Quinidine has an established place in the management of certain cardiac arrhythmias, although the toxic effects produced by this drug remain a potential hazard. With the relatively recent advances in determining the plasma concentration of quinidine and the rather specific indications and cautions stressed when this drug is used in clinical practice, the severe toxic reactions can be minimized but probably never will be completely eliminated. The toxic effects produced by quinidine are varied and unpredictable. This paper will review the cardiotoxic effects and their management, placing special emphasis on the clinical and experimental evidence for the use of molar sodium lactate in combating this disorder. The results of recent animal experiments regarding the pharmacologic action of quinidine will be summarized. Recently we encountered the problem of severe cardiac depression in two patients while attempting conversion from auricular fibrillation to normal sinus rhythm by the use of quinidine. Dramatic reversal