Electrocardiographic evaluation studies on quinidine-induced changes of myocardial conduction

Quinidine slows the rate of depolarization of both auricle and ventricle, as indicated by a widening of the P wave and the QRS complex; this is an effect which may well be responsible for the drug's effectiveness in atrial fibrillation. Precordial lead records show no change in contour of the QRS complex following large doses of quinidine; the initial and terminal portions of the QRS complex are equally prolonged. That there is no alteration in the sequence of ventricular depolarization by quinidine is confirmed in that there is neither change of contour nor axis of QRS vector loop. These observations would rule out the production of left or right bundle branch block by quinidine. Quinidine does not delay atrial or ventricular repolarization. The prolongation of P-R and Q-T intervals by quinidine can be attributed to its reduction of the heart rate. Lethal doses of quinidine present many of the electrocardiographic features of potassium intoxication at a time when the influence of hypoxia can be ruled out. Although large doses of quinidine do not significantly alter plasma ion concentrations, left ventricular tissue shows the drug to have caused a loss of sodium and a retention of potassium ion; this apparently reflects intracellular changes. Sodium lactate administered to dogs dying from quinidine poisoning exerts a respiratory stimulant action, but cannot restore to normal the quinidine-prolonged QRS complex or width of the P wave. Nearly lethal doses of quinidine were followed at no time by ventricular tachycardia nor other ventricular arrhythmias, despite considerable prolongation of myocardial depolarization and slowing of heart rate.