FIO2 and positive end-expiratory pressure as compensation for altitude-induced hypoxemia in an acute respiratory distress syndrome model: Implications for air transportation of critically ill patients

Objectives: To determine whether increases in Fio(2) or positive end-expira tory pressure will compensate for hypoxemia resulting from exposure to 8000 feet (2440 m) of altitude in a model of acute respiratory distress syndrom e. Design: Intervention and crossover design. Setting: Military research altitude chamber. Subjects: Sixteen Yucatan miniature swine (Sus scrota). Interventions: Swine initially were placed on mechanical ventilation (zero positive end-expiratory pressure, 21% Fio(2)). Twelve animals had moderate to severe acute respiratory distress syndrome (50% to 70% Fio(2) at sea lev el to maintain Pao(2) of 50-70 torr [6.65-9.3kPa]) induced by intravenous o leic acid. Four animals were controls (no lung injury). The animals were ta ken to 8000 feet (2440 m) in an altitude chamber, and then stepwise increas es of either 5% Fio(2) (six animals) or 2.5 cm H2O positive endexpiratory p ressure (six animals) were made until Pao(2). values exceeded 75 torr (10.0 kPa). If Pao(2) did not reach 75 torr (10.0 kPa), and time permitted, the animal was crossed over to the other group. Measurements and Main Results: Arterial blood gases were drawn at baseline (sea level and at altitude) and after every change in ventilator settings. Positive end-expiratory pressure increases from 5 to 12.5 cm H2O were requi red to bring the Pao(2) in the injured pigs to 75 torr (10.0 kPa). Fio(2) i ncreases did not achieve a Pao(2) of 75 torr (10.0 kPa) for three of six an imals despite reaching 100% Fio(2). One animal crossed over from Fio, to po sitive end-expiratory pressure and achieved a Pao(2) of 75 torr (10.0 kPa) with 5 cm H2O of positive end-expiratory pressure. Conclusions. Fifty percent of the animals with lung injury had altitude-ind uced hypoxia that was resistant to increases in Fio(2). Increases in positi ve end-expiratory pressure are more reliable than increases in Fio(2) for c orrecting altitude-induced hypoxia in this model of acute respiratory distr ess syndrome.