BIPHASIC DEFIBRILLATION WAVE-FORMS REDUCE SHOCK-INDUCED RESPONSE DURATION DISPERSION BETWEEN LOW AND HIGH SHOCK INTENSITIES

Mechanisms underlying defibrillation threshold reduction with biphasic waveforms remain unclear. The interaction of local shock-induced voltage gradients, which change with distance from the shocking electrode, and the slate of membrane repolarization results in different cellular responses that may influence the success of defibrillation. We used intracellular microelectrodes and S1S2 pacing protocols in myocardial cell aggregates to determine the effects of shock intensity and waveform on refractory period responses during simulated fibrillation (3 s of S-1 pacing at 180-ms cycle length). We simulated defibrillation by electric field stimulation S-2 using 8-ms monophasic (MS?) and 4/4 biphasic (BS2) waveforms (65% total tilt) delivered at intensities of 1.5, 3, and 5 times S-1 diastolic threshold, or approximate to 2 to 7 V/cm. Responses following MS(2) varied with S-2 intensity and coupling interval (P<.001). When averaged over the last 10 ms of the refractory period, MS(2) produced a negligible response (8.8+/-1.4 ms) at 1.5 times diastolic threshold and a prolonged response (53.0+/-3.1 ms) at 5 times diastolic threshold (P<.01). In contrast, BS2 response duration did not change significantly (P=NS) between 1.5 times diastolic threshold (35.1+/-12.6 ms) and 5 times diastolic threshold (46.2+/-2.7 ms). Our results suggest that biphasic waveforms not only prolong response duration at low shock intensity but reduce dispersion of refractoriness produced by differing local potential gradients generated by defibrillation shocks compared with monophasic waveforms. Preventing dispersion of refractoriness and prolonging shock-induced responses may improve biphasic waveform efficacy at low shock intensity.