Quinidine: Arterial, Venous, Coronary Sinus and Myocardial Concentrations*

Most of the current knowledge of relationships between blood levels of quinidine and therapeutic or toxic effects were ascertained by determining peripheral venous levels following oral administration. After single oral administration of quinidine sulfate to patients with atrial fibrillation, Wegria and Boyle (1) observed that the intensity of the cardiac effect of the drug and its plasma concentration were grossly parallel but not parallel in a strictly quantitative manner. Discrepancies were found between the intensity of cardiac effect and quinidine plasma concentration, the plasma level of the drug decreasing faster than the intensity of its cardiac effect. Some investigators utilize quinidine concentration of venous blood as a guide in determining optimal therapy (2-6). Wegria and Boyle (1) reported no significant difference between the arterial and venous concentration of quinidine a few hours after oral administration. Higher levels were found in the myocardium than in the peripheral venous blood. A recent publication (7) contains a review of the pertinent literature on the subject. In spite of the clinical practice of administering quinidine intravenously to patients with certain life-threatening arrhythmias for immediate therapeutic effects, there is a paucity of data relative to blood levels