Der Anaesthesist
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In a recent German multicenter study, 25% of the patients who suffered a witnessed cardiac arrest outside the hospital were resuscitated successfully and were discharged from the hospital. Approximately 100,000 people suffer a fatal cardiac arrest in Germany annually, which is about ten times more than deaths resulting from motor vehicle accidents. New devices and techniques for cardiopulmonary resuscitation (CPR) have been developed in order to enhance the efficacy of chest compressions during CPR. ⋯ In summary, since the rediscovery of chest compressions more than 35 years ago, this intervention has not changed significantly. Objective data from laboratory and clinical studies such as systolic blood pressure, CPP, and the gold standard for the efficacy of CPR, long-term survival and neurological outcome, will determine if a new device or technique can replace standard-CPR. Despite the new developments, it is mandatory to perform standard CPR correctly with a chest compression rate of 80-100/min and a depth of 38-50 mm.
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Ketamine is a racemic mixture containing equal parts of S-(+)-ketamine and R-(-)-ketamine. Their potency relation is approximately 4:1. In early human studies S-(+)-ketamine was presumed to produce the desired anaesthetic effects and R-(-)-ketamine the undesired psychic emergence reactions. ⋯ With only one exception, the recovery phase was clearly shorter after S-(+)-ketamine compared to racemic ketamine irrespective of its application as a single bolus, a bolus followed by continuous infusion, or an intramuscular injection. However, the incidence of psychic emergence reactions was lower after S-(+)-ketamine in only a single study. In conclusion, S-(+)-ketamine should be always combined with a hypnotic or sedative drug in clinical anaesthesia.
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Among anaesthetic drugs, ketamine occupies a special position. biochemically, ketamine is a racemate consisting of equal shares of two optical enantiomers. Pharmacological investigations show differences between those enantiomers in both qualitative and quantitative properties. ⋯ The main problems associated with the ketamine racemate in clinical use are desirable psychological dysfunction and a prolonged period of arousal. There are grounds for the assumption that the use of S-(+)-ketamine will minimise those problems without reducing anaesthetic potency or restricting the advantages of ketamine anaesthesia.
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As the mechanism of action of ketamine, particularly its non-competitive antagonism at the N-methyl-D-aspartate receptor (NMDA), has become better understood, the use of the drug as a neuroprotective agent has received increasing interest. Although the potential prometabolic effects of ketamine might be counterproductive to neuroprotection, the increase in intracranial pressure it has repeatedly been reported to produce does not appear to be relevant clinically under certain conditions, e.g. in patients with normocapnia and a stable blood pressure. Also, the drug has been shown to be anticonvulsant in clinically applied doses rather than epileptogenic, as was previously assumed. ⋯ But as both in vitro and in vivo studies are inconclusive, the benefits of the drug are still controversial. In addition, the potential neurotoxicity attributed to extremely high ketamine doses is poorly understood. Consequently, well controlled animal experiments and studies in humans would be necessary to establish the role of ketamine and its more potent enantiomer S-(+)-ketamine in combination with other neuroprotective measures and to shed light on its true neuroprotective potential and its possible neuroregenerative effects.
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Although ketamine has been in clinical use for 3 decades, the neuropharmacological basis of its analgesic, anaesthetic, sympathomimetic, and psychotomimetic effects is still a subject of controversial discussion and intensive investigational efforts. In recent years, however, new experimental approaches to its effects on the cellular and molecular level and the availability of pure ketamine enantiomers contributed substantially to the understanding of its complex neuropharmacology. ⋯ In contrast to the uncertainty surrounding the potential role of opioid receptors, there is now considerable evidence that NMDA antagonism is a central mechanism that contributes to the amnesic, analgesic, anaesthetic, and psychotomimetic as well as the neuroprotective actions of ketamine. Moreover, the involvement of non-NMDA glutamate receptors, muscarinic and nicotinic cholinergic transmission, interactions with 5-HT receptors, and L-Type Ca2+ channels may account for some of its anaesthetic and neuroprotective properties.