Adenosine: electrophysiologic effects and therapeutic use for terminating paroxysmal supraventricular tachycardia.

Adenosine was administered intravenously to 17 patients undergoing intracardiac electrophysiologic studies. At a mean dose of 179 +/- 88 micrograms/kg (+/- SD), adenosine suppressed sinus node automaticity and depressed atrioventricular (AV) nodal conduction. These effects were less than 20 sec in duration and were not influenced by muscarinic blockade with atropine (0.02 to 0.03 mg/kg). Adenosine at this dose had no effect on antegrade conduction over accessory pathways in patients with Wolff-Parkinson-White syndrome. No independent hemodynamic effects were observed. In six patients, adenosine was administered intravenously during stimulation-induced paroxysmal supraventricular tachycardia. In the five patients in whom the reentry loop of their tachycardia included the AV node, adenosine at a mean dose of 83 +/- 35 micrograms/kg (+/- SD) terminated their tachycardia within 20 sec after peripheral intravenous injection. The dose of adenosine required to terminate these tachycardias did not produce manifest sinus node suppression, and sinus rhythm promptly resumed in all patients. Adenosine did not terminate either supraventricular tachycardia due to intra-atrial reentry or atrial flutter, but did produce transient AV block during these arrhythmias. Our findings demonstrate that the human sinus and AV nodes are sensitive to physiologic doses of adenosine and that adenosine may be used safely and effectively to terminate acute episodes of supraventricular tachycardia that involve the AV node in the reentry pathway.