Guidelines for Use of Ketamine

Ketamine is commonly used in many laboratory species for anesthesia and chemical restraint. Ketamine is classified as a dissociative anesthetic, which means it produces dose-related unconsciousness and analgesia, but not classical anesthesia.

Its primary site of action in the central nervous system (CNS) appears to be the thalamoneocortical projection system. It selectively depresses neuronal function of the neocorticothalamic axis and the central nucleus of the thalamus while it stimulates parts of the limbic system, including the hippocampus.

Ketamine induces significant increase in cerebral blood flow, intracranial pressure, and cerebrospinal fluid pressure as a result of cerebral vasodilatation and elevated systemic blood pressure. In animals known to be epileptic, the administration of Ketamine has been associated with the induction of seizures. Hallucinatory behavior, which may progress to delirium, may occur during emergence from Ketamine anesthesia. Ketamine-induced depression of the inferior colliculus and medial geniculate nucleus, leading to misperception of auditory and visual stimuli, may be responsible for this reaction.

The cardiovascular effects of Ketamine are characterized by indirect cardiovascular stimulation. Various effects include sympathomimetic effects mediated within the CNS, inhibition of neuronal uptake of catecholamine by sympathetic nerve endings, direct vasodilatation of vascular smooth muscle, and an isotropic effect on the myocardium. Heart rate and arterial blood pressure increase as a result of direct stimulation of the CNS. Increased myocardial stimulation is associated with increased cardiac work and myocardial oxygen consumption.

The cardiovascular effect of Ketamine appears to depend on an intact and normally functioning CNS. Unlike most other anesthetics, Ketamine does not depress ventilatory responses to hypoxia. Skeletal muscle tone is maintained or even increased. Respiratory rate and minute volume may decrease initially after Ketamine administration, but return to baseline values within 15 minutes.

Ketamine may produce a transient apnea which appears to be dose dependent. Ketamine often causes increased salivation and respiratory secretions. Laryngeal and pharyngeal reflexes are usually well maintained during Ketamine anesthesia. In most species, Ketamine undergoes extensive hepatic metabolism. Rapid recovery following Ketamine administration is caused by rapid redistribution of Ketamine from the CNS to all body tissues (primarily body fat, lung, liver, and kidney).

Clinically, animals with hepatic dysfunction or renal dysfunction do not recover from Ketamine anesthesia as rapidly as normal animals.

Ketamine is rarely administered alone due to its poor muscle relaxation. Ketamine has been used in combination with various other anesthetic drugs, but it is most commonly combined with xylazine, acetylpromazine, or diazepam.

Ketamine has a wide range of safety (i.e. wide dose range in most species). It has been shown to be safe to use in pregnant animals (i.e. no significant adverse effects on the fetus). The duration of Ketamine anesthesia is very dose dependent and ranges from 15 minutes (dog), 20-45 minutes (cat) , 10-30 minutes (pig), and 10-20 minutes (rabbit).

Because of some of the very advantages for which we use Ketamine in research medicine, Ketamine can also be abused. Recent newspaper accounts of Ketamine abuse / misuse even at certain school campuses across the country have clearly demonstrated the problem. It is the abuse potential of Ketamine that has caused its recent inclusion into the federal DEA controlled drug inventory system.