Refractoriness prolongation by defibrillation shocks.

Refractoriness prolongation by defibrillation shocks.

Ventricular refractory period extension caused by defibrillation shocks.

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 ener...

A Simulation Study of Biphasic Defibrillation Shocks

0.1. Background This article presents a study, which examines the effects of biphasic defibrillation shocks on human ventricular tissue. The effects of this type of shock are not yet fully understood. Animal experiments showed the superiority of biphasic shocks over monophasic ones. A mathematical computer simulation can increase the knowledge of human heart behavior. 0.2. Methods and Results T...

Extension of Refractoriness in a Model of Cardiac Defibrillation

This simulation study presents an inquiry into the mechanisms by which a strong electric shock halts life-threatening cardiac arrhythmias. It examines the "extension of refractoriness" hypothesis for defibrillation which postulates that the shock induces an extension of the refractory period of cardiac cells thus blocking propagating waves of arrhythmia and fibrillation. The present study uses ...

The effect of rate on prolongation of ventricular refractoriness by quinidine in humans.

In this study, the rate dependent effect of quinidine on the ventricular effective refractory period (VERP) was evaluated in 30 patients undergoing electropharmacological testing with quinidine. The VERPs were measured in the baseline state and after at least 2 days of treatment with 1,458-2,044 mg/day of quinidine gluconate (mean plasma quinidine concentration 2.2 +/- 0.7 mcg/mL). In 20 patien...