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Circulation, Vol 82, 965-972, Copyright © 1990 by American Heart Association

ARTICLES

Ventricular refractory period extension caused by defibrillation shocks

RJ Sweeney, RM Gill, MI Steinberg and PR Reid
Department of Electrophysiology Research, Eli Lilly and Company, Indianapolis, Ind. 46285.

In pentobarbital-anesthetized dogs, transcardiac shocks of up to 30 J or pacing stimuli were delivered to myocardial tissue at different times in the electrical cycle. When delivered midway or later into electrical systole, shocks, but not pacing stimuli, greatly extended the refractory period as determined by left ventricular pacing. There was a positive correlation between both the shock energy and timing and the amount of delay. A 30-J shock given 10 msec before the end of the refractory period extended the refractory period by 63 +/- 15 msec (p less than 0.001), whereas the same shock given 40 msec earlier produced only 25 +/- 10 msec (p less than 0.001) of extension. By comparison, a 5-J shock given at those times produced 36 +/- 18 (p less than 0.005) and 10 +/- 8 msec (p less than 0.001) of extension, respectively. When delivered early into electrical systole, both a pacing stimulus and a shock had no substantial effect on the tissue refractory period. Because the tissue that is late in electrical systole would otherwise be the first to repolarize if no shock were given, the selective refractory period extension may create a period after the shock during which no tissue is repolarized to a level sufficient for wavefront propagation. Thus, the energy- and time-dependent refractory period extension may help explain the mechanism by which ventricular defibrillation occurs during transcardiac shocks.

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