Der Anaesthesist
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Clinical Trial
[Axillary blockade of the brachial plexus. A prospective study of blockade success using electric nerve stimulation].
Axillary block is a common anesthetic technique for operations on the hand and forearm. In our hospital, with many trainees in anaesthesia, only 250-300 axillary blocks per year are performed by about 30 colleagues. This implies a small number of blocks for each anaesthetist. ⋯ Prior to injection of the local anaesthetic, the current for nerve stimulation should be reduced to < 0.5 mA. The time between the end of injection and the beginning of surgery should be no less than 30 min because complete sensory blockade can more often be achieved. The dose of mepivacaine should be no less than 6 mg/kg body weight.
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Posttraumatic cardiopulmonary resuscitation (CPR) is associated with a poor outcome. When evaluating the literature according to the Utstein method, there were only 2 survivors (0.18%) out of 1,135 CPR attempts after trauma (Table 1). Differences in the study populations and levels of prehospital trauma care led us to analyse the results of a physician-staffed prehospital trauma care system in Cologne. ⋯ Survival has to be regarded as an individual fate; the overall results are discouraging. Even though this study analyses the largest population of posttraumatic CPR ever published, prognostic factors could not be identified due to the few survivors. Nevertheless, the result does not justify general omission of CPR after trauma as: (1) prognostic factors for survival have not been identified thus far; and (2) no significant additional costs arise from posttraumatic CPR.
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Clinical Trial
[Topographic electroencephalometry following anesthesia induction with ketamine-midazolam].
The neurophysiological action of ketamine has attracted increasing interest in recent years, with special interest in receptor action and in neurophysiological differences between and psychomimetic side effects of the two enantiomorphs. Most of the neurophysiological examinations published deal with ketamine as a single anaesthetic agent, although it has been suggested to that psychomimetic side-effects and haemodynamic deterioration could be avoided by combining ketamine with a sedative drug. The primary aim of our study was to examine the combined ketamine-midazolam action on cerebral activity; secondly, we planned to look at these interactions topographically at different points of the cortex to evaluate topographical differences in the combination's action; thirdly, the cerebral and haemodynamic reactions to anaesthesiological stimuli (intubation, gastric tube) were evaluated and compared. ⋯ Thus, the action of combined ketamine and midazolam on cerebral function is not an additive, but an interactive process. Despite a relatively high induction dosage, haemodynamic changes during intubation occurred and were accompanied by changes in cerebral activity. This can be regarded as incomplete cerebral suppression even by these induction dosages.
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Review Randomized Controlled Trial Clinical Trial
[Medical therapy for coronary heart disease. Perioperative relevance].
The aim of our review is to summarize relevant data on the perioperative use of anti-ischaemic drugs in patients at risk for or with proven coronary heart disease. ⋯ Beta-blockers, calcium channel blockers, nitrates, and possibly alpha 2-agonists lead to reduced rates of PMI and other cardiac complications in risk patients. Current anti-anginal medications, with the exception of anti-platelet agents, should be maintained to the day of surgery and continued as soon as possible thereafter. All of these drugs except anti-platelet agents may also be used intra-operatively, however, possible interactions with anaesthetic agents should be carefully considered.
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Randomized Controlled Trial Comparative Study Clinical Trial
[Ketamine racemate versus S-(+)-ketamine with or without antagonism with physostigmine. A quantitative EEG study on volunteers].
The potency of S-(+)-ketamine is approximately double that of the racemic ketamine. This study was carried out to investigate the recovery of cerebral electrical function after a bolus of 1.3 mg/kg ketamine or 0.65 mg/kg S-(+)-ketamine and subsequent continuous application of 4 mg/kg h ketamine per h or 2 mg/kg S-(+)-ketamine, per h for 15 min. Furthermore, the centrally acting, cholinergic agonist physostigmine has been reported to antagonize ketamine and to shorten the recovery period. ⋯ The spectral edge frequency did not differ between measurement points, and is therefore not suitable for assessment of the depth of anaesthesia reached with ketamine/S-(+)-ketamine. The dose of physostigmine tested was probably too low to produce antagonism of S-(+)-ketamine. An increased dosage of physostigmine has yet to be studied, but is likely to cause a higher rate of side effects, such as nausea, vomiting and bradycardia, and possibly even tonic-clonic seizures.