serious form of second-degree heart block. Its characteristic feature is the sudden appearance of a single, nonconducted sinus P wave without (1) the progressive prolongation of PR intervals seen in classic Mobitz type I (Wenckebach) AV block, and (2) shortening of the PR interval in the beat after the nonconducted P wave as seen with type I block.^[*]

Mobitz type II block is generally a sign of severe conduction system disease involving the region below the AV node (i.e., the His-Purkinje system). Because Mobitz type II block often progresses into complete heart block, cardiologists generally consider it an indication for a pacemaker. Unlike Wenckebach AV block, Mobitz type II block is not usually caused by beta-blocker therapy, digitalis excess, or inferior wall MI. Mobitz type II block may be seen, however, with anterior wall MI, and these patients often progress into complete heart block. Therefore cardiologists generally treat patients with anterior wall MI and Mobitz type II AV block by inserting a pacemaker.

Mobitz I and Mobitz II AV blocks are compared in Table 17-2 .

TABLE 17-2   -- Mobitz Type I and Mobitz Type II AV Blocks

*  For clarification of a point of common confusion, it should be noted that 2:1 AV block per se does not necessarily indicate a Mobitz type II block. Not uncommonly, 2:1 AV block is due to a type I mechanism in which the block in the AV node occurs after every other P wave. In such cases a careful search of a long rhythm strip often reveals 3:2, 4:3, and other types of classic Wenckebach block in addition to the 2:1 periods. Furthermore, in most (but not all) cases of Wenckebach AV block, the QRS complex is of normal duration. By contrast, when 2:1 block is due to a type II mechanism, the His-Purkinje system (not just the AV node) is involved and the QRS duration is often prolonged. Thus 2:1 block with a narrow QRS complex most likely represents a type I mechanism. However, 2:1 block with a wide QRS complex may be due to either mechanism. Definitive assessment in any case of 2:1 block may require an intracardiac electrophysiologic study. Therefore pure 2:1 block should be labeled as such without specifying a type I or type II mechanism.
ADVANCED SECOND-DEGREE AV BLOCK

The term advanced second-degree AV block refers to the distinct ECG finding of two or more consecutive nonconducted sinus P waves ( Fig. 17-4 ). For example, with sinus rhythm and 3:1 block, every third P wave is conducted; with 4:1 block, every fourth P wave is conducted, and so forth. This type of advanced block does not necessarily indicate a Mobitz II mechanism. However, unless advanced second-degree AV block has a reversible cause (e.g., drug toxicity or hyperkalemia), a permanent pacemaker is usually required.

THIRD-DEGREE (COMPLETE) HEART BLOCK

First- and second-degree heart blocks are examples of incomplete block because the AV junction conducts at least some stimuli to the ventricles. With complete heart block, no stimuli are transmitted from the atria to the ventricles. Instead, the atria and ventricles are paced independently. The atria generally continue to be paced by the sinus node, or sinoatrial (SA) node. The ventricles, however, are paced by an escape pacemaker located somewhere below the point of block in the AV junction. The resting ventricular rate with complete heart block may be lower than 30 beats/min or as high as 50 to 60 beats/min. The atrial rate is generally faster than the ventricular rate.

Examples of complete heart block are shown in Figures 17-5 and 17-6 [5] [6]. The ECG with sinus rhythm and complete heart block has the following three characteristics:

Complete heart block may also occur in patients whose basic atrial rhythm is flutter or fibrillation. In these cases, the ventricular rate is very slow and almost completely regular (see Fig. 15-10 ).

With complete heart block, the QRS complexes may be either of normal width (see Fig. 17-5 ) or abnormally wide (see Fig. 17-6 ) with the appearance of a bundle branch block pattern. The width of the QRS complexes depends in part on the location of the block in the AV junction. If the block is in the first part (the AV node), the ventricles are stimulated normally by a junctional pacemaker and the QRS complexes are narrow (see Fig. 17-5 ) unless the patient has an underlying bundle branch block. If the block is within, or particularly below, the bundle of His, the ventricles are paced by anidioventricular pacemaker,^[*] producing wide QRS complexes (see Fig. 17-6 ). As a general clinical rule, complete heart block with wide QRS complexes tends to be less stable than complete heart block with narrow QRS complexes because the ventricular escape pacemaker is usually slower and less consistent.

Complete heart block can occur for a number of reasons. It is most commonly seen in older patients who have chronic degenerative changes (sclerosis or fibrosis) in their conduction systems not related to MI. Digitalis intoxication, which can cause second-degree heart block, may also lead to complete heart block (see Chapter 18 ). Varying degrees of AV block, including some cases of complete block, have been reported with Lyme disease. Complete heart block may occur abruptly after open heart surgery, particularly with aortic valve replacement. Complete heart block occurring with bacterial endocarditis is an ominous finding that suggests a perivalvular abscess involving the conduction system.

Complete heart block may also be seen acutely as a complication of MI. The course and therapy of complete heart block with MI depend to a large extent on whether the infarct is anterior or inferior. Transient AV conduction disturbances are commonly seen with acute inferior wall MI because of the common blood supply to the AV node and inferior wall (via the right coronary artery). Occlusion of the right coronary artery with inferior MI also often leads to temporary ischemia of the AV node, sometimes resulting in complete heart block. (In addition, acute inferior MI may cause an increase in vagal tone.) Complete heart block occurring with inferior wall MI is often a transient and reversible complication that does not usually require a temporary pacemaker unless the patient is hypotensive or is having concomitant episodes of tachyarrhythmia.

With acute anterior MI and complete heart block, the situation is more serious. Patients with anterior wall infarcts and complete heart block generally have extensive myocardial damage. Theidioventricular escape rhythm that develops is usually slow and unstable. Therefore if complete heart block occurs with an acute anterior MI, cardiologists insert a temporary pacemaker (and subsequently a permanent one).

Regardless of its cause, complete heart block is a serious and potentially life-threatening arrhythmia. If the ventricular rate becomes too slow, the cardiac output drops and the patient may faint. Fainting spells associated with complete heart block (or other types of bradycardia) are referred to as Stokes-Adams attacks. In some patients, complete heart block is a chronic and persistent finding. In others, the block may occur transiently and may be recognized only with more prolonged monitoring.

*  An idioventricular pacemaker may be located in the His-Purkinje system or the ventricular myocardium.

BIFASCICULAR BLOCK, TRIFASCICULAR BLOCK, AND COMPLETE HEART BLOCK

Cardiologists have been interested in developing criteria to predict which patients with acute MI (particularly, anterior wall infarcts) will develop life-threatening complete heart block. Current information suggests that certain high-risk patients can be identified, although precise predictions are not possible. Specifically, patients with acute anterior wall MI and complete heart block often have other conduction disturbances before the onset of complete heart block. These conduction disturbances are referred to as bifascicular blocks.

Recall from Chapter 7 that the ventricular conduction system is trifascicular, consisting of the right bundle branch and the left bundle branch, the latter further dividing into left anterior and left posterior fascicles. Blockage of just the left anterior fascicle produces left anterior fascicular block (hemiblock) with left axis deviation (LAD). Blockage of just the left posterior fascicle produces left posterior fascicular block (hemiblock) with right axis deviation (RAD). Bifascicular block indicates blockage of any two of the three fascicles. For example, right bundle branch block (RBBB) with left anterior fascicular block produces an RBBB pattern with marked LAD (see Figs. 8-20 and 17-7 ); RBBB with left posterior fascicular block ( Fig. 17-8 ) produces an RBBB pattern with RAD (provided other causes of RAD, especially right ventricular hypertrophy and lateral MI, are excluded). Similarly, a complete LBBB may indicate blockage of both the anterior and posterior fascicles.

Bifascicular blocks are potentially significant because they make ventricular conduction dependent on the single remaining fascicle. Additional damage to this third remaining fascicle may completely block AV conduction, producing complete heart block (trifascicular block). Therefore the acute development of new bifascicular block (especially with a prolonged PR interval) during an acute anterior wall MI is an important warning signal of possible impending complete heart block.

An important distinction must be made between acute bifascicular blocks occurring with anterior wall MI (see Fig. 8-20 ) and chronic bifascicular blocks (Figs. 17-7 and 17-8 [7] [8]). Many asymptomatic people have ECGs resembling the one in Figure 17-7 showing RBBB with left axis deviation due to left anterior fascicular block. Patients with chronic bifascicular block of this kind do not generally require a permanent pacemaker unless they develop second- or third-degree AV block ( Fig. 17-9 ). The risk of complete heart block in asymptomatic patients with chronic bifascicular block is relatively low. By contrast, patients with acute anterior MI in whom bifascicular block suddenly occurs have a poor prognosis because of underlying extensive myocardial necrosis, and they are also at higher risk of abruptly developing complete heart block.

AV DISSOCIATION

Cardiologists use the term AV dissociation in two related though not identical ways. This classification continues to cause considerable (and understandable) confusion among students and clinicians.

AV dissociation is widely used as a general term for any arrhythmia in which the atria and ventricles are controlled by independent pacemakers. The definition includes complete heart block, as well as some instances of ventricular tachycardia in which the atria remain in sinus rhythm (see Chapter 16 ).

AV dissociation is also used as a more specific term to describe a particular family of arrhythmias that are often mistaken for complete heart block. With this type of AV dissociation, the SA node and AV junction appear to be “out of synch”; thus the SA node loses its normal control of the ventricular rate. As a result, the atria and ventricles are paced independently—the atria from the SA node, the ventricles from the AV junction. This situation is similar to what occurs with complete heart block. With AV dissociation, however, the ventricular rate is the same as or slightly faster than the atrial rate.When the atrial and ventricular rates are almost the same, the term isorhythmic AV dissociation is used. (Iso is the Greek root for “same.”)

The critical difference between AV dissociation (resulting from “desynchronization” of the SA and AV nodes) and actual complete heart block (resulting from true conduction failure) is as follows: with AV dissociation (e.g., isorhythmic) a properly timed P wave can be conducted through the AV node, whereas with complete heart block no P wave reaches the ventricles.

AV dissociation ( Fig. 17-10 ) therefore can be regarded as a “competition” between the SA node and the AV node for control of the heartbeat. It may occur either when the SA node slows down (e.g., because of the effects of beta blockers or calcium channel blockers or with increased vagal tone) or when the AV node is accelerated (e.g., by ischemia or digitalis toxicity). Not uncommonly, isorhythmic AV dissociation is seen in healthy young individuals, particularly when they are sleeping.

Figure 17-10 presents an example of isorhythmic AV dissociation. Notice the P waves with a variable PR interval because the ventricular (QRS) rate is nearly the same as the atrial rate. At times, the P waves may merge with the QRS complexes and become imperceptible for several beats. If the sinus rate speeds up sufficiently (or the AV junctional rate slows), the stimulus may be able to penetrate the AV junction, reestablishing sinus rhythm.

REVIEW

Three types of atrioventricular (AV) heart block may occur:

Complete heart block with acute anterior wall myocardial infarction (MI) is sometimes preceded by the sudden appearance of bifascicular block (right bundle branch block with left anterior or posterior fascicular block or a new complete left bundle branch block). Patients with chronic bifascicular block who have no symptoms, however, usually do not require any special therapy.

The significance of complete heart block with acute MI depends on the location of the infarct. Complete heart block occurring with acute inferior wall MI is usually transient and can sometimes be managed without a pacemaker. By contrast, complete heart block with acute anterior wall MI is usually associated with a very poor prognosis and requires a pacemaker.

Complete heart block must be distinguished from other forms of AV dissociation. With isorhythmic AV dissociation, the atria and ventricles beat independently; however, the ventricular rate is about the same as the atrial rate. AV dissociation of this type is a minor, usually transient arrhythmia.

Current guidelines for pacemaker therapy of AV heart block syndromes are given on the websites of the American Heart Association and the American College of Cardiology.

QUESTIONS