Anesthesia and analgesia
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Anesthesia and analgesia · Apr 1999
Randomized Controlled Trial Clinical TrialOptimization of the dose of intrathecal morphine in total hip surgery: a dose-finding study.
We designed this study to determine the optimal intrathecal dose of morphine in total hip surgery. The optimal intrathecal dose was defined as that providing effective analgesia and minimal side effects 24 h after total hip surgery. Patients (n = 143) scheduled for total hip surgery were randomized to four double-blinded groups with a standardized bupivacaine dose but different doses of intrathecal morphine (Group I = 0.025 mg, Group II = 0.05 mg, Group III = 0.1 mg, and Group IV = 0.2 mg). Pain scores, i.v. morphine intake (patient-controlled analgesia), and morphine-related side effects (respiratory depression, postoperative nausea and vomiting, itching, urinary retention) were recorded for 24 h after surgery. Excellent postoperative pain relief was present in all groups. The highest pain scores were found in Group I. The mean use of systemic morphine administered by patient-controlled analgesia infusion pump was 23.7, 17.8, 10.9, and 9.9 mg in Groups I-IV, respectively (P < 0.01 for Groups III and IV versus Group I). We conclude that 0.1 mg of intrathecal morphine is the optimal dose for pain relief after hip surgery with minimal side effects. ⋯ Earlier studies showed excellent postoperative pain relief after intrathecal morphine. However, the severity of side effects resulted in decreased enthusiasm for this anesthesia technique. In the present study, we show that an intrathecal dose of 0.1 mg of morphine can be used safely in total hip surgery with excellent postoperative pain relief.
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Anesthesia and analgesia · Apr 1999
Randomized Controlled Trial Comparative Study Clinical TrialLess core hypothermia when anesthesia is induced with inhaled sevoflurane than with intravenous propofol.
Hypothermia after the induction of anesthesia results initially from core-to-peripheral redistribution of body heat. Sevoflurane and propofol both inhibit central thermoregulatory control, thus causing vasodilation. Propofol differs from sevoflurane in producing substantial peripheral vasodilation. This vasodilation is likely to facilitate core-to-peripheral redistribution of heat. Once heat is dissipated from the core, it cannot be recovered. We therefore tested the hypothesis that the induction of anesthesia with i.v. propofol causes more core hypothermia than induction with inhaled sevoflurane. We studied patients undergoing minor oral surgery randomly assigned to anesthetic induction with either 2.5 mg/kg propofol (n = 10) or inhalation of 5% sevoflurane (n = 10). Anesthesia in both groups was subsequently maintained with sevoflurane and 60% nitrous oxide in oxygen. Calf minus toe skin temperature gradients <0 degrees C were considered indicative of significant vasodilation. Ambient temperature and end-tidal concentrations of maintenance sevoflurane were comparable in each group. Patients in both groups were vasodilated throughout most of the surgery. Nonetheless, core temperatures in patients who received propofol were significantly lower than those in patients who received inhaled sevoflurane. These data support our hypothesis that even a brief period of vasodilation causes substantial redistribution hypothermia that persists throughout surgery. ⋯ Core temperatures in patients who received i.v. propofol were consistently lower than those in patients who received inhaled sevoflurane, although anesthesia was subsequently maintained with sevoflurane in nitrous oxide in both groups. This suggests that even a brief period of propofol-induced vasodilation during anesthetic induction causes substantial redistribution hypothermia that persists throughout surgery.
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Anesthesia and analgesia · Apr 1999
Isoflurane and sodium nitroprusside reduce the depressant effects of protamine sulfate on isolated ischemic rat hearts.
The administration of protamine sulfate (protamine) to reverse the action of heparin is associated with adverse reactions. We studied the effects of protamine and isoflurane on isolated, perfused rat hearts previously subjected to cardioplegic ischemia. Hearts were perfused with oxygenated Krebs-Henseleit (KH) solution for 30 min, then subjected to cardioplegic ischemia for 30 min (KCl 16 mEq/L at 31 degrees C) and 5 min reperfusion. Drug exposure lasted 15 min, and the recovery period was 60 min. Test groups were control, protamine (10 microg/mL), isoflurane (1.5%), protamine +/- isoflurane, sodium nitroprusside (SNP) (2.5 ng/mL), and SNP +/- protamine. Left ventricular developed pressure (LVP), coronary flow, and myocardial oxygen consumption were depressed by protamine to 30% +/- 4%, 47% +/- 4%, and 39% +/- 4% of baseline (P < 0.001 versus control), respectively. Isoflurane and SNP afforded partial protection from the effects of protamine: LVP was 57% +/- 5% and 51% +/- 3% of baseline, respectively (P < 0.05 versus protamine alone and control); coronary flow was 70% +/- 6% and 97% +/- 12% of baseline, respectively (P < 0.05 versus protamine alone; P < 0.05 for isoflurane versus control); and O2 consumption was 69% +/- 6% and 88% +/- 15% of baseline, respectively (P < 0.05 versus protamine; P < 0.05 for isoflurane versus control). In this model, protamine-induced myocardial depression and coronary vasoconstriction were less pronounced in the presence of either isoflurane or SNP. ⋯ We examined the interactions of isoflurane, sodium nitroprusside, and protamine in a rat heart model and found that both isoflurane and sodium nitroprusside partially protect the heart from the depressant effects of protamine. This finding is significant, as these drugs are often used in heart surgery.