The effects of procainamide and propafenone on the composition of the excitable gap (EG) were studied in a canine model of atrial flutter (AFI) around the tricuspid valve. In 14 open-chest, chloralose-anesthetized dogs, a Y-shaped incision was made in the intercaval area extending to the right atrial appendage. Atrial effective refractory period (ERP) was measured at constant stimulation cycle lengths (CLs) (200 and 300 msec) at each of five recording sites around the tricuspid valve. The EG as defined by the reset-response curve was determined by introducing premature stimuli during AFI induced by burstpacing. Seven dogs each received procainamide or propafenone as a bolus followed by infusion. At constant plasma levels, both drugs increased ERP at constant paced CL and prolonged the reentry CL. In the absence of drug, reset-response curves were mixed, demonstrating an EG composed of both partially (increasing portion) and fully (flat portion) excitable tissue. Procainamide and propafenone shifted the curve upward and to the right and prolonged ERP during AFI, but did not change the duration of the EG. On procainamide, fully excitable tissue was preserved, but on propafenone, in some cases, the fully excitable part of the gap was reduced markedly or even eliminated. In conclusion, both drugs can prolong AFI CL by a direct effect on conduction velocity in fully excitable tissue. In addition, propafenone's effect on refractoriness can contribute significantly in some cases to slowing of AFI.