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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ANAESTHETICS, ENDOCRINE SYSTEM, AND STRESS: The effects of anaesthetics on the nervous system are invariably associated with endocrine reactions, which are of great importance for the general characterization of anaesthetics or anaesthetic regimens. In this context, the endocrine stress response is mainly represented by adrenaline (A), noradrenaline (NA), antidiuretic hormone/vasopressin (ADH), adrenocorticotropic hormone (ACTH), and cortisol. PHARMACOLOGICAL PROFILE AND ANAESTHETIC ACTION OF KETAMINE: The pharmacological profile of ketamine is characterized by the term "dissociative anaesthesia." At the present time, the anaesthetic action of ketamine cannot be explained by a single mechanism. ⋯ The combination of S-(+)-ketamine and midazolam has weaker sympathomimetic and general endocrine-stimulating properties, and can be used for analgosedation in patients with cardiovascular instability and exogenous catecholamine requirements. In combination with propofol, the sympathomimetic and general endocrine-stimulating effects of S-(+)-ketamine are less pronounced because of contrasting properties of both drugs. This combination might be useful in patients with endocrine deficits and for analgosedation, when rapid recovery is necessary and negative circulatory effects should be avoided.
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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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A key question in cellular neuroprotection is how pharmacologic agents may protect neurons when applied after injury in clinically relevant concentrations. Of special importance is the N-methyl-D-aspartate (NMDA) antagonist ketamine, which offers the potential for regulation of intracellular calcium levels and pathophysiological NO induction by blocking excessive NMDA-receptor stimulation. This may reduce progressive neuronal degeneration and cell death. ⋯ S(+)-ketamine demonstrated a unique neuroregenerative potential that was associated with greater re-outgrowth of axonal neurites after mechanical injury and increased expression of growth-associated proteins after glutamate damage. S(+)-ketamine has a two- to four-fold higher affinity for the phencyclidine receptor of the NMDA receptor complex than ketamine racemate, and it is conceivable that the induction of a differentiated pattern of genes induces cellular growth activities via ketamine-mediated NMDA-receptor activation or blockade. However, further investigations elucidating ketamine's effects in animals and humans have to be performed before final decisions regarding a potential application of ketamine as a neuroprotective agent in the clinical setting can be made.