Ketamine is described as producing 'dissociative anaesthesia'. Its primary mechanism and a unique clinical feature is:
- A Antagonism of NMDA receptors via open-channel block; produces bronchodilation, cardiovascular stimulation, and profound analgesia; risk of emergence delirium ✓
- B GABA-A potentiation, causing loss of consciousness with maintained pharyngeal reflexes and bronchodilation
- C Alpha-2 adrenoceptor agonism, producing sedation without amnesia
- D Blockade of voltage-gated sodium channels with excellent muscle relaxant properties
Explanation
Ketamine blocks NMDA receptors by entering the open channel and binding within the pore (use-dependent, non-competitive block). It produces a unique dissociative state with profound somatic analgesia, amnesia, and sedation while preserving airway reflexes and respiratory drive. It causes sympathetic stimulation (tachycardia, hypertension) via central catecholamine release and is a bronchodilator — making it useful in status asthmaticus. Emergence delirium (vivid dreams, hallucinations) is reduced by concurrent benzodiazepine use.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.