Der Anaesthesist
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The efferent sympathetic nervous system is organized into subsystems that innervate and regulate via separate peripheral sympathic pathways the different autonomic target organs. This review discusses mechanisms through which this efferent system may be causally involved in the generation of pain. Clinical pain syndromes in which this may be the case are "complex regional pain syndromes" (CRPS) type I (previously reflex sympathetic dystrophy) and type II (recently causalgia). ⋯ From this follows that the pathophysiologal processes operating in CRPS may occur at four levels of integration that interact with each other: effector organ, peripheral afferent and sympathetic neurone, spinal cord, supraspinal centres. Recent experimental investigations on rats show that the sympathetic nervous system is possibly also causally involved in the generation of inflammation and inflammatory pain. The mechanisms by which this occurs are different from those operating in SMP during CRPS.
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General cardiovascular properties of ketamine: "In vitro", ketamine has moderate negative inotropic effects. "In vivo", a significant central sympathomimetic action with consecutive hemodynamic effects is dominant. The sympathomimetic potency of ketamine is one of the most significant pharmacological features of the substance with direct clinical implications. Monoanaesthesia with S-(+)-ketamine: After application of racemic ketamine or S(+)-ketamine as well, identic and significant increases in plasma catecholamines, arterial pressure and heart rate are observed. This outstanding sympathomimetic action is beneficial in induction of patients with shock or asthmatic state. TIVA and analgosedation with S-(+)-ketamine and midazolam: The sympathomimetic effect of S(+)-ketamine, and racemic ketamine as well, is mitigated by midazolam. Nevertheless, significant increases in heart rate and arteriel pressure might be observed. Clinical use of the combination is common in short procedures like reposition maneuvers. Of greater importance is the use for analgosedation in patients with cardiovascular instability, particularly in patients with exogenous catecholamine demand. TIVA and analgosedation with S-(+)-ketamine and propofol: When S(+)-ketamine is combined with propofol, the sympatholytic effects of propofol are counteracted by S(+)-ketamine, and stable hemodynamic conditions are presented. This combination seems useful for TIVA in patients with hypotonic dysregulation or endocrine deficits like hypothyreosis and adrenal insufficiency. Furthermore, analgosedation with S(+)-ketamine and propofol is advantageous, when rapid recovery is necessary and negative circulatory effects should be avoided. ⋯ Sympathoadrenergic and hemodynamic effects of S(+)-ketamine and racemic ketamine are generally identical. The distinctest action is observed, when S(+)-ketamine is used as a monoanaesthetic. In combination with midazolam, a significant reduction is achieved. In combination with propofol, the sympatholytic effects of this hypnotic agent are compensated by S(+)-ketamine. With respect to sympathoadrenergic and hemodynamic reactions, the clinical position of S(+)-ketamine is unchanged. Nevertheless, a significant clinical progress can be expected due to improved recovery and reduced substance load, when racemic ketamine is replaced by S(+)-ketamine.
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The pharmacological profile of ketamine: Until recently, clinically available ketamine was a racemic mixture containing equal amounts of two enantiomers, (S)- and (R)-ketamine. The pharmacological profile of racemic ketamine is characterized by the so called dissociative anesthetic state and profound sympathomimetic properties. Among the different sites of action, N-methyl-D-aspartate (NMDA)-receptor antagonism is considered to be the most important neuropharmacological mechanism of ketamine. ⋯ In combination with midazolam and propofol, excellent control of analgosedation was found, making both combinations suitable for situations in which repeated neurological assessment of patients is necessary. In emergency and disaster medicine, (S)-ketamine is of outstanding importance because of its minimal logistic requirements, the chance for intramuscular administration and the broad range of use for analgesia, anaesthesia and analgosedation as well. Further perspectives of (S)-ketamine may be the treatment of chronic pain and the assumed neuroprotective action of the substance.
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The perioperative morbidity and mortality is mainly influenced by the type and duration of surgery as well as the patient's preoperative state of health. Anesthesia per se, however, may also result in severe perioperative (patho) physiological changes, which may be both desired (e.g. analgesia, vasodilation in vascular surgery) or detrimental (e.g. hypothermia, ventilatory depression) and which may differ depending on the anesthetic technique used (e.g. general anesthesia vs. regional anesthesia). Yet, all anaesthetic techniques have in common, that their effects are not limited to the duration of the surgical intervention, but may expand far into the postoperative period. ⋯ The fact that clear advantages for a single technique have not yet been demonstrated must not, however, result in anesthetic 'nihilism'. Rather there may be good reasons in the individual patient (e.g. lack of a recovery room), to prefer a certain anesthetic technique or drug over another, in order to lower the individual risk of anesthesia. Whether the use of a certain technique-e.g. spinal or epidural anesthesia-may contribute to a reduction of specific postoperative surgical complications (e.g. rate of reocclusion subsequent to peripheral vascular surgery) is presently under investigation.
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The extent of myocardial damage occurring during acute myocardial infarction is time dependent, and there is abundant evidence from most clinical trials that mortality reduction is greatest in patients treated early with thrombolytic agents, although beneficial effects have been shown with treatment initiated up to 12 h after onset of symptoms. All studies on prehospital thrombolysis have conclusively shown the practicability and safety of patient selection and administration of the thrombolytic agent. The accuracy of diagnosis in the prehospital setting was comparable to trials of in-hospital thrombolysis, e.g., in the Myocardial Infarction Triage and Intervention Project (MITI) 98% of the patients enrolled had subsequent evidence of acute myocardial infarction. ⋯ The results of randomized studies comparing the results of prehospital and in-hospital thrombolysis seem to justify the prehospital institution of thrombolytic therapy, especially in rural areas where transport times to the hospital are long and the expected time gain is largest. The choice of the thrombolytic agent seems to be of minor importance and should follow prehospital practicability (bolus injection) and costs. Aspirin should be given to all prehospital patients with suspected myocardial infarction regardless of thrombolytic therapy.