Circulation, Vol 68, 1254-1263, Copyright © 1983 by American Heart Association
JP DiMarco, TD Sellers, RM Berne, GA West and L Belardinelli
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.
ARTICLES
Adenosine: electrophysiologic effects and therapeutic use for terminating paroxysmal supraventricular tachycardia
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