Anesthesia and analgesia
-
Anesthesia and analgesia · Aug 1999
Randomized Controlled Trial Clinical TrialJugular bulb oxygen saturation during propofol and isoflurane/nitrous oxide anesthesia in patients undergoing brain tumor surgery.
We investigated, in brain tumor patients, the jugular bulb venous oxygen partial pressure (PjO2) and hemoglobin saturation (SjO2), the arterial to jugular bulb venous oxygen content difference (AJDO2), and middle cerebral artery blood flow velocity (Vmca) during anesthesia, and the effect of hyperventilation on these variables. Twenty patients were randomized to receive either isoflurane/ nitrous oxide/fentanyl (Group 1) or propofol/fentanyl (Group 2). At normoventilation (PacO2 35 +/- 2 mm Hg in Group 1 and 33 +/- 3 mm Hg in Group 2), SjO2 and PjO2 were significantly higher in Group 1 than in Group 2 (SjO2 60% +/- 6% and 49% +/- 13%, respectively; P = 0.019) (PjO2 32 +/- 3 and 27 +/- 5 mm Hg, respectively; P = 0.027). In Group 2, 5 of 10 patients had SjO2 < 50%, and 3 of these patients had SjO2 < 40% and AJDO2 > 9 mL/dL. All patients in Group 1 had SjO2 > 50%. During hyperventilation, there were no differences in SjO2, PjO2, or AJDO2 between the two groups. On hyperventilation, there was no correlation between the relative decreases of Vmca and 1/AJDO2 (r = 0.21, P = 0.41). The results indicate during propofol anesthesia, half of the brain tumor patients showed signs of cerebral hypoperfusion, but not during isoflurane/nitrous oxide anesthesia. Furthermore, during PacO2 manipulations, shifts in Vmca are inadequate to evaluate brian oxygen delivery in these patients. ⋯ During propofol anesthesia at normoventilation, 50% of brain tumor patients showed signs suggesting cerebral hypoperfusion, but this could not be demonstrated during isoflurane/nitrous oxide anesthesia. During PacO2 manipulations, consecutive measurements of the cerebral blood flow velocity may be inadequate to assess cerebral oxygenation.
-
Anesthesia and analgesia · Aug 1999
Randomized Controlled Trial Clinical TrialIntraoperative phenylephrine infusion decreases the magnitude of redistribution hypothermia.
Core hypothermia during the first hour after induction of general anesthesia results largely from an internal core-to-peripheral redistribution of body heat. This redistribution results from both central inhibition of tonic thermoregulatory vasoconstriction in the arteriovenous shunt and anesthetic-induced vasodilation. We therefore tested the hypothesis that acute administration of phenylephrine, a pure alpha-adrenergic agonist, reduces the magnitude of anesthetic-induced core-to-peripheral redistribution of body heat. Patients undergoing minor oral surgery were randomly assigned to an infusion of 0.5 microgram.kg-1.min-1 phenylephrine i.v. or no treatment (control). The phenylephrine infusion was started immediately before anesthesia was induced with 2.5 mg/kg propofol i.v. Subsequently, anesthesia was maintained with sevoflurane and 60% nitrous oxide in oxygen. Calf minus toe, skin-temperature gradients < 0 degree C were considered indicative of significant arteriovenous shunt vasodilation. Ambient temperature and end-tidal concentrations of maintenance sevoflurane were comparable in each group. Although there were no significant differences in skin-temperature gradients, core temperatures in the untreated patients decreased significantly more (1.2 +/- 0.4 degrees C) than in those given phenylephrine (0.5 +/- 0.2 degree C, P < 0.001). These data suggest that maintaining precapillary vasoconstriction of blood vessels, not in the arteriovenous shunt reduces the magnitude of redistribution hypothermia. ⋯ Core hypothermia immediately after induction of general anesthesia results largely from core-to-peripheral redistribution of body heat. Core temperature reduction during the first hour of anesthesia decreased less in patients given phenylephrine than in untreated controls. These data suggest that maintaining precapillary vasoconstriction possibly reduces the magnitude of redistribution hypothermia.
-
Anesthesia and analgesia · Aug 1999
Ventilatory response to CO2 in children with obstructive sleep apnea from adenotonsillar hypertrophy.
We measured the ventilatory response to CO2 as an indicator of respiratory control dysfunction in children with obstructive sleep apnea (OSA) scheduled for adenotonsillectomy. Measurements were performed in unpremedicated children via an endotracheal tube under 0.4%-0.5% end-tidal halothane anesthesia. Mean ventilatory CO2 response slopes for 11 children with OSA requiring adenotonsillectomy (Group I) were compared with those for 14 children without OSA requiring adenotonsillectomy (Group II) and 15 children without OSA requiring nonairway surgery (Group III). The mean ventilatory slope corrected for body surface area for Groups I, II, and III were 539 +/- 338, 828 +/- 234, and 850 +/- 380 mL.min-1.mm Hg ETCO2(-1).m-2, respectively (P < 0.05, Group I versus Groups II and III). Historical data--including snoring, apneic episodes > 10 s, daytime hypersomnolence, and nocturnal enuresis--defined those with OSA. Obesity occurred more frequently in patients with OSA and with depressed ventilatory responses (P < 0.001). Children with OSA from adenotonsillar hypertrophy have a diminished ventilatory response to CO2 stimulation, compared with those without OSA symptoms. The depressed response may account, in part, for the reported increased risk of perioperative respiratory complications in this population. ⋯ Children with obstructive sleep apnea undergoing adenotonsillar surgery are at risk of postoperative respiratory compromise. We found that patients with a clinical history suggesting obstructive sleep apnea have a diminished ventilatory response to CO2 rebreathing, compared with controls.
-
Anesthesia and analgesia · Aug 1999
Effects of one minimum alveolar anesthetic concentration sevoflurane on cerebral metabolism, blood flow, and CO2 reactivity in cardiac patients.
We investigated the cerebral hemodynamic effects of 1 minimum alveolar anesthetic concentration (MAC) sevoflurane anesthesia in nine male patients scheduled for elective coronary bypass grafting. For measurement of cerebral blood flow (CBF), a modified Kety-Schmidt saturation technique was used with argon as an inert tracer gas. Measurements of CBF were performed before the induction of anesthesia and 30 min after induction under normocapnic, hypocapnic, and hypercapnic conditions. Compared with the awake state under normocapnic conditions, sevoflurane reduced the mean cerebral metabolic rate of oxygen by 47% and the mean cerebral metabolic rate of glucose by 39%. Concomitantly, CBF was reduced by 38%, although mean arterial pressure was kept constant. Significant changes in jugular venous oxygen saturation were absent. Hypocapnia and hypercapnia caused a 51% decrease and a 58% increase in CBF, respectively. These changes in CBF caused by variation of Paco2 indicate that cerebrovascular CO2 reactivity persists during 1 MAC sevoflurane anesthesia. ⋯ We used a modified Kety-Schmidt saturation technique to investigate the effects of 1 minimum alveolar anesthetic concentration (MAC) sevoflurane on cerebral blood flow, metabolism, and CO2 reactivity in cardiac patients. We found that the global cerebral blood flow and global cerebral metabolic rate of oxygen remained coupled and that cerebrovascular CO2 reactivity is not impaired by the administration of 1 MAC sevoflurane.
-
Anesthesia and analgesia · Aug 1999
Epidural anesthesia and analgesia are not impaired after dural puncture with or without epidural blood patch.
Previous reports have noted a decrease in the success of subsequent epidural anesthesia and analgesia in patients who have undergone prior dural puncture with or without an epidural blood patch. Our retrospective study evaluated the success of epidural anesthesia and analgesia in all patients at the Mayo Clinic who had received a prior epidural blood patch over a 12-yr period. Each epidural blood patch patient was matched to two patients undergoing epidural anesthesia after previous dural puncture (without epidural blood patch) and to two patients undergoing epidural anesthesia after previous epidural anesthetic (without dural puncture/blood patch). These patients were matched for the duration of time between the initial procedure and subsequent epidural anesthetic and the indication (surgery, labor analgesia, postoperative analgesia) for which the subsequent epidural was performed. Subsequent epidural anesthesia was successful in 28 of 29 (96.6%, exact 95% CI 82.2%-99.9%) patients who had undergone prior blood patch, 55 of 58 (94.8%, 85.6%-98.9%) patients with a history of dural puncture, and 55 of 58 (94.8%, 85.6%-98.9%) patients who had had previous epidural anesthesia. There was no significant difference in the success rate of subsequent epidural anesthesia among groups. We conclude that prior dural puncture, with or without epidural blood patch, does not affect the success rate of subsequent epidural anesthesia. ⋯ Patients with postdural puncture headache should not be denied the benefits of an epidural blood patch because of concerns about the impairment of subsequent epidural anesthetics. The success rate of subsequent epidural anesthesia and analgesia in patients who have undergone dural puncture with or without epidural blood patch is similar to that of patients who have undergone two prior epidural anesthetics.