Anesthesia and analgesia
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Anesthesia and analgesia · Nov 1998
Randomized Controlled Trial Clinical TrialThe cholecystokinin antagonist proglumide enhances the analgesic efficacy of morphine in humans with chronic benign pain.
The analgesic efficacy of morphine is sometimes only partial in patients with chronic benign pain. Among the possible factors contributing to this limitation are increased levels of cholecystokinin (CCK). We performed this prospective, placebo-controlled, double-blind, cross-over study to examine the effect of proglumide, a nonspecific CCK agonist, on analgesia in patients taking morphine on a chronic basis. Forty patients with intractable pain who were taking sustained-release morphine were recruited, and we obtained results from 36 of these patients. Median visual analog scale scores before the study were 8 and 7 after the addition of placebo for 2 wk (P = 0.16), and 6 after proglumide for 2 wk (P = 0.002). Mobility was unchanged by proglumide or placebo. Of the 36 patients, 13 elected to continue receiving proglumide after the study. We conclude that proglumide enhances the analgesia produced by morphine in some, but not all, patients with chronic benign pain. ⋯ The pain-killing effect of morphine is incomplete in some patients. Increasing doses may be needed to maintain the initial effect. The peptide cholecystokinin may be partially responsible for this. In this study, we demonstrated that the cholecystokinin antagonist proglumide increases the analgesic effect of morphine in some patients with chronic benign pain.
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Anesthesia and analgesia · Nov 1998
Randomized Controlled Trial Clinical TrialThe effects of propofol, isoflurane, and sevoflurane on oxygenation and shunt fraction during one-lung ventilation.
Propofol's effect on hypoxic pulmonary vasoconstriction during one-lung ventilation (OLV) has not been determined. Twenty patients who had long-term OLV for esophageal surgery were allocated randomly to one of two study groups; one in which isoflurane administration preceded propofol, and another in which sevoflurane administration preceded propofol. Arterial and mixed venous blood samples and hemodynamics were measured as follows: before OLV, during OLV, OLV at 4 cm of positive end-expiratory pressure (PEEP), OLV after conversion from volatile anesthetics to propofol, OLV at 4 cm of PEEP, and after OLV. After the application of 4 cm of PEEP during propofol anesthesia, PaO2 increased significantly in both groups. The shunt fraction (Qs/Qt) increased significantly after the initiation of OLV in both groups and decreased significantly after the conversion from volatile anesthetics to propofol in both groups. Propofol can be used safely during OLV because PaO2 increased after the application of 4 cm of PEEP during propofol anesthesia, and Qs/Qt decreased significantly after the conversion from inhaled anesthetics to propofol anesthesia. ⋯ During one-lung ventilation, the arterial partial pressure of oxygen values with propofol were greater than those with isoflurane and sevoflurane, and shunt fraction values with propofol were lower than those with both volatile anesthetics. Propofol improved oxygenation and shunt fraction during one-lung ventilation compared with volatile anesthetics.
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Anesthesia and analgesia · Nov 1998
Randomized Controlled Trial Clinical TrialCough during emergence from isoflurane anesthesia.
We evaluated the effects of smoking history and albuterol treatment on the amplitude and frequency of cough during emergence from anesthesia. Before induction of anesthesia, 68 patients were randomized to receive two puffs of a placebo or two puffs of albuterol via a metered dose inhaler. Anesthesia was then induced with thiopental, fentanyl, and succinylcholine. The patients' tracheas were intubated with an 8.0 mm-endotracheal tube, and isoflurane administration was initiated. At the end of surgery, isoflurane was discontinued, and the pressure in the endotracheal tube cuff was monitored via the pilot balloon while the end-tidal isoflurane concentration was recorded. Of the 68 patients, 52 coughed before responding to command, but the incidence did not differ between smokers and nonsmokers (33 of 43 vs 19 of 25), nor did it differ between albuterol-treated and untreated patients. There was no difference in the frequency or amplitude of coughs between smokers and nonsmokers, nor did albuterol affect either variable. The mean end-tidal concentration at which cough first occurred was 0.30%+/-0.02%, and only 5% of patients coughed at values >0.6%. We conclude that 1) cough is frequent during emergence; 2) smoking does not affect emergence cough; 3) albuterol treatment does not affect emergence cough; and 4) patients are unlikely to cough at end-tidal values of isoflurane >0.6%. ⋯ Most patients cough as they awaken from general anesthesia given via an endotracheal tube. In our study population, cough was frequent but generally did not occur until the end-tidal concentration of isoflurane was <0.6%. Smokers were no more likely to cough than nonsmokers, and the beta-adrenergic agonist albuterol did not prevent cough.
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Anesthesia and analgesia · Nov 1998
Clinical TrialRespiratory effects of desflurane anesthesia on spontaneous ventilation in infants and children.
Volatile anesthetics depress spontaneous ventilation in a dose-dependent manner with variations in effects among different drugs. The goal of this prospective study was to assess respiratory changes during spontaneous ventilation using desflurane/O2/N2O anesthesia in two groups of children. Both groups were undergoing minor surgery and consisted of children < 2 yr old (Group I) and children > 2 yr old (Group II). They were examined at 0.5, 1, and 1.5 minimum alveolar anesthetic concentration desflurane anesthesia. Induction of anesthesia was performed via a face mask and a mixture of O2/N2O (40:60) with halothane. At lease 20 min after stopping halothane, the respiratory variables were recorded on desflurane anesthesia. Tidal volume and minute ventilation decreased significantly (P <0.05) as desflurane increased from 0.5 to 1.5 MAC in both groups. At 1.5 MAC, the respiratory rate was greater in Group II than in Group I (P <0.05). In both groups, the increase in end-tidal CO2 was significant at 1.5 MAC versus 1 and 0.5 MAC (P <0.05). Apnea, i.e., no respiratory movement for 20 s, occurred at 1.5 MAC in one patient in each group. The respiratory duty cycle did not change in any of the groups. Both indices of paradoxical respiration--amplitude index and delay index--did not change. ⋯ Desflurane induces respiratory depression at concentrations higher than 1 minimum alveolar anesthetic concentration mainly due to a decrease in tidal volume. Therefore, desflurane at high concentrations should be used cautiously in infants and children with spontaneous ventilation.
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Anesthesia and analgesia · Nov 1998
Clinical TrialIncreased anticoagulation during cardiopulmonary bypass by prostaglandin E1.
Prostaglandin E1 (PGE1) inhibits tissue factor/factor VIIa-dependent thrombin formation and platelet procoagulant activity. These pathways may trigger thrombin generation during cardiopulmonary bypass (CPB). We hypothesized that the therapeutic combination of PGE1 and heparin increases the degree of anticoagulation as measured by reduced thrombin generation during CPB. Patients undergoing primary coronary artery bypass grafting using CPB were anticoagulated with unfractionated porcine heparin and 12.5 ng x kg(-1) x min(-1) PGE1 (n = 20) or placebo (n = 20). Plasma markers that reflect thrombin generation (prothrombin fragment F1+2, thrombin-antithrombin complex) were determined, and postoperative bleeding was documented. Thrombin generation gradually increased in both groups during and after CPB but was lower in the PGE1 group. After CPB, the difference between mean levels of prothrombin fragment F1+2 was 1.9 nmol/L (95% confidence interval for difference 1.1 to 2.8; P = 0.001). The difference between mean levels of thrombin-antithrombin complex was 43.6 ng/mL (21.2 to 66.1; P = 0.001). A trend in reduced postoperative bleeding was observed in the PGE1 group with a difference of sample means of 183 mL (-5 to 371; P = 0.056). Adding PGE1 to unfractionated heparin enhances anticoagulation during CPB. The results suggest that reduced thrombin generation during surgery may decrease postoperative bleeding. ⋯ Cardiopulmonary bypass is associated with extensive thrombin generation even in the presence of clinically sufficient heparin anticoagulation. The addition of prostaglandin E1 to heparin enhances the degree of anticoagulation as measured by reduced thrombin formation during cardiopulmonary bypass.