Anesthesiology
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Postoperative epidural bupivacaine-morphine therapy. Experience with 4,227 surgical cancer patients.
We prospectively studied surgical cancer patients who received epidural bupivacaine-morphine to determine perioperative morphine use, side effects, and complications. ⋯ Continuous epidural analgesia with 0.05-0.1% bupivacaine and 0.01% morphine is an effective method of postoperative analgesia with a low incidence of side effects, that can be safely administered on the surgical wards with no special monitoring equipment.
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Comparative Study
Echocardiographic and hemodynamic indexes of left ventricular preload in patients with normal and abnormal ventricular function.
Transesophageal echocardiography (TEE) is used to diagnose hypovolemia despite the lack of validation studies. The objective was to determine the effects of acute graded hypovolemia on TEE and conventional hemodynamic determinants of left ventricular (LV) preload in anesthetized patients with normal and abnormal LV function. ⋯ TEE and hemodynamic determinants of LV preload detected changes in LV function caused by acute blood loss. Acute blood loss caused directional changes in LV end-diastolic area, pulmonary artery occlusion pressure, and LV end-diastolic wall stress even in patients with LV wall motion abnormalities. Changes in LV end-diastolic wall stress, derived from both TEE and hemodynamic measurements corresponded to changes in cardiac output, stroke volume, and mixed venous oxygen saturation that occurred during acute blood loss.
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Previous studies have noted a high incidence of adverse outcomes in the postanesthesia care unit (PACU), but few have examined associated factors and patient outcomes. To determine the frequency of acute, unanticipated respiratory problems and to examine the associated patient, surgical, and anesthetic factors, we prospectively collected preoperative, intraoperative, and postoperative data on 24,157 consecutive PACU patients who received a general anesthetic during a 33-month period. ⋯ A CRE is relatively rare. Multiple patient and surgical factors and specific aspects of anesthetic management are associated with the occurrence of a CRE in the PACU.
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Results from previous studies on the effect of nitrous oxide (N2O) on the cerebral circulation are conflicting. Early reports claim N2O to have no effect whereas recent findings demonstrate a cerebral cortical vasodilatation during N2O inhalation, but the regional cerebral blood flow (CBF) in the subcortical structures is unknown. ⋯ Inhalation of 50% N2O increased global CBF mainly by augmenting flow in frontal brain structures. In contrast, changes in carbon dioxide without N2O affected CBF uniformly in the brain. The uneven change in distribution of the CBF when N2O was added during hypocapnia, the reduced carbon dioxide response, and the lack of effect of N2O on isolated human pial arteries suggest that N2O may increase metabolism in selected brain areas.
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Depression of myocardial contractility associated with the volatile anesthetics is well established clinically and experimentally. The molecular mechanisms underlying this effect, however, have not been completely characterized. Whereas the Ca2+ release channel of cardiac sarcoplasmic reticulum (SR) has been implicated as a potential target contributing to anesthetic-induced myocardial depression, the effect of the volatile anesthetics on this protein have not been characterized at the isolated, single-channel level. The authors sought to identify changes in channel gating and conductance resulting from exposure to halothane, enflurane, and isoflurane that would contribute to the associated negative inotropy, as well as to explain the observation that isoflurane causes less contractile depression than either halothane or enflurane. ⋯ Halothane and enflurane gate the Ca2+ release channel into the open state without altering the channel conductance. An increase in the duration of open events results from halothane and enflurane, but does not occur in the presence of isoflurane. Activation of the SR Ca2+ release channel would lead to loss of SR stores of Ca2+ into the cytoplasm, which is rapidly mobilized to the extracellular space. A net depletion of Ca2+ available for excitation-contraction coupling would result. The observation that isoflurane does not alter gating of this channel contributes to the understanding of the molecular mechanisms by which isoflurane depresses myocardial contractility less than halothane and enflurane.