Electrophysiology of ventricular fibrillation and defibrillation

The survival rate from ventricular fibrillation is very high for short-duration fibrillation (<30 secs) but decreases to approximately 3% to 30% in out-of-hospital conditions. During short-duration fibrillation, action potentials occur rapidly with no intervening period of electrical diastole; a shock defibrillates by interacting with the fibrillation action potential to produce a uniformly long postshock extension of refractoriness. In contrast, during long-duration fibrillation, ischemia-induced degradation of cellular electrophysiology occurs, which causes intervening periods of electrical diastole between fibrillation action potentials and, thus, slowing of fibrillation frequency. A successful defibrillation shock must now not only prolong refractoriness when delivered during the action potential but must also excite cells during the periods of depolarized diastole. Biphasic waveforms enhance both effects by causing premature membrane repolarization with the first pulse, thereby allowing sodium channel recovery from inactivation so that the second pulse produces better-formed responses both during the cellular action potential and during the depolarized diastole. Therefore, biphasic waveforms remain superior to monophasic waveforms for treatment of long-duration fibrillation. Improved understanding of the ischemia-induced changes in cellular electrophysiology will suggest further improvements in both defibrillator waveforms and resuscitation techniques.