Anesthesia and analgesia
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Anesthesia and analgesia · Jul 1998
Tramadol reduces the sweating, vasoconstriction, and shivering thresholds.
The analgesic tramadol inhibits the neuronal reuptake of norepinephrine and 5-hydroxytryptamine, facilitates 5-hydroxytryptamine release, and activates mu-opioid receptors. Each of these actions is likely to influence thermoregulatory control. We therefore tested the hypothesis that tramadol inhibits thermoregulatory control. Eight volunteers were evaluated on four study days, on which they received no drugs, tramadol 125 mg, tramadol 250 mg, and tramadol 250 mg with naloxone, respectively. Skin and core temperatures were gradually increased until sweating was observed and then decreased until vasoconstriction and shivering were detected. The core temperature triggering each response defined its threshold. Tramadol decreased the sweating threshold by -1.03 +/- 0.67 degrees C microgram-1.mL (r2 = 0.90 +/- 0.12). Tramadol also decreased the vasoconstriction threshold by -3.0 +/- 4.0 degrees C microgram-1.mL (r2 = 0.94 +/- 0.98) and the shivering threshold by -4.2 +/- 4.0 degrees C microgram-1.mL(r2 = 0.98 +/- 0.98). The sweating to vasoconstriction interthreshold range nearly doubled from 0.3 +/- 0.4 degree C to 0.7 +/- 0.6 degree C during the administration of large-dose tramadol (P = 0.04). The addition of naloxone only partially reversed the thermoregulatory effects of tramadol. The thermoregulatory effects of tramadol thus most resemble those of midazolam, another drug that slightly decreases the thresholds triggering all three major autonomic thermoregulatory defenses. In this respect, both drugs reduce the "setpoint" rather than produce a generalized impairment of thermoregulatory control. Nonetheless, tramadol nearly doubled the interthreshold range at a concentration near 200 ng/mL. This indicates that tramadol slightly decreases the precision of thermoregulatory control in addition to reducing the setpoint. ⋯ The authors evaluated the effects of the analgesic tramadol on the three major thermoregulatory responses: sweating, vasoconstriction, and shivering. Tramadol had only slight thermoregulatory effects. Its use is thus unlikely to provoke hypothermia or to facilitate fever.
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Anesthesia and analgesia · Jul 1998
Clinical TrialOvernight hospitalization after radical prostatectomy: the impact of two clinical pathways on patient satisfaction, length of hospitalization, and morbidity.
Changes in health care have prompted efforts to reduce length of hospitalization while maintaining quality care. Therefore, we evaluated short-term outcomes after radical retropubic prostatectomy on 100 consecutive men undergoing surgery for clinically localized prostate cancer performed under epidural anesthesia followed by epidural morphine or combined with spinal anesthesia using bupivacaine and fentanyl (25 micrograms) and followed by i.m. methadone (10-20 mg). All patients received oral acetaminophen and ibuprofen beginning 4 h after surgery. Length of hospital stay, responses to written satisfaction survey, postoperative morbidity and readmission to the hospital were recorded. Using either pathway, 83% of the patients were discharged after one night in the hospital. The mean hospital stay was 1.34 +/- 1.10 and 1.28 +/- 1.0 days, respectively. Although three men were rehospitalized, it was not because of the early discharge. More than 95% of patients were satisfied with pain control, and patients discharged after one night were not more likely to be dissatisfied than patients hospitalized longer. ⋯ Both clinical pathways provide excellent anesthesia and analgesia and allow discharge 1 day after radical retropubic prostatectomy. Shortened hospital stay does not increase patient dissatisfaction or add to postoperative morbidity. Patients undergoing other pelvic and abdominal operations may also derive similar benefits using these pathways.
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Anesthesia and analgesia · Jul 1998
Comparative StudyThe hemodynamic effects of hypoxemia in anesthetized pigs: a comparison between right heart catheter and echocardiography.
During hypoxemia, hypoxic pulmonary vasoconstriction and tachycardia are often observed in association with increases in pulmonary artery pressure and cardiac output. Nevertheless, the hemodynamic consequences of hypoxemia have never been evaluated by echocardiography and simultaneously compared with invasive hemodynamic variables. Fourteen open-chest, anesthetized piglets (weight 29-36 kg) were submitted to progressive hypoxemia and reoxygenation. Usual invasive hemodynamic variables were obtained from peripheral and central heart catheters. Direct epicardial echocardiography was used to measure right and left ventricular areas on a short-axis view at mid-papillary level. The mean pulmonary artery pressure (MPAP) increased with pulmonary vascular resistance in a dose-related manner as the fraction of inspired oxygen (FIO2) declined from 0.5 to 0.12. The MPAP correlated with right ventricular end-diastolic area (RVEDA) only at FIO2 0.08. There was a 49% reduction in left ventricular end systolic wall stress (LVESWS) between FIO2 0.5 and 0.08. Left ventricular ejection fraction area (LVEFA) increased by 33% above baseline and correlated with the decrease in LVESWS. No correlation was observed between left ventricular end-diastolic area and pulmonary artery occlusion pressure or left atrial pressure and between cardiac output and LVEFA. Systemic vascular resistance underestimates the magnitude of changes in LVESWS but overestimates the afterload compared with LVESWS. This study demonstrates that, for the lowest FIO2 (0.08), changes in MPAP correlated with changes in RVEDA but not in pulmonary vascular resistance. Moreover, LVESWS decreases significantly in a dose-related manner under progressive hypoxemia and normalizes immediately after reoxygenation. This study also shows that, under hypoxemic conditions, echocardiography enhances understanding of hemodynamic changes compared with right heart catheterization alone. ⋯ Acute hypoxemia in pigs is responsible for pulmonary vasoconstriction-induced pulmonary hypertension (which is restricted by the right ventricular failure), as well as a PaO2-dependent decrease in left ventricular afterload. These changes are better displayed by echocardiography than by right heart catheter.
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Anesthesia and analgesia · Jul 1998
Clinical TrialLateral approach to the sciatic nerve in the popliteal fossa.
We describe a modification of the sciatic nerve (SN) block in the popliteal fossa through the lateral approach. After a brief anatomic study using previously reported landmarks, we propose a new needle orientation associated with a double injection technique after identification of the tibial and the common peroneal nerve. Thirty-four patients undergoing ankle or foot surgery were enrolled in this study. With patients in the supine position, the upper edge of the patella and the groove between the posterior border of the vastus lateralis and the anterior border of the tendon of the biceps femoris were identified. The needle was directed posteriorly with a 20-30 degrees angle relative to the horizontal plane and slightly caudal. Both nerves were individually located with a nerve stimulator and blocked with a mixture of lidocaine-bupivacaine and clonidine. In all but one case, the two nerves were easily located, and no vascular puncture was evident. Effective analgesia was obtained for a minimum of 15 h (first analgesic demand). We conclude that this technique, with a modified direction of the needle and a double stimulation, provides a very high rate of success for SN blockade in the popliteal fossa. ⋯ We describe a new lateral approach to the sciatic nerve in the popliteal fossa. The needle was directed caudad and posteriorly while seeking with a nerve stimulator for the tibial and the peroneal nerves, which were blocked separately. This technique was very successful.