Virtual electrodes and deexcitation: new insights into fibrillation induction and defibrillation.
Previous models of fibrillation induction and defibrillation stressed the contribution of depolarization during the response of the heart to a shock. This article reviews recent evidence suggesting that comprehending the role of negative polarization (hyperpolarization) also is crucial for understanding the response to a shock. Negative polarization can "deexcite" cardiac cells, creating regions of excitable tissue through which wavefronts can propagate. These wavefronts can result in new reentrant circuits, inducing fibrillation or causing defibrillation to fail. In addition, deexcitation can lead to rapid propagation through newly excitable regions, resulting in the elimination of excitable gaps soon after the shock and causing defibrillation to succeed.
Efimov
I R
IR
Department of Cardiology, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA. efimovi@ccf.org
Gray
R A
RA
Roth
B J
BJ
D003198:Computer Simulation; D016757:Death, Sudden, Cardiac / Q000209:etiology; D017147:Defibrillators, Implantable; D004554:Electric Countershock / Q000009:adverse effects*; D006329:Heart Conduction System / Q000503:physiopathology; D006339:Heart Rate; D006801:Humans; D008564:Membrane Potentials; D008955:Models, Cardiovascular; D017180:Tachycardia, Ventricular / Q000503:physiopathology / Q000628:therapy*; D017211:Treatment Failure; D014693:Ventricular Fibrillation / Q000209:etiology* / Q000503:physiopathology