Decreased defibrillator-induced dysfunction with biphasic rectangular waveforms.
High-intensity electric shocks used for cardiac defibrillation produce arrhythmias, S-T segment changes, and a low percent success in situ. Cultured myocardial cells exhibit similar postshock arrhythmias that are caused by a prolonged depolarization of the cell membrane. Since this dysfunction is ameliorated by biphasic RLC-type waveforms, we examined rectangular biphasic waveforms to maximize this beneficial effect and clarify the dysfunction-inducing mechanism. Cultured myocardial cells were subjected to electric field stimulation with monophasic 5-ms rectangular waveforms of about 80 V/cm to produce a postshock arrest of contractile activity lasting 4 s. Shocks given with this control waveform were alternated with biphasic test waveforms having the same initial portion followed by negative "tails" 1-100 ms in duration and 5-100% of the initial positive portion in amplitude. Results from 31 biphasic waveforms demonstrated significant alterations in postshock dysfunction. Waveforms with up to 10% undershoot and ranging from 5 to 100 ms in duration decreased arrest time by up to 50%; waveforms with greater than 20% undershoot led to protracted postshock arrest times. These results strengthen the hypothesis that electromechanical breakdown of the myocardial cell membrane underlies postshock dysfunction and show that biphasic waveforms with low amplitude tails ameliorate this dysfunction.
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology* / Q000517:prevention & control; D002478:Cells, Cultured; D002642:Chick Embryo; D004554:Electric Countershock / Q000009:adverse effects*; D004558:Electric Stimulation; D006801:Humans; D008564:Membrane Potentials; D009200:Myocardial Contraction; D009206:Myocardium / Q000166:cytology