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Adenosine SVT Mechanism — FRCA Primary MCQ

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ModeratePharmacology - CardiovascularAdenosine SVT MechanismFRCA Primary

A haemodynamically stable adult has a regular narrow-complex tachycardia in which the atrioventricular node forms part of the re-entry circuit. A rapid intravenous bolus of adenosine terminates the tachycardia. Which receptor–effector mechanism most directly accounts for this effect?

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Correct answer: E — A1-receptor activation with increased potassium conductance in atrioventricular nodal cells

Adenosine activates Gi-coupled A1 receptors in the AV node. The G-protein beta-gamma subunits increase an inwardly rectifying potassium conductance, causing potassium efflux and membrane hyperpolarisation; reduced cyclic AMP also diminishes calcium-dependent nodal currents. These effects transiently slow or block AV nodal conduction and terminate re-entry when the AV node is an essential limb. Adenosine is not a direct calcium-channel blocker or beta-1 antagonist. Na+/K+-ATPase inhibition is the mechanism of cardiac glycosides, while potassium-channel blockade generally prolongs repolarisation rather than producing adenosine's brief AV nodal block. Its blood half-life is under 10 seconds, explaining the need for rapid intravenous bolus administration followed by a flush.

Reference: Brignole M et al. Adenosine, Adenosine Receptors and Neurohumoral Syncope: From Molecular Basis to Personalized Treatment. Biomedicines. 2022. https://pubmed.ncbi.nlm.nih.gov/35625864/