Adenosine (Adenocard) is an endogenous nucleoside that is a product of the metabolism of adenosine triphos-phate. It is used for the rapid termination of supraven-tricular arrhythmias following rapid bolus dosing.
Adenosine receptors are found on myocytes in the atria and sinoatrial and A-V nodes. Stimulation of these re-ceptors acts via a G-protein signaling cascade to open an acetylcholine-sensitive outward potassium current. This leads to hyperpolarization of the resting mem-brane potential, a decrease in the slope of phase 4 spon-taneous depolarization, and shortening of the action po-tential duration.
The effects on the A-V node may result in a con-duction block and the termination of tachycardias that use the A-V node as a limb of a reentrant circuit. Adenosine does not affect the action potential of ven-tricular myocytes because the adenosine-stimulated potassium channel is absent in ventricular myocardium.
The most profound effect of adenosine is the induction of an A-V block within 10 to 20 seconds of administra-tion. Mild sinus slowing may be observed initially fol-lowed by sinus tachycardia. There is no effect on the QRS duration or QT interval. Rarely, an adenosine bo-lus injection is accompanied by atrial fibrillation or ven-tricular tachyarrhythmias.
The administration of a bolus dose of adenosine is asso-ciated with a biphasic pressor response. There is an ini-tial brief increase in blood pressure followed by vasodi-lation and secondary tachycardia.
The pharmacokinetic characteristics of adenosine:
Oral bioavailability : Not measured
Onset of action : 10 seconds (IV)
Peak response : Not measured
Duration of action : 10–20 seconds
Plasma half-life : 10 seconds
Primary route of metabolism : Red blood cells
Primary route of excretion metabolites : Renal; inactive
Therapeutic serum concentration : Not applicable
Adenosine is approved for the acute management and termination of supraventricular tachyarrhythmias, in- cluding A-V nodal reentrant tachycardia and A-V recip-rocating tachycardia. Adenosine may be helpful in the diagnosis of atrial flutter.
Adverse reactions to the administration of adenosine are fairly common; however, the short half-life of the drug limits the duration of such events. The most common ad-verse effects are flushing, chest pain, and dyspnea. Adenosine may induce profound bronchospasm in pa-tients with known reactive airway disease. The mecha-nism for bronchospasm is unclear, and the effect may last for up to 30 minutes despite the short half-life of the drug.
Patients with second- or third-degree A-V block should not receive adenosine. As indicated previously, the use of adenosine in asthmatic patients may exacerbate the asthmatic symptoms.
Metabolism of adenosine is slowed by dipyridamole, in-dicating that in patients stabilized on dipyridamole the therapeutically effective dose of adenosine may have to be increased. Methylxanthines antagonize the effects of adenosine via blockade of the adenosine receptors.
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