Pathophysiology of second degree atrioventricular block: a unified hypothesis.

An in vivo and in vitro correlative study of second degree atrioventricular (A-V) block in the canine proximal His-Purkinje system after ligation of the anterior septal artery is reported. Evidence is presented to suggest that Mobitz type II and the Wenckebach ypte of conduction represent different degrees of the same disorder rather than two distinct electrophysiologic processes. The in vivo study showed that an increment of conduction delay almost always preceded the blocked impulse in second degree A-V block. The increment, as 1 or 2 msec at the early stage of block, often increased gradually up to 180 msec. The in vitro study consistently showed an increment of conduction delay preceding the blocked impulse. The same experiments revealed a greater increment in conduction delay early after excision that, on recovery during superfusion, gradually decreased to a few milliseconds (the reverse order of the in vivo observation). Characteristic changes in duration and configuration of action potentials in the ischemic proximal His-Purkinje system were observed depending on the state of transmission and the temporal relation of the impaled cell to areas of slow propagation and block. The study revealed a remarkable similarity between characteristics of conduction in the ischemic His-Purkinje system and conduction in both the normal A-V doe and Purkinje fibers subjected to various pathophysiologic interventions. It is suggested that in the pathologic situation--exemplified in this study by acute myocardial ischemia--the normal His-Purkinje system may gradually lose the characteristics of the fast response and start showing properties of the slow response. At an early stage of departure from normal, the proximal His-Purkinje system may show second degree A-V block with no perceptible to a few milliseconds' increment of conduction delay (the equivalent of Mobitz type II block). On further departure from normal, the His-Purkinje system resembles the A-V node in showing a significant increment of conduction delay prior to the blocked impulse (the equivalent of Wenckebach periodicity). Both the in vivo and in vitro observations demonstrated a clear propensity of the ischemic proximal His-Purkinje system to develop paroxysmal A-V block during the stage of second degree A-V block when there is no perceptible to a few milliseconds' increment of conduction delay. A new classification of second degree A-V block is presented based on the suggested electrophysiologic mechanism.