Calcium and digoxin vs calcium alone for severe verapamil toxicity

Calcium chloride (CaCl2) is ineffective in severe calcium channel antagonis t overdoses. Digoxin increases intracellular calcium by inhibiting the sodi um-potassium adenosine triphosphatase enzymes. Objective: To examine the ef fect of calcium and digoxin on the treatment of verapamil toxicity. Methods : Sixteen dogs were instrumented to monitor hemodynamics. Verapamil toxicit y (50% decrease in mean arterial pressure) was induced with verapamil (VER) at 6 mg/kg/hr and maintained for 30 minutes by titrating the VER rate. Fol lowing toxicity, the dogs received either digoxin (0.018 mg/kg) (DIG) (n = 8) or saline (No-DIG) (n = 8). Both groups received VER at three sequential rates (1 mg/kg/hr from 0 to 90 min, 6 mg/kg/hr from 90 to 130 min, and 18 mg/kg/hr from 130 to 170 min). Calcium boluses were given (500 mg at 0 and 15 min; 1 g at 140, 150, and 160 min). Data were analyzed using a repeated- measures analysis of covariance comparing DIG vs No-DIG across the infusion rates and time. Animal weight, dose of VER administered during the toxicit y phase, and baseline values were included as covariates. Mortality rates w ere compared at 230 minutes following a total dose of 500 mg of VER. Result s: The DIG group had a higher systolic blood pressure (SBP) than the No-DIG group during the 1-mg/kg/hr (early p = 0.028, late p = 0.01), 6-mg/kg/hr ( p = 0.051), and 18-mg/kg/hr (p = 0.038) VER infusion rates. There were no d eaths in the DIG group and four deaths in the No-DIG group (Fisher = 0.08). Neither ventricular tachycardia nor ventricular fibrillation developed in either group. Other hemodynamic parameters did not show significant changes . Conclusions: In a model of severe verapamil toxicity digoxin plus calcium raised SEP and did not result in ventricular arrhythmias when compared wit h calcium alone.