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Effects of Antiarrhythmic Drugs on AV Nodal and Intraventricular Conduction as Assessed in the Isolated, Blood‐Perfused AV Node Preparation of the Dog

Summary The effects of seven antiarrhythmic drugs on atrioventricular (AV) nodal and intraventricular (His-Purkinje-ventricular muscle) conduction were investigated in the isolated, blood-perfused AV node preparation of the dog. When injected into the posterior septal artery (PSA), which supplies mainly the AV node, quinidine, ajmaline, disopyramide, lidocaine, mexiletine, phenytoin, and procainamide increased AV nodal conduction time; and in high doses, these drugs produced second- or third-degree AV conduction block. However, quinidine, ajmaline, disopyramide, and lidocaine had less propensity to induce second- or third-degree AV conduction block than did phenytoin, mexiletine, and procainamide. When injected into the anterior septal artery (ASA), which supplies the His-Purkinje-ventricular muscle, all seven drugs prolonged intraventricular conduction time. The relative suppressant effects of these drugs on AV nodal and intraventricular conduction varied. Quinidine, disopyramide, and ajmaline suppressed AV nodal conduction as much as intraventricular conduction. Lidocaine and mexiletine suppressed AV nodal conduction more than intraventricular conduction, and phenytoin suppressed AV nodal conduction much more than intraventricular conduction. In contrast, procainamide suppressed intraventricular conduction rather than AV nodal conduction. All drugs increased blood flow in the ASA and the PSA.