Lawless N, Tobias S, Mayorga M A
Department of Respiratory Research, Walter Reed Army Institute of Research, Washington, DC 20307-5100, USA.
Crit Care Med. 2001 Nov;29(11):2149-55. doi: 10.1097/00003246-200111000-00017.
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.
Intervention and crossover design.
Military research altitude chamber.
Sixteen Yucatan miniature swine (Sus scrofa).
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.
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.
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.
在急性呼吸窘迫综合征模型中，确定增加吸入氧分数（FiO₂）或呼气末正压（PEEP）是否能代偿因暴露于8000英尺（2440米）海拔高度而导致的低氧血症。
干预和交叉设计。
军事研究海拔舱。
16只尤卡坦小型猪（猪属）。
猪最初接受机械通气（呼气末正压为零，FiO₂为21%）。12只动物通过静脉注射油酸诱导出中度至重度急性呼吸窘迫综合征（海平面时FiO₂为50%至70%，以维持动脉血氧分压[PaO₂]为50 - 70托[6.65 - 9.31千帕]）。4只动物为对照组（无肺损伤）。将动物置于海拔舱升至8000英尺（2440米），然后对6只动物逐步增加5%的FiO₂，对另外6只动物逐步增加2.5厘米水柱的呼气末正压，直至PaO₂值超过75托（10.0千帕）。如果PaO₂未达到75托（10.0千帕）且时间允许，将动物交叉至另一组。
在基线（海平面和海拔高度）以及每次呼吸机设置改变后采集动脉血气。受伤猪的PaO₂要达到75托（10.0千帕），呼气末正压需从5厘米水柱增加到12.5厘米水柱。6只动物中有3只尽管FiO₂达到100%，但仍未使PaO₂达到75托（10.0千帕）。1只动物从FiO₂组交叉至呼气末正压组，呼气末正压为5厘米水柱时PaO₂达到了75托（10.0千帕）。
50%的肺损伤动物存在海拔诱导的低氧血症，对FiO₂增加具有抵抗性。在该急性呼吸窘迫综合征模型中，增加呼气末正压比增加FiO₂更可靠地纠正海拔诱导的低氧血症。
