A case of complex atrioventricular block

Key Teaching Points.

• •Periodic, grouped ventricular beating excludes a diagnosis of complete atrioventricular block and should prompt investigation of an alternative mechanism.
• •There can be multiple levels of block within the AV junction, with each level exhibiting a different refractory period or a different Wenckebach ratio, leading to a complex, but periodic atrioventricular relationship.
• •If there are two different, but fixed, PR intervals in a tracing, then there is the possibility of alternating antegrade conduction via a slow and fast atrioventricular pathway during sinus rhythm.

Introduction

A 68-year-old man with a history of hypertension presents with bradycardia. A 12-lead electrocardiogram is presented (Figure 1). What is the atrioventricular (AV) relationship?

Figure 1.

Twelve-lead electrocardiogram.

Discussion

The grouped, periodic beating excludes complete AV block, but there is not a clear Mobitz pattern. Therefore, it is likely that there are multiple levels of block in the AV junction. Here we present 5 possible mechanisms.

In our first proposed mechanism (Figure 2a), there is 4:3 Wenckebach in the upper level of the AV junction. There is 2:1 block in the lower level, owing to diseased tissue with a prolonged effective refractory period (ERP), which in this case is ∼720 milliseconds. P wave #1 conducts normally through the upper level, while P waves #2 and #3 conduct with increasing delay owing to latency in the AV node, and P wave #4 blocks as it encounters completely refractory tissue in the upper level (ie, it is the last P wave in the Wenckebach cycle). Once in the second level, P waves #1 and #3 conduct normally while #2 encounters refractory tissue in the lower level.

Figure 2.

A section of the rhythm strip from lead V₁ is shown, with enumerated P waves and the associated ladder diagrams for 5 possible mechanisms (a–e). AVJ = atrioventricular junction; ERP = effective refractory period.

The second possible mechanism (Figure 2b) also involves 2 levels of block within the AV junction, though there is Wenckebach in both levels with 2 different periodicities, a phenomenon that has been previously reported.¹ Note that the P waves have been labeled differently than in Figure 2a. P wave # 1 conducts “normally” (but with vagally mediated delay) down both the upper and lower levels. P wave #2 begins to delay in the upper and lower levels. P wave #3 continues to delay even further in the upper level, but it blocks in the lower level (completing a “3:2” Wenckebach cycle). P wave #4 blocks in the upper level, completing a “4:3”cycle.

The third and fourth mechanisms (Figure 2c and 2d) invoke an “escape-capture” phenomenon previously described.² In Figure 2c, P wave #1 conducts normally. P waves #2 and #3 encounter refractory tissue in the AV junction, again owing to diseased conduction tissue with a particularly prolonged ERP (in this case over 1000 ms). As a result of the blocked P waves, a junctional escape beat (at an escape interval of ∼1520 ms) conducts in a concealed retrograde manner, which prevents the incoming P wave #4 from conducting to the ventricle. In contrast, a fourth mechanism is shown in Figure 2d. P wave #1 conducts normally and P wave #2 blocks in diseased tissue within the AV junction, just as before. However, P wave #3 blocks not owing to an excessively prolonged ERP as in the previous mechanism, but rather owing to brady-dependent “phase 4” block in the AV junction. The following junctional escape beat still prevents P wave #4 from conducting antegrade owing to concealed retrograde conduction (as in the third mechanism described above), but also resets repolarization such that the subsequent P wave #1 can conduct with a normal PR.

Finally, the fifth mechanism (Figure 2e) considers instead the possibility of dual AV node physiology in addition to a level of 2:1 block in the upper common pathway. There are 2 fixed PR intervals, so it is possible that, when the PR is long, conduction occurs down the slow pathway, whereas when the PR is short, conduction proceeds along the fast pathway. Here the fast pathway ERP must be quite prolonged (more than 1000 ms), which has been described previously in patients with sustained slow pathway conduction during sinus rhythm.³ P wave #1 conducts to the ventricle via the fast pathway (and may also travel retrograde up the slow pathway). P wave #2 encounters block in the upper level. P wave #3 is blocked in the fast pathway (owing to the long ERP) and therefore conducts via the slow pathway. P wave #4 blocks in the upper level, and the cycle repeats.

The patient subsequently underwent permanent pacemaker implantation for symptomatic high-grade AV block.

Disclosures

None relevant to the manuscript.