Anesthesiology
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The proliferation of monitors and alarms in the operating room may lead to increased confusion and misdiagnosis unless the information provided is better organized. Intelligent alarm systems are being developed to organize these alarms, on the assumption that they will shorten the time anesthesiologists need to detect and correct faults. This study compared the human response time (the time between the sounding of an alarm and the resolution of a fault) when anesthesiologists used a conventional alarm system and when they used an intelligent alarm system. ⋯ The standard deviations in response time were only half as large for the intelligent alarm system. It appears that the computer-based neural network in the intelligent alarm system diagnosed faults more rapidly and consistently than did the anesthesiologists. This study indicates that breathing circuit faults may be more rapidly corrected when the anesthesiologist is guided by intelligent alarms.
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Sixty-one patients ASA physical status 1-2 aged 1 month to 12 years undergoing elective surgery were included in the study. Anesthesia was induced via a mask with sevoflurane up to 5% and 66% nitrous oxide in oxygen. After paralysis with vecuronium (0.12 mg/kg iv), the trachea was intubated and the lungs were ventilated manually with 3% sevoflurane in oxygen until the end-tidal nitrous oxide decreased to less than 5%. ⋯ The patients with symptomatic upper respiratory infection required less time for Spo2 to decrease to 95% compared to the asymptomatic children. We conclude that younger children require less time for Spo2 to decrease to 95%. The presence of upper respiratory infection is an additional factor increasing the susceptibility of small children to hypoxemia.
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In the absence of data on the anatomic localization of the cuff of the laryngeal mask airway (LMA) in children, radiologic images were obtained from 50 infants and children (aged 1 month to 15 yr) undergoing diagnostic radiologic procedures during halothane and N2O:O2 anesthesia. In 46 patients, the cuff of the LMA was in the pharynx and covered the laryngeal opening. The upper (proximal) section was adjacent to the base of the tongue at the level of C1 or C2 vertebrae pushing the tongue forward and its lower (distal) end was in the inferior recesses of the hypopharynx at the levels of C4 to T1 vertebrae. ⋯ In four patients, the cuff of the LMA was located in the oropharynx. No correlation was found between the size of the LMA and the position of the epiglottis with respect to end-tidal CO2, respiratory rate, or the leak pressures. The size of the LMA, its anatomic location, and the position of the epiglottis had no significant effect on the respiratory parameters of spontaneously breathing children.
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Sevoflurane, a new inhalational anesthetic agent has been shown to produce degradation products upon interaction with CO2 absorbants. Quantification of these sevoflurane degradation products during low-flow or closed circuit anesthesia in patients has not been well evaluated. The production of sevoflurane degradation products was evaluated using a low-flow anesthetic technique in patients receiving sevoflurane anesthesia in excess of 3 h. ⋯ Mean maximum inhalation concentration of compound A using baralyme was 20.28 +/- 8.6 ppm (mean +/- SEM) compared to 8.16 +/- 2.67 ppm obtained with soda lime, a difference that did not reach statistical significance. A single patient achieved a maximal concentration of 60.78 ppm during low-flow anesthesia with baralyme. Exhalation concentrations of compound A were less than inhalation concentrations, suggesting patient uptake.(ABSTRACT TRUNCATED AT 250 WORDS)
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Sevoflurane previously has been reported to undergo extensive degradation in the presence of soda lime. To more completely characterize the extent and significnce of this reaction, we studied degradation of sevoflurane with and without soda lime, as well as the toxicity and mutagenicity of the degradation products. Two degradation products detected were CF2 = C(CF3)OCH2F (compound A) and CH3OCF2CH(CF3)OCH2F (compound B). ⋯ Exposure of fibroblasts to 7,500 ppm of compound A for 1 h, compound A did not induce structural change. In a study of acute toxicity of compound B, there was no toxicity in Wistar rats after 3 h of exposure at 2,400 ppm. The reverse (Ames) test for compound B was negative at 625-1,250 micrograms/dish.(ABSTRACT TRUNCATED AT 400 WORDS)