Objectives : To determine whether increases in Fio2 or positive end-expiratory pressure will compensate for hypoxemia resulting from exposure to 8000 feet (2440 m) of altitude in a model of acute respiratory distress syndrome.
Design : Intervention and crossover design.
Setting : Military research altitude chamber.
Subjects : Sixteen Yucatan miniature swine (Sus scrofa).
Interventions : Swine initially were placed on mechanical ventilation (zero positive end-expiratory pressure, 21% Fio2). Twelve animals had moderate to severe acute respiratory distress syndrome (50% to 70% Fio2 at sea level to maintain Pao2 of 50–70 torr [6.65–9.31kPa]) induced by intravenous oleic acid. Four animals were controls (no lung injury). The animals were taken to 8000 feet (2440 m) in an altitude chamber, and then stepwise increases of either 5% Fio2 (six animals) or 2.5 cm H2O positive end-expiratory pressure (six animals) were made until Pao2 values exceeded 75 torr (10.0 kPa). If Pao2 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 required to bring the Pao2 in the injured pigs to 75 torr (10.0 kPa). Fio2 increases did not achieve a Pao2 of 75 torr (10.0 kPa) for three of six animals despite reaching 100% Fio2. One animal crossed over from Fio2 to positive end-expiratory pressure and achieved a Pao2 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-induced hypoxia that was resistant to increases in Fio2. Increases in positive end-expiratory pressure are more reliable than increases in Fio2 for correcting altitude-induced hypoxia in this model of acute respiratory distress syndrome.