Adenosine for the Management of Neonatal and Pediatric Supraventricular Tachycardia

Contributing Editor: Marcia L. Buck, Pharm.D.; Editorial Board: Kristi N. Hofer, Pharm.D.; Michelle W. McCarthy, Pharm.D.


Pediatr Pharm. 2008;14(8) 

In This Article

Mechanism of Action

Adenosine is an endogenous purine nucleoside present in cells throughout the body. It is formed by breakdown of adenosine triphosphate (ATP) or 5-adenosylhomocysteine. While the multiple roles of endogenous adenosine are still being investigated, it is known to aid in maintaining the balance between oxygen delivery and demand by dilating the coronaries and slowing heart rate. These effects result from binding to adenosine A1 receptors in the sinoatrial (SA) node, the atrioventricular (AV) node, atrial myocytes, and coronaries.[2,3,7,8]

Binding at cardiac A1 receptors results in direct activation of an outward potassium current (IK,Ado) and inhibition of cyclic adenosine monophosphate (cAMP), resulting in hyperpolarization of atrial myocardial cell membranes and a shortened action potential duration in the sinus node which impairs conduction. Adenosine also has an indirect effect through antagonism of the β-adrenergic system, resulting in inhibition of β-adrenergic-mediated increases in the inward calcium current and slowing of the pacemaker current.[2,3,7,8]

These same mechanisms result in the ability of exogenous adenosine to slow conduction through the SA, AV node, and atrial tissue. Adenosine is effective in terminating SVT associated with AV nodal re-entry, AV re-entry tachycardia associated with an accessory pathway, sinus node re-entry, and automatic atrial tachycardia. It has also been shown to produce cardioversion in patients with Wolff-Parkinson-White (WPW) syndrome. In addition to its use in cardioversion of SVT, adenosine has been used to induce arrhythmias during electrophysiologic (EP) studies to aid in the diagnosis and evaluation of patients with intermittent tachycardias.[2,3,7–9]


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