Intraoperative dexmedetomidine infusion reduces anaesthetic requirements through which receptor mechanism, and what is the unique pharmacological property that makes it distinct from clonidine?
- A Mu-opioid receptor agonism; no withdrawal
- B GABA-A receptor potentiation; ultra-short half-life of 2 minutes
- C NMDA receptor antagonism; less psychomimetic than ketamine
- D Alpha-2 adrenergic receptor agonism; 8-fold greater selectivity for alpha-2 over alpha-1 compared to clonidine ✓
Explanation
Dexmedetomidine is a highly selective alpha-2 adrenergic agonist with an alpha-2:alpha-1 selectivity ratio of approximately 1620:1, compared to clonidine's ratio of ~200:1. This greater alpha-2 selectivity reduces unwanted alpha-1 mediated peripheral vasoconstriction. Dexmedetomidine provides sedation, anxiolysis, analgesia (spinal cord alpha-2 receptors), and opioid-sparing effects without respiratory depression. It is unique in producing a 'cooperative sedation' where patients can be easily roused. It reduces intraoperative anaesthetic requirements (MAC sparing ~30%), attenuates haemodynamic responses to intubation, and is used for awake intubation sedation.
Reference: Morgan & Mikhail's Clinical Anesthesiology, 6th ed.
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