K B Milne | PubMed Health

PubMed1994

Refractory period prolongation by biphasic defibrillator waveforms is associated with enhanced sodium current in a computer model of the ventricular action potential.

Mechanisms through which biphasic waveforms lower defibrillation threshold are unknown. Previous work showed that low-intensity biphasic shocks (BS2), delivered during the refractory period of a control action potential (S1), produced significantly longer responses than monophasic shocks (MS2). To test the hypothesis that longer responses are due to hyperpolarization-induced excitation channel recovery during the first portion of the biphasic waveform, we used the Beeler-Reuter ventricular action potential computer model with the Drouhard-Roberge (BRDR) modification to study refractory period stimulation with MS2 (10 msec) and symmetrical BS2 (10 msec each pulse). At 1.5 times diastolic threshold, BS2 prolonged action potential duration when delivered 50 msec into the S1 refractory period, and produced a maximum BS2 versus MS2 response duration difference of 62 msec. Longer BS2 responses corresponded to enhanced BS2-induced sodium current compared to MS2. Maximum BS2 vs MS2 sodium current difference was 400 uA/cm2. These results show that, in a computer model of the ventricular action potential, hyperpolarization by the first phase of a biphasic waveform enhances S2 sodium current and prolongs duration of refractory-period responses. This effectively shortens the cellular refractory period. Prolonged refractory period responses, produced by biphasic defibrillator waveforms, may underlie enhanced defibrillating efficacy at low shock intensities.

Action Potentials↗

PubMed1994

Dysfunction and safety factor strength-duration curves for biphasic defibrillator waveforms.

Newly developed biphasic waveforms significantly lower defibrillation threshold in animal and clinical models. However, underlying mechanisms and optimum waveform shape are unknown. Defibrillation shocks produce dysfunction; safety factor, the ratio of shock intensity inducing dysfunction to that producing stimulation of partially refractory cells, is an important parameter for defibrillator waveforms. We determined dysfunction and safety factor strength-duration curves for symmetric and asymmetric (50% undershoot) monophasic and biphasic rectangular (0%-tilt) waveforms. Dysfunction threshold, defined as the voltage producing a 4-s postshock contractile arrest, was determined for waveforms with total durations from 1 to 40 ms. For all waveforms, dysfunction threshold decreased with waveform duration. At all durations, dysfunction threshold was similar for symmetric monophasic and biphasic waveforms with the same total duration. In contrast, asymmetric biphasic waveforms increased dysfunction threshold 14 +/- 3% (P < 0.005) compared with monophasic control waveforms. Because long-duration, low-tilt, biphasic waveforms improve excitation threshold for refractory cells, they should improve defibrillation threshold. Asymmetric waveforms have the additional advantage of improving safety factor by reducing postshock dysfunction.

Animals↗