Transient hypoxemia during sleep in chronic obstructive pulmonary disease is not a sleep apnea syndrome

The American review of respiratory disease (Impact Factor: 10.19). 08/1983; 128(1):24-9.
Source: PubMed


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.

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    • "In patients with severe COPD, oxygen saturation may fall during REM sleep by 20–30% [9] [10] and PAP may rise by as much as 20 mm Hg [11]. "
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    ABSTRACT: The development of pulmonary hypertension in COPD adversely affects survival and exercise capacity and is associated with an increased risk of severe acute exacerbations. Unfortunately not all patients with COPD who meet criteria for long term oxygen therapy benefit from it. Even in those who benefit from long term oxygen therapy, such therapy may reverse the elevated pulmonary artery pressure but cannot normalize it. Moreover, the recent discovery of the key roles of endothelial dysfunction and inflammation in the pathogenesis of PH provides the rationale for considering specific pulmonary vasodilators that also possess antiproliferative properties and statins.
    Pulmonary Medicine 08/2012; 2012(2090-1836):203952. DOI:10.1155/2012/203952
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    • "Although pulmonary hypertension in COPD is usually mild (mPAP 20–35 mm Hg), it may increase markedly during exercise (Horsfi eld et al 1968; Weitzenblum 2003), sleep (Coccagna et al 1978; Catterall et al 1983; Fletcher et al 1984), and exacerbations (Weitzenblum et al 1994). Frequent exacerbations can promote the development of right heart failure and this should be preventable by general management measures recommended for COPD. "
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    ABSTRACT: Hypoxia and endothelial dysfunction play a central role in the development of pulmonary hypertension. Cor pulmonale is a maladaptive response to pulmonary hypertension. The presence of peripheral edema in cor pulmonale is almost invariably associated with hypercapnia. Correction of abnormalities of gas exchange and ventilation can ameliorate pulmonary hypertension and improve survival. This review focuses on new information about the pathogenesis and treatment of pulmonary hypertension in COPD including information derived from lung volume reduction surgery, the role of brain natriuretic peptide, exhaled nitric oxide for diagnosis, and the treatment of cor pulmonale with recently available specific pulmonary vasodilators.
    International Journal of COPD 02/2007; 2(3):273-82. · 3.14 Impact Factor
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    • "The most common finding is a small SaO2 reduction, while the breathing pattern remains substantially regular. Instead, prolonged oxygen desaturations are often observed throughout rapid eye movement (REM) sleep (Douglas et al 1979; Catterall et al 1983) (Figure 1). Long duration (often several minutes) and a slow resolution distinguish such desaturations from the typical desaturations of sleep apneas that rarely exceed a minute and are rapidly reverted (Bonsignore et al 1990). "
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    ABSTRACT: Patients with COPD may show slow, progressive deteriorations in arterial blood gases during the night, particularly during rapid eye movement (REM) sleep. This is mainly due to hypoventilation, while a deterioration of ventilation/perfusion mismatch plays a minor role. The severity of gas exchanges alterations is proportional to the degree of impairment of diurnal pulmonary function tests, particularly of partial pressure of oxygen (PaO2) and of carbon dioxide (PaCO2) in arterial blood, but correlations between diurnal and nocturnal blood gas levels are rather loose. Subjects with diurnal PaO2 of 60-70 mmHg are distinguished in "desaturators" and "nondesaturators" according to nocturnal oxyhemoglobin saturation behavior. The role of nocturnal hypoxemia as a determinant of alterations in sleep structure observed in COPD is dubious. Effects of the "desaturator" condition on pulmonary hemodynamics, evolution of diurnal blood gases, and life expectancy are also controversial. Conversely, it is generally accepted that occurrence of sleep apneas in COPD is associated with a worse evolution of the disease. Nocturnal polysomnographic monitoring in COPD is usually performed when coexistence of sleep apnea ("overlap syndrome") is suspected, while in most other cases nocturnal oximetry may be enough. Nocturnal oxygen attenuates sleep desaturations among stable patients, without increases in PaCO2 of clinical concern. Nocturnal treatment with positive pressure ventilators may give benefit to some stable hypercapnic subjects and patients with the overlap syndrome.
    International Journal of COPD 02/2006; 1(4):363-72. DOI:10.2147/copd.2006.1.4.363 · 3.14 Impact Factor
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