Effect of hyperkalemia on experimental myocardial depression by verapamil.

Three patients with systemic hypotension and sinus bradycardia that were initially refractory to conventional therapy responded well to intravenous calcium administration. Two-dimensional echocardiography revealed immediate reversal of severe left ventricular dysfunction after intravenous administration of calcium in two instances. Common factors were hyperkalemia and verapamil therapy. This interaction was examined further by evaluation of contractility, heart rate, and arterial blood pressure in anesthetized dogs. Controls (n = 9) received saline infusion, and a second group (n = 10) received saturated potassium chloride (approximately 0.2 ml/min intravenously). In control dogs, administration of verapamil (1195 +/- 181 micrograms/kg intravenously) reduced systemic arterial pressure from 113 +/- 7 mm Hg to 74 +/- 5 mm Hg, and heart rate from 147 +/- 9 beats/min to 86 +/- 11 beats/min. Potassium chloride infusion alone increased blood [K+] from 3.4 +/- 0.1 to 6.2 +/- 0.2 mEq/L, but was without hemodynamic effects. In hyperkalemic dogs, a significantly lower dose of verapamil (428 +/- 42 micrograms/kg intravenously) reduced systemic arterial pressure from 102 +/- 8 mm Hg to 36 +/- 4 mm Hg, and heart rate from 150 +/- 5 beats/min to 104 +/- 15 beats/min. Myocardial contractile function was examined with right ventricular isometric contractile force and left ventricular segment length changes. In normokalemic and hyperkalemic groups, contractility was decreased by verapamil. Effects of verapamil on arterial pressure and contractility could be reversed significantly by administration of calcium, 0.4 mEq/kg intravenously. The present results support the theory that the negative hemodynamic effects of verapamil may be exaggerated to a harmful degree by concomitant hyperkalemia. These adverse events may be reversed by calcium administration.