Threshold reduction with biphasic defibrillator waveforms. Role of charge balance.
Mechanism underlying improved defibrillation efficacy of biphasic waveforms at low shock intensities remain poorly understood. Recent studies suggest that biphasic waveforms produce a longer mean postshock response throughout the ventricle. This prolongs the cellular refractory period, blocks fibrillation wave fronts, and causes fibrillation to cease. Previous studies showed that hyperpolarizing monophasic waveforms, delivered during the refractory period, can shorten action potential duration (APD90), which would be deleterious for defibrillation. This study tested the hypothesis that a balanced-charge biphasic waveform produces a longer mean total mean APD than a comparable monophasic waveform by preventing this shortening in hyperpolarized regions as well as by prolonging APD in depolarized regions. To test this hypothesis, the authors examined transmembrane potential changes produced by hyperpolarizing and depolarizing monophasic and balanced-charge symmetrical biphasic waveforms using a computer model of the ventricular action potential. Shock intensities within the low-intensity "window," where biphasic waveforms defibrillate with higher efficacy than monophasic waveforms (1.5-3 times diastolic threshold), were used. Results show that biphasic S2 produced a significantly longer response both under hyperpolarizing and depolarizing conditions. The hyperpolarizing/depolarizing biphasic S2 produced a prolonged response with a well-defined plateau. Following the depolarizing/hyperpolarizing S2, APD90 did not shorten as with the hyperpolarizing monophasic S2. Rather, repolarization continued near the original S1 times course, but with slight prolongation of S1 APD90. These results suggest that biphasic waveforms enhance the prolonged refractory periods required for defibrillation throughout the heart, including regions exposed to both anodal and cathodal stimulation.
Jones
J L
JL
Department of Physiology and Biophysics, Georgetown University, Washington, DC, USA.
Tovar
O H
OH
D000200:Action Potentials; D003198:Computer Simulation; D004554:Electric Countershock / Q000145:classification / Q000379:methods*; D004558:Electric Stimulation; D004594:Electrophysiology; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D008564:Membrane Potentials; D008959:Models, Neurological; D012032:Refractory Period, Electrophysiological; D013997:Time Factors; D014693:Ventricular Fibrillation / Q000503:physiopathology