Background: Isoflurane inhibits baroreflex control of heart rate (HR) by poorly understood mechanisms. The authors examined whether suprapontine central nervous system cardiovascular regulatory sites are required for anesthetic depression. Methods: The effects of isoflurane (1 and 2 rat minimum alveolar concentration [MAC]) on the baroreflex control of HR were determined in sham intact and midcollicular-transected decerebrate rats. Intravenous phenylephrine (0.2-12 microg/kg) and nitroprusside (1-60 microg/kg) were used to measure HR responses to peak changes in mean arterial pressure (MAP). Sigmoidal logistic curve fits to HR-MAP data assessed baroreflex sensitivity (HR/MAP), HR range, lower and upper HR plateau, and MAP at half the HR range (BP50). Four groups (two brain intact and two decerebrate) were studied before, during, and after isoflurane. To assess sympathetic and vagal contributions to HR baroreflex, beta-adrenoceptor (1 mg/kg atenolol) or muscarinic (0.5 mg/kg methyl atropine) antagonists were administered systemically. Results: Decerebration did not alter resting MAP and HR or baroreflex parameters. Isoflurane depressed baroreflex slope and HR range in brain-intact and decerebrate rats. In both groups, 1 MAC reduced HR range by depressing peak reflex tachycardia. Maximal reflex bradycardia during increases in blood pressure was relatively preserved. Atenolol during 1 MAC did not alter maximum reflex tachycardia. In contrast, atropine during 1 MAC fully blocked reflex bradycardia. Therefore, 1 MAC predominantly depresses sympathetic components of HR baroreflex. Isoflurane at 2 MAC depressed both HR plateaus and decreased BP50 in both groups. Conclusions: Isoflurane depresses HR baroreflex control by actions that do not require suprapontine central nervous system sites. Isoflurane actions seem to inhibit HR baroreflex primarily by the sympathetic nervous system.
For patients suspicious of cervical spine injury, a Philadelphia cervical collar is usually applied. Application of Philadelphia cervical collar may cause difficult airway. The aim of this study was to evaluate the laryngeal view and the success rate at first intubation attempt of the Airtraq and conventional laryngoscopy in patients with simulated cervical spine injury after application of a Philadelphia cervical collar. Anesthesia was induced with propofol, remifentanil, and rocuronium. After a Philadelphia cervical collar applied, patients were randomly assigned to tracheal intubation with an Airtraq (Group A, n = 25) or with conventional laryngoscopy (Group L, n = 25). Measurements included intubation time, success rate of first intubation attempt, number of intubation attempts, and percentage of glottic opening (POGO) score. Mean blood pressure and heart rate were also recorded at baseline, just before and after intubation. The success rate of the first attempt in Group A (96%) was significantly greater than with the Group L (40%). POGO score was significantly greater in Group A (84 ± 20%) than in Group L (6 ± 11%). The duration of successful intubation at first tracheal intubation attempt and hemodynamic changes were not significantly different between the two groups. The Airtraq offers a better laryngeal view and higher success rate at first intubation attempt in patients who are applied with a Philadelphia cervical collar due to suspicion of cervical spine injury.