Dexmedetomidine is increasingly used for procedural sedation and ICU analgosedation. Its primary mechanism of action is:

• A GABA-A potentiation at cortical inhibitory interneurons
• B Mu-opioid receptor agonism combined with weak NMDA antagonism
• C H1 receptor blockade with central anticholinergic activity
• D Selective alpha-2 adrenoceptor agonism at locus coeruleus and spinal cord ✓

Explanation

Dexmedetomidine is a highly selective alpha-2 adrenoceptor agonist (alpha-2:alpha-1 selectivity ratio approximately 1600:1). Sedation and anxiolysis result from activation of alpha-2 receptors in the locus coeruleus (reducing noradrenergic outflow); analgesia from activation of spinal dorsal horn alpha-2 receptors (reducing substance P release). Unlike benzodiazepines, it preserves respiratory drive and produces 'cooperative sedation' — patients are easily rousable. Bradycardia and transient hypertension followed by hypotension are the key adverse effects.

Reference: Morgan & Mikhail's Clinical Anesthesiology, 6th ed.

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Written and medically reviewed by the StethoPrep medical team.