Anesthesiology
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Hypothermia is common in surgical patients and victims of major trauma; it also results from environmental exposure and drug abuse. In most cases, hypothermia results largely from drug-induced inhibition of normal thermoregulatory control. Although opioids are given to a variety of patients, the thermoregulatory effects of opioids in humans remain unknown. Accordingly, the hypothesis that opioid administration impairs thermoregulatory control was tested. ⋯ The observed pattern of thermoregulatory impairment is similar to that produced by most general anesthetics: a slight increase in the sweating threshold and a substantial, linear decrease in the vasoconstriction and shivering thresholds.
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Systemic vascular resistance (the ratio of mean aortic pressure [AP] and mean aortic blood flow [AQ]) does not completely describe left ventricular (LV) afterload because of the phasic nature of pressure and blood flow. Aortic input impedance (Zin) is an established experimental description of LV afterload that incorporates the frequency-dependent characteristics and viscoelastic properties of the arterial system. Zin is most often interpreted through an analytical model known as the three-element Windkessel. This investigation examined the effects of isoflurane, halothane, and sodium nitroprusside (SNP) on Zin. Changes in Zin were quantified using three variables derived from the Windkessel: characteristic aortic impedance (Zc), total arterial compliance (C), and total arterial resistance (R). ⋯ The major difference between the effects of isoflurane and halothane on LV afterload derived from the Windkessel model of Zin was related to R, a property of arteriolar resistance vessels, and not to Zc or C, the mechanical characteristics of the aorta. No changes in arterial wave reflection patterns determined from Zin spectra occurred with isoflurane and halothane. These results indicate that isoflurane and halothane have no effect on frequency-dependent arterial properties.
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Measurement of motor evoked responses to transcranial stimulation (tc-MER) is a technique for intraoperative monitoring of motor pathways in the brain and spinal cord. However, clinical application of tc-MER monitoring is hampered because most anesthetic techniques severely depress the amplitude of motor evoked responses. Because paired electrical stimuli increase tc-MER responses in awake subjects, we examined their effects in anesthetized patients undergoing surgery. METHODS. Eleven patients whose neurologic condition was normal and who were undergoing spinal or aortic surgery were anesthetized with sufentanil-N20-ketamine. Partial neuromuscular blockade (single-twitch height 25% of baseline) was maintained with vecuronium. Single and paired electrical stimuli were delivered to the scalp, and compound action potentials were recorded from the tibialis anterior muscle. The amplitude and latency of the tc-MERs were measured as the interval between paired stimuli was varied between 0 (single stimulus) and 10 ms. All recordings were completed before spinal manipulation or aortic clamping. ⋯ Application of paired transcranial electrical stimuli increases amplitudes and reproducibility of tc-MERs during anesthetic-induced depression of the motor system. The effect may represent temporal summation of stimulation at cortical or spinal sites. The results of this study warrant further clinical evaluation of paired transcranial stimulation.
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Changes in basal temperature of > or = 1 degree C (e.g., fever-induced hyperthermia or anesthesia-related hypothermia) are a common occurrence in neurologically impaired patients. The current study tested the hypothesis that temperature changes as small as 1 degree C or 2 degrees C would significantly alter post-ischemic functional neurologic outcome and cerebral histopathology. The hypothesis was tested in a canine model of transient, complete cerebral ischemia. ⋯ Small, clinically relevant changes in temperature (1 degree C or 2 degrees C) resulted in significant alterations in both postischemic neurologic function and cerebral histopathology. Assuming that our results are transferable to humans, the results suggest that, in patients at imminent risk for ischemic neurologic injury, body temperature should be closely monitored. Further, the clinician should aggressively treat all episodes of hyperthermia until the patient is no longer at risk for ischemic neurologic injury.
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Jugular venous catheters and near-infrared spectroscopy can measure cerebral venous blood hemoglobin oxygen saturation (SvO2). We used computer simulation to characterize the relation between Sv02 and cerebral metabolic rate for oxygen (CMR02) during hypothermic cardiopulmonary bypass (CPB). ⋯ High Sv02 observed during hypothermic CPB may indicate impaired oxygen transfer from hemoglobin to brain, not "luxury perfusion." The relation between Sv02 and CMR02 depends dramatically on the temperature of the patient. Sv02 per se may not be reliable index of normal CMR02 during hypothermic CPB.