Sweeney R J, Gill R M, Reid P R
Department of Electrophysiology Research, Eli Lilly and Co, Indianapolis, Ind, USA.
Circulation. 1996 Dec 1;94(11):2947-52. doi: 10.1161/01.cir.94.11.2947.
Measurements of refractory period extension by shocks during ventricular pacing at fast rates predict that all tissue should be refractory for a brief interval after shocks during fibrillation. This study experimentally determined whether a refractory interval was present just after a shock during fibrillation.
In pentobarbital-anesthetized dogs, rectangular monophasic (4-ms) or biphasic (2.5/1.5-ms) shocks were followed with a 2-ms postshock stimulus (PSS) delivered to the defibrillation electrodes. We measured the effect of PSS on the shock current (I50) required for 50% defibrillation success. In group 1 (n = 6), a 1.0-A PSS had no effect on I50 when delivered up to 35 ms after monophasic shocks but greatly increased I50 when delivered at 50 to 90 ms. A 0.5-A PSS had no effect at any timing. In group 2 (n = 6), we compared 1.0-A PSSs after monophasic and biphasic shocks. The effect of PSS after monophasic shocks was similar to group 1. After biphasic shocks, PSS at the same timings had similar effects but caused even greater increases in I50.
We conclude that after both monophasic and biphasic shocks during fibrillation, there is a postshock interval during which the heart is refractory to the refibrillating effect of PSS. The interval is shorter for biphasic than for monophasic shocks with the same duration and defibrillation efficacy. These findings support the refractory period extension hypothesis for defibrillation and suggest that propagating depolarization activity is absent immediately after defibrillation shocks but that it develops again at the end of the refractory interval or later.
