A patient with paroxysmal supraventricular tachycardia (PSVT) is successfully cardioverted with adenosine IV. The haemodynamic mechanism by which adenosine terminates SVT is:
- A Adenosine blocks cardiac sodium channels preventing depolarisation in re-entrant circuits
- B Adenosine activates A1 receptors causing Gi-mediated opening of IKAdo potassium channels in the AV node, transiently blocking AV conduction ✓
- C Adenosine stimulates A2 receptors increasing cAMP to slow the SA node
- D Adenosine acts as a calcium channel blocker in the AV node
Explanation
Adenosine activates A1 purinoceptors in the sinoatrial and atrioventricular nodes, which are Gi-coupled. The released Gβγ subunits open IKAdo (adenosine-sensitive inward rectifier K+) channels, hyperpolarising nodal cells and transiently blocking AV conduction, interrupting re-entrant SVT circuits. Its extremely short half-life (~10 seconds, metabolised in blood) limits systemic side effects but causes transient heart block and flushing. Adenosine A2 receptors cause vasodilation via increased cAMP (used in pharmacological stress testing), not AV blockade.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.