ABSTRACT
Airway anaesthesia using atomised lidocaine for awake oral fibreoptic intubation in morbidly obese patients was evaluated using two doses of local anaesthetic. In this randomised, blinded prospective study, 40 ml of atomised 1% (n = 11) or 2% (n = 10) lidocaine was administered with high oxygen flow as carrier. Outcomes included time for intubation, patient tolerance to airway manipulation, haemodynamic parameters, the bronchoscopist's overall satisfaction, and serial serum lidocaine concentrations. Patients receiving lidocaine 1% had a longer mean (SD) time from the start of topicalisation to tracheal tube cuff inflation than those receiving lidocaine 2% (8.6 (0.9) min vs 6.9 (0.5) min, respectively; p < 0.05). Patients in the 1% cohort demonstrated increased responses to airway manipulation (p < 0.0001), reflecting lower bronchoscopist's satisfaction scores (p < 0.03). Haemodynamic responses to topicalisation and airway manipulation were similar in both groups. Peak plasma concentration was lower in the 1% group (mean (SD) 1.4 (0.3) and 3.8 (0.5) μg.ml−1, respectively; p < 0.001). Airway anaesthesia using atomised lidocaine for awake oral fibreoptic intubation in the morbidly obese is efficacious, rapid and safe. Compared with lidocaine 1%, the 2% dose provides superior intubating conditions.
Thursday, January 14, 2010
Effects of Dexmedetomidine and Propofol on Lower Esophageal Sphincter and Gastroesophageal Pressure Gradient in Healthy Volunteers
Abstract
Background: Many anesthetics reduce lower esophageal sphincter pressure (LESP). Reduced pressure and consequent reduction in the gastroesophageal pressure gradient (GEPG) thus promotes gastroesophageal reflux and may contribute to aspiration pneumonia and associated morbidity. Therefore, the authors compared LESP and GEPG during dexmedetomidine and propofol sedation.
Methods: Using a randomized, double-blind, crossover design, 11 healthy volunteers were sedated on 2 separate days. Baseline LESP and GEPG were recorded each day. Subsequently, on each day volunteers received three 40-min-long sedative infusions of increasing doses of 0.6, 1.2, and 2.4 ng/ml dexmedetomidine or 1, 2, and 4 [mu]g/ml propofol. LESP and GEPG were recorded during inhalation and expiration at 20 and 40 min after starting each infusion phase, and these measurements were averaged. Results are presented as mean (95% confidence interval).
Results: Two subjects did not return for the dexmedetomidine study day, and the dexmedetomidine results were unusable in another; propofol results in these volunteers were nonetheless retained for analysis. There were no significant differences in LESP and GEPG as a function of drug. However, there was a small but significant 7.4 (-1.6 to -13.2) mmHg (approximately 25%) dose-dependent decrease in LESP over the range of targeted low to high blood levels of each drug.
Conclusions: Both dexmedetomidine and propofol have similar effects on LESP and GEPG. Although both of the drugs cause some decrease in LESP at high concentrations, it is unlikely that this effect would promote gastroesophageal reflux during sedation.
Background: Many anesthetics reduce lower esophageal sphincter pressure (LESP). Reduced pressure and consequent reduction in the gastroesophageal pressure gradient (GEPG) thus promotes gastroesophageal reflux and may contribute to aspiration pneumonia and associated morbidity. Therefore, the authors compared LESP and GEPG during dexmedetomidine and propofol sedation.
Methods: Using a randomized, double-blind, crossover design, 11 healthy volunteers were sedated on 2 separate days. Baseline LESP and GEPG were recorded each day. Subsequently, on each day volunteers received three 40-min-long sedative infusions of increasing doses of 0.6, 1.2, and 2.4 ng/ml dexmedetomidine or 1, 2, and 4 [mu]g/ml propofol. LESP and GEPG were recorded during inhalation and expiration at 20 and 40 min after starting each infusion phase, and these measurements were averaged. Results are presented as mean (95% confidence interval).
Results: Two subjects did not return for the dexmedetomidine study day, and the dexmedetomidine results were unusable in another; propofol results in these volunteers were nonetheless retained for analysis. There were no significant differences in LESP and GEPG as a function of drug. However, there was a small but significant 7.4 (-1.6 to -13.2) mmHg (approximately 25%) dose-dependent decrease in LESP over the range of targeted low to high blood levels of each drug.
Conclusions: Both dexmedetomidine and propofol have similar effects on LESP and GEPG. Although both of the drugs cause some decrease in LESP at high concentrations, it is unlikely that this effect would promote gastroesophageal reflux during sedation.
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