The mechanism of defibrillation and cardioversion

Sudden cardiac death due to ventricular fibrillation is responsible for over 400,000 deaths per year in the United States alone. The only treatment for this fatal arrhythmia is electrical defibrillation of the ventricle. During the initial seconds of ventricular fibrillation, multiple reentry circuits cause action potentials to occur rapidly with a cycle length determined primarily by the cellular refractory period. A successful defibrillation shock stimulates cells during the refractory period to produce a prolonged postshock response throughout the ventricle. The ventricle is then refractory to propagating fibrillation wavefronts and fibrillation ceases. Biphasic defibrillator waveforms, formed by reversing the polarity partway through the shock, lower defibrillation threshold significantly thereby allowing nonthoracotomy implantation of implantable cardioverter-defibrillators (ICDs). These waveforms appear to defibrillate at lower shock intensities primarily because sodium channel recovery from inactivation by the first phase of the waveform allows the shock to produce the required prolonged responses at these lower intensities. Defibrillation becomes much more difficult at the longer fibrillation durations encountered in “out-of-hospital” cardiac arrest, due to changes in fibrillation morphology. Recent studies suggest that sodium channel recovery produced by biphasic waveforms may also have the potential to increase probability of successful resuscitation under these more stringent conditions