| Overview | – Ketamine is a phencyclidine derivative that induces dissociative anesthesia. |
| – It affects EEG by dissociating thalamocortical and limbic systems. |
| – Hypertonus and muscle movements may occur independently of surgical stimulation. |
| – Ketamine induces amnesia and intense analgesia. |
| – Emergence delirium limits its clinical use. |
| Structure Activity Relationship | – Ketamine has two optical isomers: S(+) and R(-). S(+) is clinically available. |
| – S(+) ketamine is preferred for its benefits. |
| – Ketamine can be dissolved in water and contains benzethonium chloride as a preservative. |
| Mechanism of Action | – NMDA receptor antagonism and reduction in glutamate release. |
| – Interaction with μ, δ, κ, and κ opioid receptors. |
| – Effects on monoaminergic receptors and muscarinic receptors. |
| – Interaction with voltage-gated sodium channels. |
| – Interaction with nicotinic acetylcholine receptors. |
| Pharmacokinetics | – Rapid peak plasma levels after IV and IM administration. |
| Metabolism | – Metabolized to norketamine by cytochrome P450 enzymes. |
| Clinical Uses | – Rapid induction of anesthesia and intense analgesia. |
| – Used in anesthesia, burn dressing changes, and skin grafting. |
| – Treatment for opioid tolerance recovery. |
| Adverse Effects | – Cardiovascular stimulation, emergence delirium. |
| – Effects on cerebral blood flow, bronchospasm treatment. |
| – Minimal risk of allergic reactions and histamine release. |
| Drug Interactions | – Interference with inhaled anesthetics and neuromuscular blockers. |
