Oh

Figure 22.6 • Metabolism of ketamine.

concentration from building and triggering excitatory synaptic transmissions in the brain and spinal cord.

Ketamine causes a transient increase in blood pressure after administration and is contraindicated in patients whom a significant elevation of blood pressure would constitute a serious hazard. Ketamine has also been found to bind to mu, delta, and kappa opioid receptors as well as the sigma receptors. The S(+) ketamine is two to three times more potent than the R(—) ketamine as an analgesic.51 Ketamine has different effects at different doses on the opioid receptors and the use of ketamine as a postoperative analgesic or for chronic pain requires more study.52,53

Ketamine is classified as a "dissociative anesthetic," and psychological manifestations during emergence of anesthesia occur in 12% of patients. These vary from pleasant dreamlike states to vivid hallucinations and delirium. The duration is usually for only a few hours but patients have reported recurrences taking place up to 24 hours postopera-tively. The incidence of this appears to be less in children younger than 16 years of age and in patients older than 65 years of age. Like other dissociative anesthetics, ketamine is abused for its hallucinatory effects. Most of the illegally used ketamine comes from stolen legitimate sources, particularly from veterinary clinics or smuggled in from

Mexico.54

Ketamine is metabolized via N-demethylation to form the main metabolite norketamine. Norketamine has about one third the potency of the parent compound. Minor meta bolic pathways include hydroxylation of the cyclohexanone ring; hydroxylation followed by glucuronide conjugation, and hydroxylation followed by dehydration to the cyclo-hexenone derivative (Fig. 22.6).55,56

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