Anesthesia and analgesia
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Anesthesia and analgesia · Mar 2004
Randomized Controlled Trial Comparative Study Clinical TrialCombined spinal-epidural anesthesia using epidural volume extension leads to faster motor recovery after elective cesarean delivery: a prospective, randomized, double-blind study.
Epidural volume extension (EVE) via a combined spinal-epidural (CSE) technique is the enhancement of a small-dose intrathecal block by epidural saline boluses. In this prospective, randomized, double-blind study, we compared the EVE technique with single-shot spinal anesthesia with respect to its sensory and motor block profile and hemodynamic stability. Sixty-two parturients (n = 31 in each group) undergoing elective cesarean deliveries were administered either spinal anesthesia with hyperbaric 0.5% bupivacaine 9 mg and fentanyl 10 microg or CSE comprising intrathecal hyperbaric 0.5% bupivacaine 5 mg with fentanyl 10 microg, followed by 0.9% saline 6.0 mL through the epidural catheter 5 min thereafter. In each group, the lowest systolic blood pressure (SBP), sensory block level to loss of pain from pinprick, and modified Bromage scores were recorded at 2.5-min intervals. The visual analog pain score (VAS), peak sensory block height, highest modified Bromage motor score, time for sensory regression to the tenth thoracic dermatome (T10), and motor block recovery were compared between groups. Both groups were comparable in demographic data, VAS scores, peak sensory block height, time for sensory regression to T10, and lowest SBP recorded. Patients in the EVE group demonstrated significantly faster motor recovery to modified Bromage 0 (73 +/- 33 min versus 136 +/- 32 min, P < 0.05). ⋯ When compared with conventional, single-shot spinal anesthesia, epidural volume extension of a small-dose spinal block provides satisfactory anesthesia for cesarean delivery with only 55% of the bupivacaine dose required and is associated with faster motor recovery of the lower limbs.
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Anesthesia and analgesia · Mar 2004
Randomized Controlled Trial Clinical TrialThe effects of different ventilatory settings on pulmonary and systemic inflammatory responses during major surgery.
Mechanical ventilation with high tidal volumes (V(T)) and zero or low positive end-expiratory pressure increased mediator release to inflammatory stimuli or acute lung injury. We studied whether mechanical ventilation modifies the inflammatory responses during major thoracic or abdominal surgery. Sixty-four patients undergoing elective thoracotomy (n = 34) or laparotomy (n = 30) were randomized to receive either mechanical ventilation with V(T) = 12 or 15 mL/kg ideal body weight, respectively, and zero end-expiratory pressure, or V(T) = 6 mL/kg ideal body weight with positive end-expiratory pressure of 10 cm H(2)O. In 62 patients who completed the study, arterial oxygenation was not different between groups. Tumor necrosis factor, interleukin (IL)-1, IL-6, IL-8, IL-10, and IL-12 were determined by cytometric bead array in plasma after 0, 1, 2, and 3 h and in tracheal aspirates after 3 h of mechanical ventilation. Data were log-transformed and analyzed using parametric or nonparametric tests, as indicated. All plasma mediators increased more during abdominal than during thoracic surgery, although the differences were small. However, neither time course nor concentrations of pulmonary or systemic mediators differed between the two ventilatory settings. Our data suggest that the ventilatory settings we studied do not affect inflammatory reactions during major surgery within 3 h. ⋯ In 62 patients undergoing elective major thoracic or abdominal surgery, mechanical ventilation with low tidal volumes and positive end-expiratory pressure or high tidal volumes and zero end-expiratory pressure did not result in different pulmonary or systemic levels of measured inflammatory markers.
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Anesthesia and analgesia · Mar 2004
Randomized Controlled Trial Clinical TrialThe influence of ambulation time on the incidence of transient neurologic symptoms after lidocaine spinal anesthesia.
The cause of transient neurologic symptoms (TNSs) after lidocaine spinal anesthesia remains unclear. It has been proposed that early ambulation after spinal anesthesia contributes to the development of TNSs. We evaluated the influence of ambulation time on the occurrence of TNSs after spinal anesthesia with 50 mg of 2% plain lidocaine for knee arthroscopy. One-hundred-twenty patients undergoing knee arthroscopy (ASA physical status 1-2) were randomized into 3 groups, i.e., early (Group E), 6-h (Group 6-h), or late ambulation (Group L) groups. In Group E, ambulation was allowed as early as possible after regression of spinal block (on average 229 +/- 21 min; range, 135-247 min). In Group 6-h, the patients remained in bed for approximately 6 h after the block and in Group L until the next morning. The patient groups were comparable with respect to demographic, anesthetic, and surgical variables. The overall incidence of TNSs was 16%. TNSs occurred in 3 patients of Group E (7.5%), in 11 patients of Group 6-h (28%), and in 5 patients of Group L (13%). No significant differences were detected between the patients with and without TNSs. Early ambulation was not found to be a risk factor for TNSs after spinal anesthesia with 50 mg of 2% lidocaine. ⋯ This study shows that early ambulation time does not increase the incidence of transient neurologic symptoms after spinal anesthesia with 50 mg of 2% lidocaine for elective knee arthroscopy.
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Anesthesia and analgesia · Mar 2004
Comparative StudyClinical evaluation of the effects of signal integrity and saturation on data availability and accuracy of Masimo SE and Nellcor N-395 oximeters in children.
Pulse oximetry manufacturers have introduced technologies that claim improved detection of hypoxemic events. Because improvements in signal processing and data rejection algorithms may differentially affect data reporting, we compared the data reporting and signal heuristic performance and agreement among the Nellcor N-395, Masimo SET, and GE Solar 8000 oximeters under a spectrum of conditions of signal integrity and arterial oxygen saturations. A blinded side-by-side comparison of technologies was performed in 27 patients, and data were analyzed for time of data availability, measures of agreement and signal heuristics, and warnings stratified by signal integrity and SpO(2). The Solar 8000 had less total data dropout than either of the new technologies. Masimo's LoSIQ (signal quality) heuristic rejected less data than Nellcor's MOT/PS (motion/pulse search) flag. When no signal heuristic was displayed, there was little difference in precision and bias between the two newer technologies; however, agreement between devices deteriorated in the presence of SIQ, MOT, or hypoxemia. Both newer devices flagged questionable data, but their use of different rejection algorithms resulted in different probabilities of presenting data. Therefore, with poor SIQ or during hypoxemia, the Nellcor N-395 and Masimo oximeters are not clinically equivalent to each other or to the older Solar 8000 oximeter. ⋯ We compared new pulse oximeters from Nellcor and Masimo and found that, with good signal conditions, both new devices performed similarly to older technology. Overall, Masimo reported less data as questionable than Nellcor. With poor signal conditions or during hypoxemia, the new devices are not clinically equivalent to each other or to the older technology.
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Anesthesia and analgesia · Mar 2004
Amplification by hyperoxia of coronary vasodilation induced by propofol.
We tested the hypothesis that in vitro coronary and myocardial effects of propofol (10-300 microM) should be significantly modified in an isolated and erythrocyte-perfused rabbit heart model in the absence (PaO(2) = 137 +/- 16 mm Hg, n = 12) or in the presence (PaO(2) = 541 +/- 138 mm Hg, n = 12) of hyperoxia. The induction of hyperoxia provoked a significant coronary vasoconstriction (-13% +/- 7%). Propofol induced increased coronary vasodilation in the presence of hyperoxia. Because high oxygen tension has been reported to induce a coronary vasoconstriction mediated by the closure of adenosine triphosphate-sensitive potassium channels, we studied the effects of propofol in 2 additional groups of hearts (n = 6 in each group) pretreated by glibenclamide (0.6 microM) and cromakalim (0.5 microM) in the absence and presence of hyperoxia, respectively. The pretreatment by glibenclamide induced a coronary vasoconstriction (-16% +/- 7%) which did not affect propofol coronary vasodilation. The pretreatment by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. Propofol induced a significant decrease in myocardial performance for a concentration >100 micro M both in the absence and presence of hyperoxia. We conclude that propofol coronary vasodilation is amplified in the presence of hyperoxia. This phenomenon is not explained by the previous coronary vasoconstriction induced by glibenclamide. However, the pretreatment of hearts by cromakalim abolished the amplification of propofol coronary vasodilation in the presence of hyperoxia. The myocardial effects of propofol were not affected by the presence of hyperoxia. ⋯ Propofol induced a coronary vasodilation that was amplified in the presence of hyperoxia. This phenomenon does not seem to be related to previous coronary vasoconstriction. The myocardial effects of propofol were not significantly modified in the presence of hyperoxia.