Postshock potential gradients and dispersion of repolarization in cells stimulated with monophasic and biphasic waveforms.
BACKGROUND
Even though the clinical advantage of biphasic defibrillation waveforms is well documented, the mechanisms that underlie this greater efficacy remain incompletely understood. It is established, though, that the response of relatively refractory cells to the shock is important in determining defibrillation success or failure. We used two computer models of an isolated ventricular cell to test the hypothesis that biphasic stimuli cause a more uniform response than the equivalent monophasic shocks, decreasing the likelihood that fibrillation will be reinduced.


RESULTS
Models of reciprocally polarized and uniformly polarized cells were used. Rapid pacing and elevated [K]o were simulated, and either 10-msec rectangular monophasic or 5-msec/5-msec symmetric biphasic stimuli were delivered in the relative refractory period. The effects of stimulus intensity and coupling interval on response duration and postshock transmembrane potential (Vm) were quantified for each waveform. With reciprocal polarization, biphasic stimuli caused a more uniform response than monophasic stimuli, resulting in fewer large gradients of Vm (only for shock strengths < or = 1.25x threshold vs < or = 2.125x threshold) and a smaller dispersion of repolarization (1611 msec2 vs 1835 msec2). The reverse was observed with uniform polarization: monophasic pulses caused a more uniform response than did biphasic stimuli.


CONCLUSIONS
These results show that the response of relatively refractory cardiac cells to biphasic stimuli is less dependent on the coupling interval and stimulus strength than the response to monophasic stimuli under conditions of reciprocal polarization. Because this may lead to fewer and smaller spatial gradients in Vm, these data support the hypothesis that biphasic defibrillation waveforms will be less likely to reinduce fibrillation. Further, published experimental results correlate to a greater degree with conditions of reciprocal polarization than of uniform polarization, providing indirect evidence that interactions between depolarized and hyperpolarized regions play a role in determining the effects of defibrillation shocks on cardiac tissue.
Department of Biomedical Engineering, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
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D003198:Computer Simulation; D004554:Electric Countershock; D004558:Electric Stimulation; D006352:Heart Ventricles / Q000166:cytology / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D015640:Ion Channel Gating; D008564:Membrane Potentials; D014693:Ventricular Fibrillation / Q000628:therapy