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8 General anaesthetic agents100 mg.ml−^1 ,and it may be given intravenously (1–2 mg.kg−^1 )orintramuscularly
(5–10 mg.kg−^1 )for induction of anaesthesia. Intravenous doses of 0.2–0.5 mg.kg−^1
may be used to provide analgesia during vaginal delivery and to facilitate the posi-
tioning of patients with fractures before regional anaesthetic techniques are per-
formed. It has been used via the oral and rectal route for sedation and also by
intrathecal and epidural routes for analgesia. However, its use has been limited by
unpleasant side effects.Effects
Cardiovascular – ketamine is unlike other induction agents in that it pro-
duces sympathetic nervous system stimulation, increasing circulating levels of
adrenaline and noradrenaline. Consequently heart rate, cardiac output, blood
pressure and myocardial oxygen requirements are all increased. However, it
does not appear to precipitate arrhythmias. This indirect stimulation masks the
mild direct myocardial depressant effects that racemic ketamine would oth-
erwise exert on the heart. S(+)ketamine produces less direct cardiac depres-
sion in vitro compared with R(−)ketamine. In addition while racemic ketamine
has been shown to block ATP-sensitive potassium channels (the key mecha-
nism of ischaemic myocardial preconditioning), S(+)ketamine does not, which
therefore must be considered advantageous for patients with ischaemic heart dis-
ease.
Respiratory – the respiratory rate may be increased and the laryngeal reflexes rela-
tively preserved. A patent airway is often, but not always, maintained, and increased
muscle tone associated with the jaw may precipitate airway obstruction. It causes
bronchodilation and may be useful for patients with asthma.
Central nervous system – it produces a state of dissociative anaesthesia that is
demonstrated on EEG by dissociation between the thalamocortical and limbic
systems. In addition, intense analgesia and amnesia are produced. Theαrhythm
is replaced byθandδwave activity. Ketamine is different from other intravenous
anaesthetics as it does not induce anaesthesia in one arm–brain circulation time –
central effects becoming evident 90 seconds after an intravenous dose. Vivid and
unpleasant dreams, hallucinations and delirium may follow its use. These emer-
gence phenomena may be reduced by the concurrent use of benzodiazepines or
opioids. S(+)ketamine produces less intense although no less frequent emergence
phenomena. They are less common in the young and elderly and also in those left
to recover undisturbed. Cerebral blood flow, oxygen consumption and intracra-
nial pressure are all increased. Muscle tone is increased and there may be jerking
movements of the limbs.
Gut–nausea and vomiting occur more frequently than after propofol or thiopental.
Salivation is increased requiring anticholinergic premedication.