The effect of lithium chloride on the electrocardiogram of the isolated perfused heart

Abstract

Action potentials were recorded simultaneously from the cavity and the epicardium of the ventricle of the isolated perfused heart of the dog and the turtle before and after alteration of the concentrations of the various cations in the perfusate. High concentrations of lithium chloride in the perfusate slowed the cardiac rate, prolonged the S-T interval, and broadened the T waves. The width and contour of the QRS complex were unaltered, but the voltage was decreased. A very high concentration of lithium seemed to affect primarily the automaticity of the turtle heart. Lithium in a concentration of 25.72 meq. per liter or greater counteracted many of the electrocardiographic effects of an excess of potassium; more specifically, lithium shortened the delayed intraventricular conduction time, increased the shortened S-T interval, and again separated the components of electrical activity from the terminal monophasic and diphasic forms of potassium intoxication. Lithium could not substitute for calcium or sodium in the perfusing solution, although lithium tended to counteract the electrocardiographic effects of a moderately low sodium concentration in the perfusate. An excess of calcium in the perfusate caused an increase in the QRS interval, widening of the T wave, a slight increase in the amplitude of the S wave in the epicardial tracing, and atrioventricular dissociation. The absence of calcium from the perfusate prolonged the P-R interval and Q-T interval, without change in the width or contour of the QRS complex, and broadened the T waves.