A quantitative model of the single capacitor biphasic defibrillation w
aveform is proposed. The primary hypothesis of this model is that the
first phase leaves a residual charge on the membranes of the unsynchro
nized 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 str
ong enough to synchronize a critical mass of nearly 100% of the myocyt
es. Since the biphasic waveform performs this protection function by r
emoving the residual charge (with its second phase), its first phase m
ay be of a lower strength than a monophasic shock of equivalent perfor
mance. A quantitative model was developed to calculate the residual me
mbrane voltage, V-m, assuming a capacitive membrane being alternately
charged and discharged by the first and second phases, respectively. i
t was further assumed that the amplitude of the first phase would be p
redicted by a minimum value plus a term proportional to V-m(2). The mo
del was evaluated on the pooled data of three relevant published studi
es comparing biphasic waveforms. The model explained 79% of the varian
ce in the first phase amplitude and predicted optimal durations for va
rious defibrillator capacitances and electrode resistances. Assuming a
first phase of optimal duration, the optimal second phase duration ap
pears to be about 2.5 msec for all capacitances and resistances now se
en clinically. Conclusion: The effectiveness of the single capacitor b
iphasic waveform may be explained by the second phase ''burping'' of t
he deleterious residual charge of the first phase that, in turn, reduc
es the synchronization requirement and the amplitude requirements of t
he first phase.