A minimal model of the single capacitor biphasic defibrillation waveform.
A quantitative model of the single capacitor biphasic defibrillation waveform is proposed. The primary hypothesis of this model is that the first phase leaves a residual charge on the membranes of the unsynchronized cells, which can then reinitiate fibrillation. The second phase diminishes this charge, reducing the potential for refibrillation. To suppress this potential refibrillation, a monophasic shock must be strong enough to synchronize a critical mass of nearly 100% of the myocytes. Since the biphasic waveform performs this protection function by removing the residual charge (with its second phase), its first phase may be of a lower strength than a monophasic shock of equivalent performance. A quantitative model was developed to calculate the residual membrane voltage, Vm, assuming a capacitive membrane being alternately charged and discharged by the first and second phases, respectively. It was further assumed that the amplitude of the first phase would be predicted by a minimum value plus a term proportional to Vm2. The model was evaluated on the pooled data of three relevant published studies comparing biphasic waveforms. The model explained 79% of the variance in the first phase amplitude and predicted optimal durations for various defibrillator capacitances and electrode resistances. Assuming a first phase of optimal duration, the optimal second phase duration appears to be about 2.5 msec for all capacitances and resistances now seen clinically.


CONCLUSIONS
The effectiveness of the single capacitor biphasic waveform may be explained by the second phase "burping" of the deleterious residual charge of the first phase that, in turn, reduces the synchronization requirement and the amplitude requirements of the first phase.
Implantable Products Division, Angeion Corporation, Plymouth, Minnesota.
M W
MW
Kroll
D000200:Action Potentials; D004554:Electric Countershock; D004562:Electrocardiography; D004594:Electrophysiology; D006321:Heart / Q000502:physiology; D006801:Humans; D008954:Models, Biological