Abstract Paroxysmal supraventricular tachycardia most often results from atrioventricular (AV) reentry using an accessory AV pathway (Wolff-Parkinson-White syndrome) or reentry within the region of the AV node. In AV reentry, using an accessory pathway, suppression of the tachycardia may be achieved by depressing either anterograde AV nodal conduction or retrograde accessory pathway conduction. Intracardiac recordings and programmed electrical stimulation have established that β-adrenergic antagonists and calcium channel blockers principally affect AV nodal conduction (anterograde limb of the reentrant circuit), whereas class IA and IC agents principally affect the accessory AV pathway (retrograde limb). Pharmacologic therapy has been more effective when directed at the limb in which conduction is most marginal at the tachycardia rate (weak limb). In individual patients, intracardiac recordings and programmed electrical stimulation can be used to identify the weak limb, indicating the class of agents most likely to be effective. Specialized techniques allowing direct recording of accessory pathway activation suggest that limitations in accessory pathway conduction may be explained by anatomic impediments. Conduction is most limited at the atrial interface of the accessory pathway in some patients, whereas in others the ventricular interface may be the limiting factor. Class IA and IC agents appear to have the greatest effect at sites where conduction is most tenuous, i.e., at the anatomic impediments. Similar considerations apply to AV nodal reentry. Anterograde slow AV nodal pathway conduction is most often depressed by digitalis preparations, β-adrenergic antagonists, and calcium channel blockers, whereas retrograde fast AV nodal pathway conduction is more often depressed by class IA and IC agents. Intracardiac recordings and programmed electrical stimulation can also be used in these patients to identify the weak limb and direct pharmacologic therapy. Direct catheter recordings of AV nodal conduction remain elusive, limiting knowledge of the different conduction properties of the anterograde and retrograde limbs and the site(s) of drug action. Studies in progress, comparing the retrograde AV nodal conduction time during tachycardia with that during ventricular pacing at the same rate, suggest that the His bundle may be incorporated in the reentrant circuit in some patients. It appears that verapamil more readily depresses retrograde fast pathway conduction in these patients than in those in whom the His bundle does not form part of the reentrant circuit, but the reasons for this are unknown.