Resuscitation After Prolonged Ventricular Fibrillation With Use of Monophasic and Biphasic Waveform Pulses for External Defibrillation

Abstract

Background-Survival after prolonged ventricular fibrillation (VF) appears severely limited by 2 major factors: (1) low defibrillation success rates and (2) persistent post-countershock myocardial dysfunction. Biphasic (BP) waveforms may prove capable of favorably modifying these limitations. However, they have not been rigorously tested against monophasic (MP) waveforms in clinical models of external defibrillation, particularly where rescue from prolonged VF is the general rule. Methods and Results-We randomized 26 dogs to external countershocks with either MP or BP waveforms.Hemodynamics were assessed after shocks applied during sinus rhythm, after brief VF (Ͼ10 seconds), and after resuscitation from prolonged VF (Ͼ10 minutes). Short-term differences in percent change in left ventricular ϩdP/dt max (MP Ϫ16Ϯ28%, BP ϩ9.1Ϯ24%; Pϭ0.03) and left ventricular ϪdP/dt max (MP Ϫ37Ϯ26%, BP Ϫ18Ϯ20%; Pϭ0.05) were present after rescue from brief VF, with BP animals exhibiting less countershock-induced dysfunction. After prolonged VF, the BP group had lower mean defibrillation thresholds (107Ϯ57 versus 172Ϯ88 J for MP, Pϭ0.04) and significantly shorter resuscitation times (397Ϯ73.7 versus 488Ϯ74.3 seconds for MP, Pϭ0.03). Conclusions-External defibrillation is more efficacious with BP countershocks than with MP countershocks. The lower defibrillation thresholds and shorter resuscitation times associated with BP waveform defibrillation may improve survival after prolonged VF arrest.

Electrical Induction of Ventricular Fibrillation for Resuscitation From Postcountershock Pulseless and Asystolic Cardiac Arrests

“…8 A power of 80% and PϽ0.05 were assumed. ANOVA was used to screen for significant variability; then, contrast analyses were performed to isolate differences for our prospective end points.…”

“…Recently, in our own laboratory, a subgroup analysis of animals initially proving refractory to defibrillation demonstrated a surprising trend toward improved resuscitation rates and less severe myocardial stunning despite the probable selection of a more compromised population of subjects. 8 Immediately defibrillated subjects appeared to fare no better than subjects in the delayed defibrillation subgroup despite significantly shorter durations of VF, fewer countershocks, and equivalent coronary perfusion pressures during CPR. The available evidence would therefore suggest that modest delays to defibrillation do not necessarily predict poorer cardiac resuscitation outcomes when ongoing VF is counterbalanced by effective precountershock CPR.…”

“…A revealing trend toward more severe myocardial stunning, however, became apparent when resuscitated RF group animals were compared with CPR group animals that were not subjected to an additional cycle of immediate defibrillation and refibrillation. By extension, repeated high-energy countershocks administered in a systematic attempt to suppress VF may have served to potentiate typically minor degrees of electrical myocardial injury 8,24,25 and may be primarily responsible for producing the phenotype of crippling hemodynamic consequences apparent in our immediate defibrillation group. Thus, frequent defibrillatory countershocks to maintain essentially pulseless rhythms would appear not merely unproductive but ultimately deleterious to resuscitation from VF arrest.…”

Milrinone Facilitates Resuscitation From Cardiac Arrest and Attenuates Postresuscitation Myocardial Dysfunction

“…26,27 Lower current biphasic defibrillation waveforms have been shown to be more effective than monophasic waveforms for VF termination and, in selected instances, to be associated with less-pronounced alterations in cardiac contractility. 12,14 Once established, few studies have addressed the management of postresuscitation ventricular dysfunction. Dobutamine is the only drug that has been systematically evaluated in in vivo animal models of cardiac arrest and resuscitation.…”

“…9 -11 Other investigations suggest that defibrillation shocks administered to animal models with a low transthoracic impedance are associated with transient declines in ventricular systolic and diastolic function. [12][13][14] However, a critical interrelationship between shock-induced myocardial injury and the degree of hypoperfusion has recently been demonstrated, and there is evidence that suggests that defibrillation shocks do not significantly contribute to myocyte dysfunction. [15][16][17] Several studies support the concept that transient calcium overload in stunned myocardium results in a decreased sensitivity or responsiveness of cardiac myofilaments to intracellular calcium.…”