Anesthesia and analgesia
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Anesthesia and analgesia · Dec 1998
Comparative StudyA comparison of pharyngeal mucosal pressure and airway sealing pressure with the laryngeal mask airway in anesthetized adult patients.
We measured pharyngeal mucosal pressures at six different locations on the laryngeal mask airway (LMA) and tested the hypothesis that the efficacy of the seal is not related to pharyngeal mucosal pressure. Twenty anesthetized, paralyzed adult patients were studied. Microchip sensors were attached to the size 5 LMA at locations corresponding to the lateral and posterior pharynx, the hypopharynx, the pyriform fossa, the base of tongue, and the oropharynx. Mucosal pressures and airway sealing pressures were recorded during inflation of the cuff from 0 to 40 mL in 10-mL increments. The highest mean mucosal pressure was in the oropharynx (26 cm H2O), and the lowest was in the posterior pharynx (2 cm H2O). Mucosal pressures increased with increasing intracuff pressure and cuff volume, but the rate of increase varied among locations. Airway sealing pressure increased with increasing intracuff volume from 0 to 10 mL (P < 0.0001) and 10 to 20 mL (P = 0.0001), was unchanged from 20 to 30 mL, and decreased from 30 to 40 mL (P = 0.005). The airway sealing pressure was higher than pharyngeal mucosal pressure until the intracuff volume was > or =30 mL. There was no correlation between mucosal pressures and airway sealing pressure at any location. We conclude that the efficacy of the seal is not related to pharyngeal mucosal pressure. Pharyngeal mucosal pressures are generally lower than those considered safe for the tracheal mucosa during prolonged intubation. ⋯ We measured pharyngeal mucosal pressures at six different locations on the laryngeal mask airway and showed that the efficacy of the seal is not related to pharyngeal mucosal pressure. Pharyngeal mucosal pressures are generally lower than those considered safe for the tracheal mucosa during prolonged intubation.
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Anesthesia and analgesia · Dec 1998
Nitrous oxide and carbon dioxide have no effect on the blood-gas solubilities of sevoflurane and isoflurane.
Nitrous oxide (N2O) has been shown to decrease the solubility (lambdaB:G) of volatile anesthetics in human blood and, consequently, affect their rate of uptake. If this is true, then carbon dioxide (CO2) may also have an effect, which is important because methods that measure the tension of volatile anesthetics in blood washout CO2 in the process. Blood samples were obtained from fasted, healthy volunteers and patients undergoing major surgery. Each sample was divided into two aliquots: one was equilibrated at 37 degrees C in a closed glass tonometer with a mixture of isoflurane 1% and sevoflurane 2% in a test gas mixture of either 50:50 N2O/O2 or 5:95 CO2/O2; the other aliquot was equilibrated with isoflurane and sevoflurane in O2 alone as a control. Using a two-stage headspace technique using gas chromatography, we measured the lambdaB:G of isoflurane and sevoflurane in the presence and absence of the test gas in each subject. There was no significant difference between the lambdaB:G of sevoflurane and isoflurane obtained from the N2O group and their controls or between the CO2 group and their controls. We conclude that neither N2O nor CO2 has an effect on the lambdaB:G of sevoflurane or isoflurane in the concentrations tested. ⋯ The blood solubilities of sevoflurane and isoflurane were measured with and without nitrous oxide and carbon dioxide. No differences were found. Nitrous oxide does not affect the kinetics of other anesthetics by altering their solubility. Carbon dioxide tensions need not be controlled when measuring anesthetic tensions in blood.
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Anesthesia and analgesia · Dec 1998
Characteristics of tolerance to somatic and visceral antinociception after continuous epidural infusion of morphine in rats.
A continuous epidural infusion of morphine may cause a complicated tolerance to develop, depending on the spinal and supraspinal sites. We designed this study to clarify the characteristics of the tolerance to somatic and visceral antinociception after epidural morphine infusion. Rats received epidural infusion of morphine at the rates of 50 or 100 microg kg(-1) h(-1), or isotonic sodium chloride solution for 7 days. The tail-flick (TF) test and colorectal distension (CD) test were used to measure the somatic and visceral antinociceptive effects, respectively. Nociceptive tests were performed on Days 1, 2, 3, 4, and 7. After 7 days, time-response curves after epidural morphine (10 microg) or intraperitoneal morphine (3 mg) challenge tests were conducted to assess the magnitude of tolerance. Epidurally infused morphine significantly increased percent maximal possible effects (%MPEs) (P < 0.05) in both the TF and CD tests, depending on the concentration of morphine. In the epidural morphine challenge test, increases in %MPEs were significantly attenuated (P < 0.05) in the morphine-infused group compared with the isotonic sodium chloride solution-infused group. The increases in %MPEs in the intraperitoneal challenge test were also attenuated in the morphine-infused group. We conclude that morphine tolerance to both somatic and visceral antinociception develops rapidly during epidural infusion and is based on the development of tolerance at the systemic, as well as the epidural, level. ⋯ A continuous epidural infusion of morphine rapidly induces tolerance to visceral and somatic antinociception in rats. This development is based on the development of tolerance at the systemic, as well as the epidural, level.
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Anesthesia and analgesia · Dec 1998
Hypoxemia decreases the shivering threshold in rabbits anesthetized with 0.2 minimum alveolar anesthetic concentration isoflurane.
Shivering has been proposed as an etiology of postoperative hypoxemia. The difficulty with this theory is that hypoxemia inhibits shivering in unanesthetized cats, rats, and humans. However, anesthesia inhibits many protective reflexes, including the ventilatory response to hypoxemia. We therefore tested the hypothesis that arterial hypoxemia fails to inhibit shivering in lightly anesthetized rabbits. Rabbits were intubated and instrumented during exposure to surgical concentrations of anesthesia, and anesthesia was then maintained with 0.2 minimum alveolar anesthetic concentration isoflurane. The core was cooled at a rate of 2-3 degrees C/h by perfusing water at 10 degrees C through a colonic thermode. Core temperatures were recorded from the distal esophagus. Sustained, vigorous shivering was considered physiologically significant. The core temperature that triggering significant shivering identified the thermoregulatory threshold for this response. Arterial blood was sampled for gas analysis at the shivering threshold in each rabbit. Hypoxemia linearly reduced the shivering threshold from 36.7 degrees C at 130 mm Hg to 35.4 degrees C at 50 mm Hg (threshold = PaO2.0.019 + 34.3; r2 = 0.49). We failed to confirm our hypothesis: instead, even mild hypoxemia reduced the shivering threshold >1 C. A 1 C decrease in the shivering threshold is likely to prevent or stop most postoperative shivering because it exceeds the reduction produced by many effective anti-shivering drugs. These data do not support the theory that shivering causes postoperative hypoxemia. ⋯ Shivering has been proposed as an etiology of postoperative hypoxemia. Our data, in contrast, show that mild hypoxemia inhibits shivering. Shivering is thus unlikely to be a cause of postoperative hypoxemia.