The PR interval on the electrocardiogram represents the time that it takes an impulse to travel through the atrium and atrioventricular (AV) conduction system to the ventricles. Normally, activation is slowest in the AV node, and variations in PR interval most commonly parallel changes in AV nodal activation time. The AV nodal conduction time and effective refractory period are rate dependent and, in adult humans, are usually prolonged with increasing atrial paced rates. In addition, alterations in autonomic tone effect AV nodal conduction as well as sinus rate. The effect is usually in the same direction but often to different degrees. In patients with normal AV nodal function, parasympathetic and sympathetic tone are balanced at rest, but in patients with abnormal AV conduction, the effect of the parasympathetic system is more marked. Drugs including the slow channel blockers and beta blockers, affect AV nodal function. Slow channel blockers inhibit the slow inward calcium current, which may prolong conduction and refractoriness in the AV node. However, whereas diltiazem and verapamil have been shown to prolong AV nodal conduction and refractoriness in humans, nifedipine, a potent vasodilator, cannot be used in doses large enough to affect the AV node. The increase in PR interval caused by verapamil is minimal, and at doses of less than 480 mg/d, AV block occurs infrequently. When AV block occurs, it is first degree block in most patients, and it is usually asymptomatic. The electrophysiologic effects of diltiazem are similar to those of verapamil. Beta blockers also have a negative dromotropic effect on the AV node. They prolong the AH interval and AV nodal refractory periods and may lengthen the PR interval. The prolonged PR interval rarely results in more than first degree AV block in patients receiving maintenance therapy. In selected patients, combination therapy with a slow channel blocker and a beta blocker rarely causes second-degree AV block.