Objective: Despite a history of widespread use, the utility of lidocaine as an antiarrhythmic and antifibrillatory agent is questionable. The objective of this article is to examine the theoretical basis for the use of lidocaine in light of recent experimental and clinical data. This article reviews the effects of lidocaine on: a) ventricular arrhythmias under ischemic and nonischemic conditions; b) the energy and current requirements for defibrillation; and c) the propensity for asystole during cardiac arrest.
Design: A contemporary review of the literature.
Findings: There appears to be a theoretical basis for the use of lidocaine in treating ventricular arrhythmias secondary to acute ischemia largely based on voltage- and pH-dependent binding and inactivation of sodium channels by lidocaine under ischemic conditions. However, clinical and experimental data failed to establish enhanced survival following prophylactic treatment for acute ischemic events or when treatment is administered during cardiac arrest. Moreover, there are no data supporting the use of lidocaine in treating sustained and life-threatening ventricular arrhythmias in the absence of acute ischemia. Experimental data demonstrate that lidocaine can reduce countershock efficacy, i.e., increase the current and energy requirements for defibrillation. Experimental and clinical data suggest that the administration of lidocaine increases the propensity for asystole during cardiac arrest.
Conclusions: While lidocaine may possess an antifibrillatory effect under experimental conditions, the clinical relevance of such an effect is questionable. If cardiac arrest occurs, lidocaine has limited utility and may be deleterious secondary to diminished countershock efficacy or lidocaine-induced asystole. Reconsideration of the use of lidocaine should be included in future guidelines for management of cardiac arrest.