Both the electrophysiological and antiarrhythmic effects of some antiarrhythmic agents may differ markedly depending on their route of administration. Flecainide acetate, a new class 1 agent, was therefore administered both intravenously and orally to 13 patients with recurrent paroxysmal tachycardia to assess whether the acute response to intravenous flecainide accurately predicts the response to oral therapy. Eight patients had atrioventricular re-entrant tachycardia (AVRT) and five patients intra AV nodal re-entrant tachycardia (AVNRT). When administered by either route, flecainide markedly prolonged both the anterograde and retrograde conduction intervals during constant rate pacing and the anterograde and retrograde Wenckebach cycle lengths during incremental pacing. Five of the 13 patients developed complete retrograde block after both routes of administration of the drug. All 13 patients received intravenous flecainide during tachycardia with successful reversion to sinus rhythm in all cases. Tachycardia could be reinitiated in five of the patients with AVRT after intravenous flecainide and in one further patient after oral administration. It was not possible to reinitiate tachycardia in any of the five patients with AVNRT after either intravenous or oral flecainide. The size of the tachycardia initiation windows, by either atrial or ventricular premature stimuli, were significantly reduced by both intravenous and oral flecainide. In those patients in whom tachycardia could be reinitiated, tachycardia cycle length was significantly increased, and to a similar degree, by both routes of administration of the drug. This increase in cycle length was predominantly due to prolongation in retrograde conduction. It is concluded that flecainide acetate is a potent antiarrhythmic agent for use in patients with junctional tachycardia. The intravenous administration of flecainide reliably predicts the subsequent response to oral therapy.