Dillard T A, Moores L K, Bilello K L, Phillips Y Y
Department of Medicine, Walter Reed Army Medical Center, Washington, DC 20307-5001.
Chest. 1995 Feb;107(2):352-7. doi: 10.1378/chest.107.2.352.
We sought to compare arterial oxygen partial pressure (PaO2) relationships between a 15.1% hypoxia inhalation test (HIT) at sea level and a hypobaric chamber exposure equivalent to 2,438 m (8,000 feet) of altitude above sea level in patients with chronic obstructive pulmonary disease (COPD) and healthy subjects.
Comparison of physiologic variables before and during intervention.
A referral-based pulmonary disease clinic at a US Army medical center in a metropolitan area.
The study included three groups: group 1, 15 patients, 3 women and 12 men, with COPD (forced expiratory volume in the first second [FEV1, mean +/- SD], 41 +/- 14% of predicted); group 2, 9 healthy men; and group 3, 18 men with COPD (FEV1, 31 +/- 10% of predicted) previously reported in detail.
We evaluated each group at sea level followed by one of two different types of hypoxic exposures. Group 1 received exposure to 15.1% oxygen at sea level, the HIT. Groups 2 and 3 received hypobaric chamber exposure equivalent to 2,438 m (8,000 feet) above sea level.
For all three groups combined, the arterial oxygen tension at sea level (PaO2SL) explained significant variability in PaO2 during hypoxic exposure according to the following formula: PaO2 during exposure = 0.417 (PaO2SL)] + 17.802 (n = 42; r = 0.756; p < 0.001). Neither the type of hypoxic exposure (HIT vs hypobaric), status as patient vs control, sex, nor age explained significant variability in PaO2 during hypoxia exposure after inclusion of PaO2SL as a covariate in analysis of variance. Subsequent analysis revealed that forced expiratory spirometric variables FEV1 and FEV1 to FVC ratio served as second order covariates with PaO2SL to improve description of PaO2 during hypoxia exposure for the combined samples (n = 42; p < 0.05). Analysis of residuals from regression analysis revealed approximately normal distribution.
The PaO2 relationships did not differ between the 15.1% HIT at sea level and hypobaric exposures of 2,438 m (8,000 feet) above sea level. Normal subjects and patients with COPD formed a single relationship. The present study extends descriptive models to a larger range of subjects. Regression models have definable accuracy in predicting PaO2 during hypoxia exposure that increases with inclusion of spirometric variables.
我们试图比较海平面15.1%低氧吸入试验（HIT）与模拟海拔2438米（8000英尺）的低压舱暴露条件下，慢性阻塞性肺疾病（COPD）患者和健康受试者的动脉血氧分压（PaO2）关系。
干预前后生理变量的比较。
大都市地区一家美国陆军医疗中心的转诊式肺病诊所。
该研究包括三组：第1组，15例患者，3名女性和12名男性，患有COPD（第1秒用力呼气量[FEV1，均值±标准差]，为预测值的41±14%）；第2组，9名健康男性；第3组，18名患有COPD的男性（FEV1，为预测值的31±10%），此前已详细报道。
我们在海平面评估每组受试者，然后进行两种不同类型的低氧暴露之一。第1组在海平面接受15.1%氧气暴露，即HIT。第2组和第3组接受模拟海拔2438米（8000英尺）的低压舱暴露。
对于合并的所有三组受试者，海平面动脉血氧张力（PaO2SL）可根据以下公式解释低氧暴露期间PaO2的显著变异性：暴露期间的PaO2 = 0.417（PaO2SL）+ 17.802（n = 42；r = 0.756；p < 0.001）。在方差分析中将PaO₂SL作为协变量纳入后，低氧暴露类型（HIT与低压舱）、患者与对照状态、性别及年龄均不能解释低氧暴露期间PaO₂的显著变异性。后续分析显示，用力呼气肺量计变量FEV1和FEV1与FVC比值作为与PaO₂SL的二阶协变量，可改善对合并样本低氧暴露期间PaO₂的描述（n = 42；p < 0.05）。回归分析残差分析显示近似正态分布。
海平面15.1%的HIT与模拟海拔2438米（8000英尺）的低压舱暴露条件下，PaO₂关系无差异。正常受试者和COPD患者形成单一关系。本研究将描述模型扩展到更大范围的受试者。回归模型在预测低氧暴露期间的PaO₂方面具有可定义的准确性，随着肺量计变量的纳入，准确性增加。
