Electrophysiologic and Hemodynamic Effects of Sodium Bicarbonate in a Canine Model of Severe Cocaine Intoxication

Abstract

Objective. Cocaine toxicity causes myocardial depression, malignant dysrhythmias, and sudden death, partially due to cocaine‐related myocardial sodium channel blockade. Because of cocaine's ability to block cardiac sodium channels, sodium bicarbonate (NaHCO₃) has been proposed as an antidote. The hypothesis of this study was that NaHCO₃ would correct cocaine‐induced conduction abnormalities and resultant hemodynamic compromise in an animal model simulating severe cocaine intoxication. Methods. Design: Prospective, controlled, experimental study in which 15 anesthetized dogs were given three successive boluses of cocaine (7 mg/kg) and then randomized to receive NaHCO₃, 2 mEq/kg (n = 8) or placebo (n = 7). Measurements: Arterial, left ventricular, and pulmonary artery pressures; cardiac output (CO); electrocardiogram (ECG); blood gases; and serum concentrations of cocaine were measured at baseline, at fixed time intervals after each bolus of cocaine, and then after administration of NaHCO₃ or placebo. Statistical significance was determined by analysis of variance (ANOVA) for repeated measures. Results. Seven dogs experienced significant arrhythmias, including VT, pulseless electrical activity, and third‐degree atrioventricular block; 2 of these dogs expired prior to receiving NaHCO₃ and were excluded. Immediately after administering NaHCO₃, QRS duration decreased by 30% (p < 0.001), returning to baseline more quickly than in the control group. This effect was associated with a brief 30% decrease in MAP (p = NS). After NaHCO₃, CO increased 78% and remained increased for 5 min (p < 0.007). One dog converted from complete heart block to sinus rhythm shortly after NaHCO₃ administration. Conclusions. NaHCO₃ improved ECG changes secondary to cocaine toxicity and improved myocardial function.