Atrioventricular (AV) Conduction Abnormalities, Part I: Delays, Blocks, and Dissociation Syndromes

First-Degree AV “Block” (Prolonged PR Interval)

First-degree AV block ( Fig. 17.2 ) is characterized by a P wave (usually but not always sinus in origin) followed by a QRS complex with a prolonged PR interval of greater than 200 msec (one big box or five small boxes in width at the standard 25 mm/sec recording speed). More precise terms for this finding are prolonged PR interval or PR interval prolongation because the electrical signal is not actually blocked but rather delayed. The PR interval can be mildly to moderately prolonged (e.g., 232 msec in Fig. 17.2 B), or it can become markedly long (occasionally up to 400–600 msec or longer) or may fluctuate from beat to beat ( Fig. 17.2 C). PR prolongation in concert with prominent sinus bradycardia ( Fig. 17.2 D) should raise strong consideration of functional (not structural) slowing of conduction, especially because of enhanced vagal tone or drugs (e.g., beta blockers).

Second-Degree AV Block

Second-degree AV block is characterized by intermittently “dropped” QRS complexes. With underlying sinus rhythm, the metaphorical term “dropped beat” means that a P wave is not followed by a QRS. As noted, there are two major subtypes of second-degree AV block: Mobitz I (AV Wenckebach) and Mobitz II.

With Mobitz I , the classic AV Wenckebach pattern ( Figs. 17.3 and 17.4 ), each stimulus (e.g., sinus P wave) from the atria encounters progressively more “difficulty” (decremental conduction) in traversing the AV node en route to the ventricles (i.e., the node becomes increasingly refractory). Finally, an atrial stimulus is not conducted at all, such that the expected QRS complex is blocked (“dropped QRS”), producing that a P wave that is not conducted despite the fact that it comes “on time.” This cycle is followed by recovery of the AV node; then the cycle starts again.

The characteristic electrocardiogram (ECG) signature of classic AV Wenckebach block, therefore, is of progressive prolongation of the PR interval from one beat to the next until a QRS complex is dropped. (Occasionally, when the PR interval gets very long, it can fluctuate from one beat to the next and show minimal or no prolongation between the last conducted beats of a cycle.) However, the PR interval after the nonconducted P wave (the first PR interval of the new cycle) is always shorter than the PR interval of the beat just before the nonconducted P wave. This observation is the most useful and, indeed, a clinically imperative means of differentiating Mobitz I block from Mobitz II in which the conducted PR interval does not vary throughout the cycle.

The number of P waves occurring before a QRS complex is “dropped” may vary with AV Wenckebach. Cardiologists employ a simple index based on the ratio of the number of P waves to QRS complexes in a given cycle. The numerator is always one higher than the denominator. In the most readily diagnosed cases, just two or three conducted P waves are seen before one is not conducted (e.g., 3:2, 4:3 AV block). In other cases, longer cycles are seen (e.g., 5:4, 10:9, etc.).

As you see from the examples, the Wenckebach cycle also produces a distinct clustering of QRS complexes separated by a pause (the “dropped” QRS). Any time you encounter an ECG with this type of group beating, you should suspect AV Wenckebach block and look for the diagnostic pattern of lengthening PR intervals and the presence of a nonconducted P wave. As discussed in the following sections, infranodal second-degree AV block (Mobitz type II) also demonstrates group beating with dropped QRS complexes but without significant progressive PR interval prolongation ( Fig. 17.5 ). Another cause of group beating is the frequent occurrence of nonconducted (blocked) premature atrial complexes (blocked PACs) as discussed in Chapter 14

Caution! Clinicians must be careful not to mistake group beating because of blocked premature atrial complexes (PACs) for second-degree AV block. In the former, the nonconducted P waves come “early,” and in the latter, the P waves come “on time” (see 14, 24 ).

Mobitz II AV block (see Fig. 17.5 ) is a less common but more serious form of second-degree heart block. Its characteristic feature is the sudden appearance of a single, nonconducted sinus P wave without two features seen in Mobitz I block: (1) progressive prolongation of PR intervals and (2) noticeable shortening of the PR interval in the beat after the nonconducted P wave versus the PR before the nonconducted P wave.

A relatively rare but important subset of second- degree heart block occurs when there are multiple consecutive nonconducted P waves present (e.g., P to QRS ratios of 3:1, 4:1, etc.). This finding is often referred to as high-degree (or advanced ) AV block. It can occur at any level of the conduction system ( Fig. 17.6 ). A common mistake is to call this pattern Mobitz II block or complete heart block.

Third-Degree (Complete) AV Block

First- and second-degree AV heart blocks are examples of incomplete block because the AV junction conducts at least some stimuli to the ventricles. With third-degree or complete heart block ( Figs. 17.7–17.9 ), no stimuli are transmitted from the atria to the ventricles. Instead, the atria and ventricles are paced independently. The atria may continue to be paced from the sinus node (or by an ectopic focus or even by atrial fibrillatory or flutter activity). The ventricles, however, are paced by a nodal or infranodal escape focus located below the point of block. Complete heart block can develop at the level of the AV node, or at the infranodal level. Typically, the escape rhythm in complete heart block at the level of the AV node tends to be narrow (junctional) with faster (40-60 beats/min) rates compared with a wide QRS escape beats with slower (30-40 beats/min or less) rates because of infranodal block.

Complete heart block can develop gradually because of the progression of first- or second-degree AV block, or a bundle branch block, noted on prior ECGs, or it may be observed suddenly without any apparent preexisting AV conduction abnormalities. The most dramatic example of the latter is referred to as paroxysmal complete AV block (see Fig. 17.9 ). Paroxysmal complete AV block occurs in severe conduction disease, which is often not apparent from the surface ECG. In susceptible individuals, paroxysmal complete heart block can be triggered by a PAC, a PVC, or an increase in heart rate, but it sometimes occurs without any identifiable precipitant. Unless the rhythm is “rescued” by ventricular or junctional (see Fig. 17.9 ) escape beats, cardiac arrest will ensue with asystole (see Chapter 21 ). Therefore, development of paroxysmal AV block because of intrinsic conduction disease is a potentially life-threatening condition requiring urgent pacemaker implantation. ^a

a Of potential confusion, the term paroxysmal AV block has also been used to describe acute and progressive AV block, including third-degree block, associated with excess vagal tone. This vagally mediated form of paroxysmal block may occur with vomiting, endotracheal suctioning, micturition, neurocardiogenic syncope, and so forth. In such cases, the sinus rate generally slows as well. A pacemaker is usually not required. In contrast, the intrinsic (degenerative) form of paroxysmal AV block described in the text may be associated with increased sinus rate and reflects primary conduction disease, requiring pacemaker insertion.

Complete AV heart block, where there is no signaling or “cross-talk” between the atria and ventricles and each of them is driven independently by a separate pacemaker at a different rate, is one generic example of AV dissociation. In the setting of complete heart block, AV dissociation usually produces more P waves than QRS complexes ( Box 17.1 ). However, as discussed later, AV dissociative rhythms are not restricted to complete heart block syndromes.