• Louise W Sturesson, Mikael Bodelsson, Anders Johansson, Björn Jonson, and Gunnar Malmkvist.
• From the Section of Anesthesiology and Intensive Care, Department of Clinical Sciences Lund, Lund University and Skane University Hospital, Lund, Sweden.
• Anesth. Analg.. 2013 Dec 1;117(6):1319-24.

BackgroundThe anesthetic conserving device (ACD) reduces consumption of volatile anesthetic drug by a conserving medium adsorbing exhaled drug during expiration and releasing it during inspiration. Elevated arterial CO2 tension (PaCO2) has been observed in patients using the ACD, despite tidal volume increase to compensate for larger apparatus dead space. In a test lung using room temperature dry gas, this was shown to be due to adsorption of CO2 in the ACD during expiration and release of CO2 during the following inspiration. The effect in the test lung was higher than in patients. We tested the hypothesis that a lesser dead space effect in patients is due to higher temperature and/or moisture attenuating rebreathing of CO2.MethodsThe lungs of 6 postoperative cardiac surgery patients were ventilated using a conventional heat and moisture exchanger (HME) or an ACD. The ACD was studied with a test lung at varying temperatures and moistures. Infrared spectrometry was used to measure apparent dead space by the single-breath test for CO2 as well as rebreathing of CO2.ResultsIn patients, the median apparent dead space was 136 mL (95% confidence interval [CI,] 120-167) larger using the ACD compared with an HME (after correction for difference in internal volume 100 and 50 mL, respectively). Median rebreathing of CO2 using the ACD was 53% (range 48-58) of exhaled CO2 compared with 29% (range 27-32) with an HME. The median difference in CO2 rebreathing was 23% (95% CI, 18-27). In the test lung apparent dead space using ACD was unaffected by body temperature but decreased from 360 to 260 mL when moisture was added. This decreased rebreathing of CO2 from 62% to 48%.ConclusionsThe use of an ACD increases apparent dead space to a greater extent than can be explained by its internal volume. This is caused by adsorption of CO2 in the ACD during expiration and release of CO2 during inspiration. Rebreathing of CO2 was attenuated by moisture. The dead space effect of the ACD could be clinically relevant in acute respiratory distress syndrome and other diseases associated with ventilation difficulties, but investigations with larger sample sizes would be needed to determine the clinical importance.

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