Acute drug treatment of recent onset atrial flutter may reduce the ventricular rate by increasing block in the A-V node (digitalis/verapamil) or act by directly affecting the atria by reducing the atrial rate or converting flutter to sinus rhythm (1a and 1c antiarrthythmic drugs). Treatment that reduces the atrial rate may cause 1:1 A-V conduction. Quinidine and disopyramide are well known for increasing A-V conduction to 1:1 in some patients, because of their anticholinergic effect on the A-V node. Flecainide, a 1c antiarrhythmic drug, slows down atrial conduction, reducing flutter rate by 1/3. Clinical studies have shown flecainide to be effective in converting atrial fibrillation, atrial tachycardia, A-V reentry and A-V nodal reentry tachycardias to sinus rhythm. The effect on atrial flutter has been less impressive. Flecainide prolongs A-V conduction and increases Wenckebach cycle length. In spite of this, 1:1 A-V conduction may occur during treatment with intravenous flecainide for atrial flutter. We present a case where this is demonstrated and review the literature.