Anesthesia and analgesia
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Anesthesia and analgesia · Mar 1999
The anesthetic and physiologic effects of an intravenous administration of a halothane lipid emulsion (5% vol/vol)
The i.v. administration of < or = 9 mL of nonvaporized liquid halothane causes significant pulmonary damage, cardiovascular decompensation, and death. To determine whether liquid halothane mixed in a lipid emulsion would alter these toxic effects, six swine were evaluated in a randomized cross-over study. The pulmonary, analgesic, hemodynamic, and histopathologic effects of liquid halothane (25 mL) mixed with a liquid carrier (475 mL, Liposyn III 20%) and administered by constant infusion were compared with halothane administered by a calibrated vaporizer. Three swine received the halothane lipid emulsion (HLE), followed by inhaled halothane. Three additional swine received inhaled halothane, followed by the HLE. There were no changes in pulmonary compliance or arterial blood gases during or after the administration of equivalent volumes of halothane (13.75 mL) either by infusion of HLE or by inhalation of halothane. The end-tidal halothane concentration for the minimum alveolar anesthetic concentration was 0.79% +/- 0.08% during HLE administration and 1.13% +/- 0.12% for inhaled halothane (P < 0.001). Hemodynamic variables and blood halothane levels by gas chromatography were measured at end-tidal concentrations of 0.6%, 1.2%, and 1.8%. Blood halothane levels (mg/mL) were significantly higher (P < 0.05) after the administration of HLE at end-tidal halothane concentrations of 1.2% (0.49 +/- 0.19 vs 0.82 +/- 0.18) and 1.8% (0.79 +/- 0.17 vs 1.29 +/- 0.34). When compared at equivalent blood levels, HLE caused fewer changes in the left ventricular end-diastolic pressure, mean arterial pressure, and dP/dt than inhaled halothane. There was no evidence of pulmonary histopathologic damage 4-8 h after the infusion of 500-700 mL of HLE. This novel method of delivery of a volatile anesthetic seems to lack the toxicity of direct i.v. administration of liquid halothane. It may be a useful alternative to traditional administration via a vaporizer. ⋯ Halothane causes pulmonary dysfunction and death when given i.v. in liquid form. Six swine received a halothane lipid emulsion i.v. to evaluate the anesthetic and physiologic effects. No pulmonary toxicity or deaths were associated with the halothane lipid emulsion. The anesthetic profile was similar to delivery of halothane via a vaporizer.
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Anesthesia and analgesia · Mar 1999
The safety and efficacy of intrathecal opioid analgesia for acute postoperative pain: seven years' experience with 5969 surgical patients at Indiana University Hospital.
To assess the efficacy of the analgesic technique and the incidence of complications, we prospectively evaluated patients who received intrathecal opioid analgesia (ITOA) to manage postsurgical pain. Daily quality assurance data were collected on the first postoperative day and tabulated for 5969 adult patients who had received ITOA for major urologic, orthopedic, general/ vascular, thoracic, and nonobstetrical gynecologic surgery. A scale of 1-10 was used to quantify each patient's satisfaction with analgesia. The incidence of side effects, complications, and naloxone usage was also recorded and tabulated. The mean satisfaction score using a 10-point numeric rating scale was 8.51, with a score of 1 connoting "complete dissatisfaction" and 10 connoting "complete satisfaction." Side effects were minor and easily managed. Pruritus was the most common (37%). Respiratory depression was the least common (3%), easily detected by nursing observation, never life-threatening, and always responsive to treatment with naloxone. There were no deaths, nerve injuries, central nervous system infections, or naloxone-related complications. Postdural puncture headaches were rare (0.54%), as was the need for epidural blood patch (0.37%). ⋯ Over a 7-yr period, intrathecal opioid analgesia was used to control acute postoperative pain on nearly 6000 patients, resulting in a high degree of patient satisfaction and a low incidence of side effects and complications.
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Anesthesia and analgesia · Mar 1999
The effects of general anesthetics on excitatory and inhibitory synaptic transmission in area CA1 of the rat hippocampus in vitro.
It is unclear whether general anesthetics induce enhancement of neural inhibition and/or attenuation of neural excitation. We studied the effects of pentobarbital (5 x 10(-4) mol/L), propofol (5 x 10(-4) mol/L), ketamine (10(-3) mol/L), halothane (1.5 vol%), and isoflurane (2.0 vol%) on both excitatory and inhibitory synaptic transmission in rat hippocampal slices. Excitatory or inhibitory synaptic pathways were isolated using pharmacological antagonists. Extracellular microelectrodes were used to record electrically evoked CA1 neural population spikes (PSs). In the presence of the gamma-aminobutyric acid type A (GABA(A)) receptor antagonist (bicuculline), the inhibitory actions of pentobarbital and propofol were completely antagonized, whereas those of ketamine, halothane, and isoflurane were only partially blocked. To induce the N-methyl-D-aspartate (NMDA) receptor-mediated PS (NMDA PS), the non-NMDA and GABA(A) receptors were blocked in the absence of Mg2+. Ketamine, halothane, and isoflurane decreased the NMDA PS, and pentobarbital and propofol had no effect on the NMDA PS. The non-NMDA receptor-mediated PS (non-NMDA PS) was examined using the antagonists for the NMDA and GABA(A) receptors. Volatile, but not i.v., anesthetics reduced the non-NMDA PS. These findings indicate that pentobarbital and propofol produce inhibitory actions due to enhancement in the GABA(A) receptor; that ketamine reduces NMDA receptor-mediated responses and enhances GABA(A) receptor-mediated responses; and that halothane and isoflurane modulate GABA(A), NMDA, and non-NMDA receptor-mediated synaptic transmission. ⋯ Volatile anesthetics modulate both excitatory and inhibitory synaptic transmission of in vitro rat hippocampal pathways, whereas i.v. anesthetics produce more specific actions on inhibitory synaptic events. These results provide further support the idea that general anesthetics produce drug-specific and distinctive effects on different pathways in the central nervous system.