© 2003 American Thoracic Society
Is Chronic Obstructive Pulmonary Disease Related to Sleep Apnea–Hypopnea Syndrome?University of British Columbia Vancouver, British Columbia, Canada Sleep is the period of greatest physiologic disturbance in chronic obstructive pulmonary disease (COPD) and the time of greatest danger to these individuals. Sleep aggravates their abnormalities of gas exchange and causes secondary pulmonary hypertension and cardiac arrhythmias. Individuals with COPD also tend to have a short and disturbed sleep. It has not been clear whether or not COPD and the sleep apnea–hypopnea syndrome (SAHS) are related. Most previous studies of sleep-disordered breathing in COPD have been performed on small numbers of selected individuals with severe disease (1, 2). The Sleep Heart Health Study (3) provides a unique opportunity to examine the association between COPD and SAHS, and predictors of sleep desaturation and sleep quality in a large community population of adult individuals with COPD who did not seek medical attention. Because COPD and SAHS are both common diseases, some individuals would be expected to have both conditions by chance alone. Both tobacco smoking and abnormal respiratory control are potential contributing factors that could predispose to SAHS in individuals with COPD. An early report found a high prevalence of SAHS in individuals with COPD (4). This finding, however, was biased in that most of the individuals underwent polysomnography because of suspected sleep apnea. Several other reports (5, 6) have suggested that the prevalence of SAHS in individuals with COPD is higher than would be expected in the general population. In this issue of AJRCCM (pp. 7–14), Sleep Heart Health Study investigators report that SAHS was not more prevalent in 1,132 participants with predominantly mild COPD (7). When the investigators accounted for confounding variables, surprisingly the severity of apnea/hypopnea tended to decrease as the degree of airflow obstruction became more marked. When COPD and SAHS occur in the same individual, they occur on the basis of chance and do not represent a common pathophysiologic link. Individuals with COPD may demonstrate gas exchange abnormalities when asleep. The mechanism, extent, and significance of these abnormalities have been the subject of much investigation. Sleep desaturation occurs in all sleep stages, but maximum desaturation usually occurs during rapid eye movement sleep. Alveolar hypoventilation, which occurs in normal sleeping individuals, is thought to be the major mechanism causing arterial oxygen desaturation (8). Oxygen saturation while awake is the best predictor of sleep desaturation in individuals with COPD. Many individuals with COPD are hypoxemic and have waking arterial oxygen tensions at or near the steep portion of the oxyhemoglobin dissociation curve. Accordingly, a decrease of alveolar ventilation will cause greater oxygen desaturation in these individuals than in normal individuals. Hypoventilation is not the only cause of hypoxemia. Oxygen desaturation during sleep in COPD is also partly due to alterations in the distribution of ventilation–perfusion relationships (9). That oxygen desaturation is usually greatest during rapid eye movement sleep also provides insight into its etiology. Oxygen uptake is increased during rapid eye movement sleep, and this may contribute to the desaturation. The dissociation between diaphragmatic and intercostal activity during rapid eye movement sleep can also result in both hypoventilation and worsening of ventilation–perfusion disturbances. The Sleep Heart Health Study investigators found that participants with an FEV1/FVC ratio of less than 65% had an increased risk of sleep desaturation independent of awake oxygen saturation and the presence of SAHS (7). Sleep desaturation is associated with reduced survival (10) and cannot be accurately predicted by symptoms or awake measurements. Accordingly, the investigators proposed that overnight oximetry be routinely considered in patients with an FEV1/FVC of less than 65%. Individuals with severe COPD sleep badly. They have decreased sleep time, less rapid eye movement sleep, and more changes in sleep stage. Poor sleep quality is probably a major factor in the chronic fatigue and impaired quality of life reported by patients with severe COPD (11). Nevertheless, sleep duration and quality are frequently overlooked in studies that evaluate the effectiveness of therapy on quality of life in individuals with COPD. The mechanism of the sleep disturbance is not clear. It may be related to gas exchange abnormalities, medications (e.g., theophylline) (12), or general debility associated with COPD. Hypoxia stimulates the reticular activating system, and there is a strong association between hypoxemia and the incidence of arousals in COPD. The frequency of arousals, however, does not decrease after nocturnal oxygen therapy (2), suggesting it is not the hypoxemia but some related phenomenon, possibly hypercapnia, that is the principal arousing stimulus. The Sleep Heart Health Study investigators found that sleep quality was minimally impaired in their participants with predominantly mild COPD without SAHS (7). Based on this finding, they recommended that when individuals with COPD have sleep-related symptoms, other sleep disorders, such as periodic limb movement disorder or SAHS, should be considered. They were unable to record limb movements, and thus it is not known whether the prevalence of periodic limb movements is increased in individuals with COPD. Although the prevalence of SAHS was not higher in the participants with COPD, sleep quality and sleep desaturation was worse when participants had both COPD and SAHS. COPD and SAHS are two common conditions that may coexist. The Sleep Heart Health Study shows that when these two conditions do coexist, this is the result of chance alone. When COPD and SAHS do coexist the individuals have more sleep desaturation and disruption than they would have with only one condition. Although awake oxygen saturation is the best predictor of sleep desaturation in COPD, the degree of airflow obstruction also independently predicts sleep desaturation. Overnight oximetry should be considered in most individuals with COPD, irrespective of whether they have symptoms of sleep disruption, to exclude significant overnight desaturation that may be associated with reduced survival. When individuals with COPD have sleep-related symptoms, other sleep disorders should be included in the differential diagnosis. REFERENCES
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