Arterial blood gases and pH during sleep in chronic obstructive pulmonary disease

Abstract

Arterial blood gases were measured during 7 hours of sleep in 15 patients with severe stable chronic obstructive pulmonary disease (COPD); 6 awake patients with COPD studied in recumbency for an average of 5 hours served as controls. Mean maximal decrease in arterial oxygen partial pressure (PaO 2) (± SD) was 13.5 ± 3.9 mm Hg for sleeping patients (p <0.005) and 5.5 ± 1.7 mm Hg for controls (p < 0.05); comparable increases for PaCO 2 were 8.3 ± 4.4 mm Hg (p < 0.005) and 4.7 ± 1.7 mm Hg (p < 0.1), respectively. Changes in pH during sleep were of the magnitude expected with acute changes in arterial carbon dioxide partial pressure (PaCO 2) in patients with chronic hypercapnia. Consistent changes In heart rate, respiratory frequency or cardiac rhythm were not observed during sleep. Nocturnal worsening of hypoxemia could be explained by alveolar hypoventilation in six sleeping patients and in five controls; in nine sleeping patients, further impairment of ventilation-perfusion mismatch also contributed to worsening of hypoxemia. There was no relationship between the decrease in PaO 2 during sleep and the degree of airways obstruction or the PaO 2 level when awake. Because of low PaO 2, when awake, a fall in PaO 2 during sleep brings values into the steep part of the oxyhemoglobin dissociation curve where slight changes in PaO 2 result in marked changes in oxygen content. All patients with COPD whose waking PaO 2 was below 60 mm Hg had PaO 2 below 50 mm Hg during sleep; nocturnal oxygen therapy should be considered in such patients, particularly in the presence of polycythemia or troublesome right-sided heart failure.