Der Anaesthesist
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Review Randomized Controlled Trial Clinical Trial
[S-(+)-Ketamine and circulation].
The S-(+) isomer of ketamine has about twice the analgesic potency of the clinically used racemic mixture. Therefore, the known side effects may be reduced when one-half of the usual dose is administered. Several prospective, randomised, and double-blinded studies have been performed to assess whether the S-(+) isomer of ketamine is superior to the racemic mixture with respect to circulatory side effects. ⋯ One patient in the S-(+)-ketamine group showed severe arterial hypertension and tachycardia after induction of anaesthesia and was withdrawn from the study. With respect to haemodynamic changes, the pharmacodynamic effects of ketamine racemate and S-(+)-ketamine are comparable. Therefore, it can be concluded that neither ketamine nor S-(+)-ketamine should be used in patients who suffer, e.g., from arterial hypertension and coronary artery disease.
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Generalized muscle weakness in critically ill patients can result in prolonged periods of artificial ventilation and longer stays in the intensive care unit. Both neuropathic (critical illness polyneuropathy) and myopathic (critical illness myopathy) abnormalities seem to play an important role for this prolonged weakness. ⋯ An efficient diagnostic plan is necessary for the exclusion of other curable causes of prolonged muscle weakness even in the presence of polyneuromyopathic changes. Psychological support of the patient and prophylaxis of secondary complications of prolonged immobilization are crucial when specific therapy is not possible.
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The phencyclidine derivative ketamine is a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist with the thalamo-neocortical projection system as the primary site of action. Racemic ketamine consists of the enantiomers S(+)-ketamine and R(-)-ketamine. Racemic ketamine has never been considered an adequate anaesthetic agent in neurosurgical patients since it produces regionally specific stimulation of cerebral metabolism (CMRO2) and increases cerebral blood flow (CBF) and intracranial pressure (ICP). ⋯ In contrast, studies in unanaesthetised humans showed increases in CBF after racemic ketamine (2-3 mg/kg). This observation is consistent with animal studies and suggests that the cerebrovascular effects of racemic ketamine are related to the pre-existing cerebrovascular tone induced by background anaesthetics. Studies in humans with and without intracranial pathology confirm the data from animal experiments. (ABSTRACT TRUNCATED)
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The present review summarises the main actions of racemic ketamine and ketamine enantiomers on central nervous system receptors. The primary CNS action of ketamine appears to be a non-competitive block of N-methyl-D-aspartate receptors. Although numerous other receptors (e.g., GABA, nicotinic acetylcholine, opiate, voltage-operated channels) have been reported to interact with ketamine, their role in inducing dissociative anaesthesia is still under discussion. ⋯ Interestingly, in contrast to many other anaesthetics, middle-latency AEP were not altered by racemic and S-(+)-ketamine. This observation may indicate insufficient suppression of auditory stimulus processing during ketamine anaesthesia. Motor evoked responses to transcranial electrical or magnetic stimulation in humans are not markedly suppressed by ketamine.
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This review focuses on the significance of S-(+)-ketamine as a neuroprotective agent. Evidence in the literature supporting or contradicting a neuroprotective or even therapeutic role of ketamine in global cerebral ischaemia is critically reviewed, and data from an ongoing study in a rat global cerebral ischaemia model (15 min ischaemia with S(+)-ketamine administered 15 min after reperfusion) are reported. ⋯ Only at higher ketamine dosages was protection found reliably, especially in models of complete forebrain ischaemia lasting over 10 min. In our own study, only after 90 mg/kg S(+)-ketamine was there significantly better preservation of cortical neurons than without treatment; 30 and 60 mg/kg did not produce this effect.