Conversion of mobitz type II AV block to 1:1 AV conduction by premature ventricular beats

Preliminary experiments in a canine model of Mobitz type II atrioventricular (AV) block showed improvement of conduction after premature ventricular beats. In this investigation, the authors studied the mechanism(s) responsible for this response. In vivo studies were performed in 16 anesthetized dogs. Block was induced by ischemia after septal artery occlusion or by mechanical trauma. Two pairs of plunge electrodes were inserted in the proximal and distal His bundle. An electrode catheter was positioned at the level of the aortic root to provide an overall view of His bundle activation. Bipolar pacing was performed from the high right atrium, right ventricular outflow tract, and proximal and distal His bundle. Infra-nodal 2:1 AV block was consistently induced at an atrial rate of 238 ± 21 beats/min. In 15 dogs a narrow time window (10-60 ms; mean, 32 ± 6 ms) was found during which premature beats resulted in transient (2-11 beats; n = 9) or persistent (n = 8) restoration of 1:1 AV conduction. Retrograde penetration of the site of block, that is, Hb, was found even when the anterograde impulse was blocked, demonstrating the asymmetric nature of anterograde versus retrograde conduction. In vitro studies were performed in the same hearts. Intracellular recordings were obtained in the damaged His bundle and proximal right bundle. The site of block showed frequent displacements along the bundle. The introduction of a retrograde stimulus during 2:1 block restored 1:1 anterograde conduction. This effect was due to two major factors: peeling back of refractoriness, as an early and short action potential ensued, and asymmetry of conduction, as retrograde stimuli depolarized the damaged area at the time of expected anterograde block. Other factors that influence this phenomenon are: dissociation of conduction and elecrotonic interaction among dissociated cells. Within a narrow time window, a retrograde stimulus can penetrate the site of block in the damaged conduction system and restore anterograde conduction by early activation of the damaged area.