Abstract
Quinidine is widely used in the therapy of various cardiac arrhythmias. Toxic effects, while well documented, are relatively uncommon. Contraindications to the use of quinidine have, however, limited clinical application. Quinidine depresses cardiac rhythmicity and conduction. This appears to be a direct effect on the myocardium, with little if any effect being mediated through the autonomic nervous system. At the present time there is no method of therapy which will reverse cardiotoxic quinidine effects. Molar sodium lactate appears to promptly reverse moderately severe cardiotoxic electrocardiographic effects, and to correct the hypotension secondary to quinidine intoxication, restoring the blood pressure to normotensive levels. These preliminary observations suggest that molar sodium lactate may be effective clinically in treating quinidine intoxication in man. Serum electrolyte and pH determinations revealed that the animals developed a moderately severe acidosis which was promptly restored to normal by molar sodium lactate. The possible mechanisms of action are discussed.
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