Pulmonary, Critical Care, and Sleep Division, Cincinnati Veterans Affairs Medical Center, Cincinnati, Ohio 45220, USA.
COPD. 2009 Dec;6(6):478-87. doi: 10.3109/15412550903341497.
Although the Centers for Medicare and Medicaid Services oxygen prescription guidelines utilize a threshold arterial oxygen tension <or=55 mmHg or an oxygen saturation <or=88%, a range of oxygen levels and relative declines have been used in investigations of exertional desaturation in patients with chronic obstructive pulmonary disease (COPD). There is no uniform definition of exertional hypoxemia or standardized exercise protocol to elicit decreases in oxygen levels in individuals with COPD. The causes for exertional desaturation in patients with COPD are multifactorial with ventilation-perfusion mismatching, diffusion-type limitation, shunting and reduced oxygen content of mixed venous blood all contributing to some degree. Neither resting oxygen saturation nor pulmonary function studies can reliably predict which patients with COPD will develop exertional desaturation. However, preserved pulmonary function, especially diffusing capacity, reliably predicts which patients with COPD will sustain oxygenation during exercise. Although exertional desaturation in patients with COPD appears to portend a poor prognosis, there is no evidence that maintenance of normoxemia during exercise improves the survival of these patients. Studies of the effect of supplemental oxygen on exercise performance in individuals with COPD who desaturate with exertion have yielded conflicting results. The use of short-term or "burst" oxygen either prior to or after exertion may not have significant clinical benefit. Differences in the definition of desaturation, mode of exercise, and characteristics of the patient population make it difficult to compare studies of exertional desaturation and its treatment and to determine their applicability to clinical practice.
虽然医疗保险和医疗补助服务中心的氧气处方指南使用动脉氧分压<55mmHg 或氧饱和度<88%作为阈值，但在慢性阻塞性肺疾病（COPD）患者运动性低氧血症的研究中，已经使用了一系列氧水平和相对下降范围。对于 COPD 患者的运动性低氧血症，没有统一的定义，也没有标准化的运动方案来诱发氧水平下降。COPD 患者运动性低氧血症的原因是多因素的，通气-灌注不匹配、弥散型限制、分流和混合静脉血氧含量降低都在一定程度上导致了这种情况。静息氧饱和度或肺功能检查都不能可靠地预测哪些 COPD 患者会出现运动性低氧血症。然而，保留的肺功能，特别是弥散能力，可以可靠地预测哪些 COPD 患者在运动期间会保持氧合。虽然 COPD 患者的运动性低氧血症似乎预示着预后不良，但没有证据表明运动期间维持正常氧合能改善这些患者的生存率。对在运动中出现低氧血症的 COPD 患者进行补充氧对运动表现影响的研究结果相互矛盾。在运动前或运动后短暂或“爆发”吸氧可能没有显著的临床益处。低氧血症的定义、运动方式和患者人群的特征差异使得比较运动性低氧血症及其治疗的研究以及确定它们在临床实践中的适用性变得困难。
