Anesthesia and analgesia
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Anesthesia and analgesia · Oct 1991
Randomized Controlled Trial Clinical TrialEpidural sufentanil for postoperative analgesia: dose-response in patients recovering from major gynecologic surgery.
To determine the lowest effective dose of epidural sufentanil given for analgesia, 41 patients undergoing elective abdominal gynecologic surgery during continuous epidural anesthesia (lidocaine 2%) were randomly assigned to one of four postoperative treatment groups. Patients received an epidural bolus of either 25 (group A), 40 (group B), 55 (group C), or 70 micrograms (group D) sufentanil in 10 mL of saline. They were evaluated for the next 8 h using a 10-cm visual analogue scale. ⋯ There were no differences among groups with regard to mean respiratory rate, level of sedation, 24-h narcotic requirements, or incidence of nausea, vomiting, and pruritus (P = NS). A single patient in group D suffered profound respiratory depression within seconds of administration. We conclude that, in patients recovering from lower abdominal surgery, a single 40-55-micrograms epidural bolus of sufentanil provides 3-3.5 h of effective analgesia, and that larger doses are not warranted.
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Anesthesia and analgesia · Oct 1991
Low concentrations of isoflurane abolish motor evoked responses to transcranial electrical stimulation during nitrous oxide/opioid anesthesia in humans.
To study the feasibility of noninvasive monitoring of motor pathways in anesthetized patients, we evaluated the effect of isoflurane on motor evoked responses to constant-voltage transcranial electrical stimulation (tce-MERs). Reproducible tce-MERs were recordable from the tibialis anterior muscle during nitrous oxide/opioid anesthesia in 11 patients. Before the introduction of isoflurane, tce-MER onset latency was 30.8 +/- 1.9 ms, and amplitude ranged from 19 microV to 2.6 mV (median, 209 microV). ⋯ The tce-MERs were completely obliterated in all subjects at end-tidal isoflurane concentrations between 0.2% and 0.6% (median, 0.24%). After discontinuation of isoflurane, the tce-MER returned in all patients. The authors conclude that, during nitrous oxide/opioid anesthesia, with the stimulus and recording variables used, isoflurane even at very low concentrations precludes recording of tce-MERs.
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Anesthesia and analgesia · Oct 1991
Treatment of acute systemic toxicity after the rapid intravenous injection of ropivacaine and bupivacaine in the conscious dog.
Two groups of six beagle dogs received rapid intravenous (IV) injections of ropivacaine or bupivacaine on two occasions in a blinded random fashion. Initially, a dose sufficient to cause convulsions (CD) was given followed by twice the CD (2 x CD), which was administered 48 h later. The CD of bupivacaine (4.3 mg/kg) and ropivacaine (4.9 mg/kg) caused significant (P less than 0.05) increases in heart rate and mean arterial blood pressure. ⋯ Another dog had two 1-s bursts of premature ventricular contractions requiring no treatment. The rapid treatment of convulsions and cardiovascular toxicity resulted in a decreased number of deaths in both groups when compared with dogs from a previously published study in which no therapy was instituted. Thus, early aggressive treatment of central nervous system and cardiovascular system toxicity is capable of reducing the incidence of mortality associated with the rapid intravenous administration of excessive doses of local anesthetics.
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Anesthesia and analgesia · Oct 1991
Adverse interaction between bupivacaine and halothane on ventricular contractile force and intraventricular conduction in the dog.
Regional anesthesia with bupivacaine in pediatric patients is often accompanied by light levels of halothane general anesthesia. To determine the potential cardiotoxicity of these two drugs when used together, we defined the interaction between moderate plasma bupivacaine concentrations (1270-1760 ng/mL) and halothane (end-tidal concentrations, 0.5%-1.0%) on ventricular contractility and conduction in 22 closed-chest dogs anesthetized with chloralose. ⋯ In other dogs given halothane but in which bupivacaine levels were held constant (1400 ng/mL), VCT remained constant and VERP lengthened slightly, whereas dP/dtmax decreased. We conclude that the combination of bupivacaine and halothane can cause adverse effects on ventricular contractility and intraventricular conduction.