• Niels D Nielsen, Gratien Andersen, Benedict Kjaergaard, Mette E Staerkind, and Anders Larsson.
• Anaesthesia Research Unit, Anaesthesia and Intensive Care Medicine, North Denmark Region, Aarhus University Hospital, Aalborg, Denmark. ndn@rn.dk
• ASAIO J. 2010 Jan 1;56(1):30-4.

AbstractIn a model of acute lung injury (ALI), previously, we have shown that apneic oxygenation, using an inspiratory O2 fraction (FiO2) of 1.0 combined with extracorporeal arteriovenous CO2 removal (AO-AVCR) maintains adequate arterial O2 and CO2 levels for a prolonged period. However, it is important that FiO2 lower than 1.0 can be used to avoid possible pulmonary oxygen toxicity. In preliminary studies, arterial oxygenation decreased to extreme low levels, when FiO2 <1 was used in apneic oxygenation. We assumed that this was caused either by alveolar accumulation/concentration of N2 or by absorption atelectasis. In four anesthetized and mechanically ventilated pigs, mild lung injury was induced. After a lung recruitment maneuver, we initiated two 20-minute periods of AO-AVCR with FiO2 of 1 and 0.5, respectively. By using FiO2 = 1, PaO2 remained above 300 mm Hg. At the end of the period, the alveolar O2 fraction (FAO2) was 0.89 (0.88-0.89; median and ranges). With FiO2 = 0.5, PaO2 decreased 90% compared with baseline values and FAO2 decreased to 0.07 (0.06-0.07). No atelectasis was visible on computed tomography after either period, and we, therefore, conclude that the alveolar hypoxia was caused by the alveolar N2 accumulation/concentration and subsequently by the O2 depletion.

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