Tatsumi K, Kimura H, Kunitomo F, Kuriyama T, Watanabe S, Honda Y
Chest. 1986 Jul;90(1):68-73. doi: 10.1378/chest.90.1.68.
Recent studies have demonstrated that oxygen desaturation occurs during sleep in some patients with chronic obstructive pulmonary disease (COPD). The degree of sleep hypoventilation in COPD may be related to an inadequate chemical control of ventilation. To investigate this relationship, we compared maximal sleep changes in arterial oxygen saturation (SaO2) with the hypercapnic and hypoxic ventilatory control during wakefulness in 24 patients with COPD. Both hypercapnic and hypoxic ventilatory responses were inversely correlated with the degree of maximal sleep desaturation in rapid-eye-movement (REM) sleep. Furthermore, the level of baseline SaO2 during wakefulness was also negatively related to the magnitude of sleep desaturation. Patients with insufficient chemical control of breathing appear to have larger falls in SaO2, particularly if they have lower baseline SaO2.
近期研究表明,一些慢性阻塞性肺疾病(COPD)患者在睡眠期间会出现氧饱和度下降。COPD患者睡眠低通气的程度可能与通气的化学调节不足有关。为了研究这种关系,我们比较了24例COPD患者在清醒时的高碳酸血症和低氧通气控制与动脉血氧饱和度(SaO2)的最大睡眠变化。高碳酸血症和低氧通气反应均与快速眼动(REM)睡眠中最大睡眠去饱和程度呈负相关。此外,清醒时的基线SaO2水平也与睡眠去饱和幅度呈负相关。呼吸化学调节不足的患者似乎SaO2下降幅度更大,尤其是基线SaO2较低的患者。