title: Effects of repetitive electrical shocks on postresuscitation myocardial function.
abstract: Whereas myocardial cell injury can occur during electrical defibrillation proportional to the energy level of individual shocks, only minimal (or no) injury seems to develop when the energy is limited to the levels typically required to terminate ventricular fibrillation. During cardiac arrest, however, multiple shocks are often required to terminate ventricular fibrillation or to treat episodes that appear subsequently during the resuscitation effort or the postresuscitation interval. Concern exists because an inverse relationship has been reported between the number of electrical shocks delivered during cardiac resuscitation and both resuscitability and survival. Repetitive electrical shocks can alter diastolic function and prompt leftward shifts of the end-diastolic pressure-volume curves. Repetitive shocks may, therefore, contribute to the recently recognized phenomenon of postresuscitation myocardial dysfunction and hamper efforts to reestablish competent myocardial function after resuscitation. Thus, strategies aimed at limiting the number of electrical shocks during cardiopulmonary resuscitation are highly desirable. These may include real-time ventricular fibrillation waveform analysis to improve targeting of individual shocks and efforts (using mechanical and pharmacologic means) to render the myocardium more responsive to individual shocks and to promote greater electrical stability after successful defibrillation.
authors: Medical Service, Section of Critical Care Medicine, North Chicago Veterans Affairs Medical Center, Illinois 60064, USA. raul.gazmuri@med.va.gov
authors: R J
authors: RJ
authors: Gazmuri
mesh_terms: D000818:Animals; D009202:Cardiomyopathies / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control; D004554:Electric Countershock / Q000009:adverse effects* / Q000379:methods*; D004594:Electrophysiology; D006323:Heart Arrest / Q000150:complications / Q000401:mortality / Q000628:therapy*; D006439:Hemodynamics; D006801:Humans; D051381:Rats; D015996:Survival Rate; D018754:Ventricular Dysfunction / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control