Reversal of the cardiovascular effects of verapamil by calcium and sodium: differences between electrophysiologic and hemodynamic responses.

The reversibility of verapamil-induced hemodynamic and electrophysiologic changes by intravenously administered CaCI2 and NaCI was tested in 34 anesthetized open-chest dogs during verapamil infusions which produced plasma verapamil concentrations of 70-2042 ng/ml. An increase of serum calcium concentration (Ca). to an average 6.5 mEq/l abolished the depressive effects of verapamil on cardiac output and left ventricular dp/dt and diminished drug-related hypotension by an average of 52%, but did not affect verapamil-induced prolongation of AH interval and slowing of sinus rate. Further increase of (Ca). to an average of 8.2 mEq/l decreased AH prolongation caused by verapamil from an average of 95% to 45% of control value, but had no effect on verapamil-induced slowing of sinus rate or second-degree atrioventricular (AV) block during atrial pacing. Rapid intravenous injection of 40 ml 2 M NaCI, transiently raised serum Na+ concentration to 162 mE/l, decreased AH prolongation caused by verapamil to an average of 22% of control value, decreased slowing of sinus rate from an average of 34% to an average of 19% of control value, and decreased the severity of second-degree AV block, but had no effect on verapamil-induced complete AV block or sinus arrest. Hypernatremia had no effect on AH interval and sinus rate without prior CaCl2 infusion. In the absence