Journal of anesthesia
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The epidural administration of local anesthetics can provide anesthesia without the need for respiratory support or mechanical ventilation. Nevertheless, because of the additional effects of epidural anesthesia on motor function and sympathetic innervation, epidural anesthesia does affect lung function. These effects, i.e., a reduction in vital capacity (VC) and forced expiratory volume in 1 s (FEV(1.0)), are negligible under lumbar and low thoracic epidural anesthesia. ⋯ In chronic obstructive pulmonary disease (COPD) patients, the use of thoracic epidural anesthesia has raised concerns about respiratory insufficiency due to motor blockade, and the risk of bronchial constriction due to sympathetic blockade. However, even in patients with severe asthma, thoracic epidural anesthesia leads to a decrease of about 10% in VC and FEV(1.0) and no increase in bronchial reactivity. Overall, epidural administration of local anesthetics not only provides excellent anesthesia and analgesia but also improves postoperative outcome and reduces postoperative pulmonary complications compared with anesthesia and analgesia without epidural anesthesia.
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Journal of anesthesia · Jan 2006
Review Meta AnalysisThe benefits of adding epidural analgesia to general anesthesia: a metaanalysis.
The purpose of this metaanalysis was to determine the benefits of postoperative epidural analgesia in patients operated on under general anesthesia. By searching the American National Library of Medicine's Pubmed database from 1966 to July 10, 2004, 70 studies were identified. These included 5402 patients, of which 2660 had had epidural analgesia. ⋯ It also reduces the first 24-h morphine consumption, OR = -13.62 mg (95%CI = -22.70, -4.54, P = 0.003), and improves the forced vital capacity (FVC), OR = 0.23 l (95%CI = 0.09, 0.37, P = 0.001) at 24 h. A thoracic epidural containing a local anesthetic reduces the incidence of renal failure: OR = 0.34 (95%CI = 0.14, 0.81, P = 0.01). Epidural analgesia may thus offer many advantages over other modes of postoperative analgesia.
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Journal of anesthesia · Jan 2005
ReviewAnesthesia management for electroconvulsive therapy: hemodynamic and respiratory management.
Recent guidelines have stated that anesthesia for electroconvulsive therapy (ECT) should be administered by a specially trained anesthesiologist, and that anesthesiologists have overall responsibility, not only for anesthesia itself, but also for cardiopulmonary management and emergency care. Accordingly, anesthesiologists who administer anesthesia for ECT should have sufficient knowledge regarding the physiologically and pharmacologically unique effects of ECT. Electrical current during ECT stimulates the autonomic nervous system and provokes unique hemodynamic changes in systemic and cerebral circulation. ⋯ Reports of serious complications of this therapy are not frequent; however, patients with ischemic heart disease or cerebrovascular problems must be managed with special care to prevent myocardial infarction or neurological disorders. Safe physical management by anesthesiologists greatly contributes to the establishment of ECT under muscle relaxation. To maintain social confidence and to refine the therapy, anesthesiologists should play an essential role both in clinical activities and in laboratory research.
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Ischemic neuronal injury is characterized by early death mediated by excitotoxicity and by delayed death caused by apoptosis. Current evidence indicates that volatile agents, barbiturates, and propofol can protect neurons against ischemic injury caused by excitotoxicity. In the case of volatile agents and propofol, neuroprotection may be sustained if the ischemic insult is relatively mild; however, with moderate to severe insults, this neuronal protection is not sustained after a prolonged recovery period. ⋯ Cerebral ischemia is characterized by continued neuronal loss for a long time after the initial ischemic insult. Therefore, in investigations of cerebral ischemia, the duration of the recovery period should be taken into consideration in the analysis of the neuroprotective effects of anesthetic agents. A combination of different approaches that target specific stages of the evolution of ischemic injury may be required for sustained neuroprotection.