A patient has atrial fibrillation with rapid ventricular rate and is haemodynamically stable. Adenosine is administered. This drug terminates paroxysmal supraventricular tachycardia primarily by:

• A Blocking L-type calcium channels in the AV node
• B Increasing intracellular cAMP to prolong AV nodal refractory period
• C Activating cardiac A1 receptors, hyperpolarising AV nodal cells via opening GIRK channels ✓
• D Blocking delayed rectifier potassium channels to prolong repolarisation

Explanation

Adenosine acts on cardiac A1 purinergic receptors coupled to Gi, which opens G-protein-regulated inward-rectifying K+ (GIRK) channels. This causes hyperpolarisation of SA and AV nodal cells, prolonging AV nodal refractory period and transiently blocking conduction through the AV node. This mechanism terminates re-entrant SVTs that involve the AV node in the circuit. It is ineffective for atrial fibrillation itself but used diagnostically.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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