Effects of a class III antiarrhythmic drug and biphasic shocks on the postdefibrillation refractory period of relatively refractory myocardium.

Abstract

This study was designed to test whether the refractory state of nondepolarized myocardium is a major determinant of electrical defibrillation. Postshock recovery interval (PSRI) was estimated by measuring the residual refractory period after an appropriately timed field stimulus (1 to 16 V). The PSRI and transcardiac defibrillation threshold (DFT) were compared before and during the administration of E-4031, a new Class III antiarrhythmic drug (group 1, n = 10), or between monophasic and biphasic shocks (group 2, n = 14) in anesthetized open chest dogs. Group 1: E-4031 reduced the DFT from 2.6 +/- 0.6 J to 1.8 +/- 0.6 J (P < 0.01). The PSRI increased with the increase of the applied voltage and was almost always greater during E-4031 infusion than at baseline. There was an inverse correlation between the changes of DFT and PSRI measured with a 14-V stimulus (r = -0.80, P < 0.01) and a 16-V stimulus (r = -0.80, P < 0.01). Group 2: Mean DFTs were not statistically different between the two waveforms (3.3 +/- 1.0 J vs 2.9 +/- 1.4 J). However, there also was an inverse correlation between the differences in individual PSRIs and DFTs of the two waveforms (10-V stimulus: r = -0.62, P < 0.05; 16-V stimulus: r = -0.75, P < 0.01). Modulation of defibrillation efficiency by E-4031 infusion or by changes of the shock waveform was related to the effect of these interventions on PSRI. These results suggest an independent role for the refractoriness of nondepolarized myocardium in the mechanism of defibrillation.