Transient Hypoxemia during Sleep in Chronic Obstructive Pulmonary Disease Is Not a Sleep Apnea Syndrome^1–3

Abstract

We measured ear oxygen saturation (SaO2), chest wall movement, and oronasal air flow, and took electroencephalographic tracings during nocturnal sleep in 20 healthy subjects and 20 similarly aged patients with chronic obstructive pulmonary disease (COPD), none of whom was obese. Thirteen of the patients with COPD were persistently hypoxemic and hypercapnic when awake ("blue and bloated", Type B); the remaining 7 maintained relatively normal arterial gas tensions when awake despite equally severe airways obstruction ("pink and puffing", Type A). Hypoxemic episodes (HE) (SaO2 falls of greater than 10%) occurred during sleep in all the blue bloaters but in only 3 of 7 pink puffers and 3 of 20 normal subjects. However, the maximal change in arterial oxygen tension (PaO2) (calculated from SaO2 values assuming normal pH) was similar in all 3 groups, averaging 24 mmHg. Furthermore, the cumulative duration of apnea and hypopnea was the same in each group. Only one patient COPD had more than 2 apneas per night, and obstructive apnea was seen only in the healthy subjects. Sleep apnea syndromes thus appear to be rare in nonobese patients with COPD. Of the 40 HE in patients with COPD, 29 occurred during periods of hypoventilation. In 10 blue bloaters whose arterial blood was sampled during sleep, the measured fall in PaO2 during the HE (mean, 11.2 mmHg) was greater than the rise in PaCO2 (mean, 4.2 mmHg). Although these changes in arterial gas tensions could be produced by an increase in ventilation-perfusion imbalance during the HE, it is suggested that unsteady-state gas exchange during transient hypoventilation could provide an alternative explanation.

Mechanisms of Endothelin-1 Elevation in Chronic Obstructive Pulmonary Disease Patients with Nocturnal Oxyhemoglobin Desaturation

“…In normal subjects alveolar ventilation during bursts of eye movement is about 40% lower than that during wakefulness [44, 45]. Ventilation has not been accurately measured during sleep in patients with lung disease, but semiquantitative assessment of the breathing pattern during REM sleep shows that it is similar to that of normal subjects [11]. As patientswith COPD have a higher, physiologic dead space than do normal subjects, the rapid shallow breathing during periods of eye movements might produce an even greater decrease in alveolar ventilation, which would contribute significantly to the REM-related hypoxemia [46].…”

“…Transient oxygen desaturation in COPD probably results from a combination of alveolar hypoventilation and gas exchange abnormalities contributing to REM sleep muscular atonia and changes in respiratory control [10, 11, 12, 13, 14, 15, 16]. These often profound decreases in oxyhemoglobin saturation (SaO 2 ) may be accompanied by marked elevation in pulmonary artery pressure [17, 18]and development of pulmonary hypertension in patients with advanced lung disease [19, 20].…”

Sleep and Sleep Disorders in Chronic Obstructive Pulmonary Disease

“…Lower pulmonary function test results (FEV 1 /FVC <60%) have been associated with NOD [30], but this finding has not been found in other studies. Unlike patients with cystic fibrosis, those with COPD who experience exercise-related desaturation do not necessarily also experience NOD [31].…”

Sleep-related O2 desaturation and daytime pulmonary haemodynamics in COPD patients with mild hypoxaemia

“…We believe that most of these patients belong to the "pink and puffer" type of COPD, whereas a number of desaturators were probably of the "blue and bloated" type. It has been shown previously that "blue bloated" COPD patients are likely to desaturate more during sleep [9,10,28], but these studies concerned patients with a very wide range of Pa,O 2 levels whilst awake, most of them exhibiting marked daytime hypoxaemia. Of interest, the same observation can be drawn from a series with a narrow range of Pa,O 2 , not including patients with severe daytime hypoxaemia.…”

“…These results do not support the hypothesis that sleep-related hypoxaemia favours the development of pulmonary hypertension. Eur Respir J 1997; 10: 1730-1735 The worsening of hypoxaemia during sleep in patients with chronic obstructive pulmonary disease (COPD) has been documented since the early 1960s [1], and has since been confirmed by polysomnographic studies [2,3], which have included continuous monitoring of oxygen saturation from the late 1970s [4][5][6][7][8][9][10]. It must be emphasized that most of these studies have included patients with severe COPD exhibiting marked daytime hypoxaemia.…”