Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/11192
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dc.contributor.authorPeyton, Philip Jen
dc.contributor.authorChao, Ianen
dc.contributor.authorWeinberg, Laurenceen
dc.contributor.authorRobinson, Gavin J Ben
dc.contributor.authorThompson, Bruce Ren
dc.date.accessioned2015-05-16T00:46:49Z
dc.date.available2015-05-16T00:46:49Z
dc.date.issued2011-03-01en
dc.identifier.citationAnesthesiology; 114(3): 596-602en
dc.identifier.govdoc21270630en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/11192en
dc.description.abstractRapid elimination of nitrous oxide from the lungs at the end of inhalational anesthesia dilutes alveolar oxygen, producing "diffusion hypoxia." A similar dilutional effect on accompanying volatile anesthetic agent has not been evaluated and may impact the speed of emergence.Twenty patients undergoing surgery were randomly assigned to receive an anesthetic maintenance gas mixture of sevoflurane adjusted to bispectral index, in air-oxygen (control group) versus a 2:1 mixture of nitrous oxide-oxygen (nitrous oxide group). After surgery, baseline arterial and tidal gas samples were taken. Patients were ventilated with oxygen, and arterial and tidal gas sampling was repeated at 2 and 5 min. Arterial sampling was repeated 30 min after surgery. Sevoflurane partial pressure was measured in blood by the double headspace equilibration technique and in tidal gas using a calibrated infrared gas analyzer. Time to eye opening and time extubation were recorded. The primary endpoint was the reduction in sevoflurane partial pressures in blood at 2 and 5 min.Relative to baseline, arterial sevoflurane partial pressure was 39% higher at 5 min in the control group (P < 0.04) versus the nitrous oxide group. At 30 min the difference was not statistically significant. Time to eye opening (8.7 vs. 10.1 min) and time to extubation (11.0 vs.13.2 min) were shorter in the nitrous oxide group versus the control group (P < 0.04).Elimination of nitrous oxide at the end of anesthesia produces a clinically significant acceleration in the reduction of concentrations of the accompanying volatile agents, contributing to the speed of emergence observed after inhalational nitrous oxide anesthetic.en
dc.language.isoenen
dc.subject.otherAgeden
dc.subject.otherAnesthesia Recovery Perioden
dc.subject.otherAnesthesia, Inhalationen
dc.subject.otherAnesthetics, Inhalation.blood.pharmacokineticsen
dc.subject.otherBlood Gas Analysisen
dc.subject.otherCarbon Dioxide.blooden
dc.subject.otherConsciousness Monitorsen
dc.subject.otherDose-Response Relationship, Drugen
dc.subject.otherDrug Interactionsen
dc.subject.otherEndpoint Determinationen
dc.subject.otherFemaleen
dc.subject.otherHumansen
dc.subject.otherMaleen
dc.subject.otherMethyl Ethers.blood.pharmacokineticsen
dc.subject.otherMiddle Ageden
dc.subject.otherNitrous Oxide.blood.pharmacokineticsen
dc.subject.otherSmoking.metabolismen
dc.titleNitrous oxide diffusion and the second gas effect on emergence from anesthesia.en
dc.typeJournal Articleen
dc.identifier.journaltitleAnesthesiologyen
dc.identifier.affiliationDepartment of Anesthesia, Austin Hospital, Melbourne, Australia. phil.peyton@austin.org.auen
dc.identifier.doi10.1097/ALN.0b013e318209367ben
dc.description.pages596-602en
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pubmed/21270630en
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