Treatment Complications
H.3 Sleep Disorders

Nocturnal oxygen desaturation in COPD patients is fairly common and often unrecognized. It is not usually caused by sleep apnea. Instead, sleep-related hypoxemia has been attributed to ventil-ation-perfusion abnormalities and transient hypo-ventilation during rapid eye movement, (REM), sleep. Nonobese patients with COPD who have daytime normoxemia and transient nocturnal hypoxemia during sleep rarely develop coexisting upper airway obstruc-tion or “obstructive sleep apnea.” But in some obese individuals with COPD an “overlap syndrome” occurs, adding an obstructive component to the typical mechanisms of transient hypoxemia.

Sleep-related hypoxemia is suggested by the presence of an expanded red cell mass as reflected by an increased hematocrit, along with a patient’s reports of morning headaches and daytime somnolence. Often, the patient's spouse is aware of intense snoring and even chooses to sleep in a separate room because of it. The spouse may also notice pauses in breathing followed by loud bursts of snoring when breathing resumes. These reports strongly suggest obstructive sleep apnea.

Diagnosis

Sleep-related hypoxemia and its mechanisms can be diagnosed via overnight home monitoring with a pulse oximeter. The pulse oximeter should be equipped with a memory system and a device to observe whether chest motion ceases during episodes of hypoxemia. Such pauses indicate that a coexisting obstructive component is present. Home sleep studies must be ordered and interpreted by a qualified specialist. Formal polysom-nography can provide additional information about the mechanisms associated with nocturnal hypoxemia, but such studies are expensive and must be conducted in a sleep lab, an unusual sleeping environment.

Treatment

Whether or not nocturnal hypoxemia should be treated with oxygen supplementation has been the subject of numerous studies. Two controlled clinical trials in patients with daytime normoxemia (PaO2 >60 mm Hg) showed a better survival rate in those who did not experience nocturnal desaturation compared with those who did. These studies also showed a trend toward increased survival in oxygen-treated desaturators, compared with desaturators who breathed room air. In fact, one double-blind trial of nocturnal oxygen supplementation for sleep desaturation in patients with daytime normoxemia showed an approximate 4 mm Hg reduction in pulmonary arterial pressures in those treated with oxygen. In contrast, patients who breathed only room air had an increase in their mean pulmonary arterial pressure of approximately 4 mm Hg.

At the present time, experts plan to conduct additional controlled clinical trials to determine whether or not mortality in COPD can be reduced when nocturnal desaturation is treated with oxygen. The outcomes of these studies will answer remaining questions about prescribing nocturnal oxygen. In light of our current knowledge in this area, what should primary care physicians do if nocturnal desaturation is suspected? If home monitoring with a pulse oximeter identifies nocturnal hypoxemia (SaO2 < 88%), and if symptoms of headache, fatigue, and poor exercise tolerance are present, it would be wise for the physician to prescribe home oxygen at a liter-flow rate sufficient to correct the hypoxemia. The oxygen “dose” can be determined by studying pulse oximeter readouts taken over several nights while the patient breathes supplemental oxygen. The physician should also ask the patient to report any symptom improvements. In the case of overlap syndrome, providing continuous positive airway pressure, (CPAP), via a well-fitting nasal mask can also be beneficial.

Caution should be used in prescribing sedative agents for insomnia in COPD patients, and patients should be warned against excessive alcohol consumption. Some of these agents may cause disordered sleep patterns and, in extreme cases, might depress respiration, thus augmenting nocturnal hypoventilation.

References

Block AJ, Boysen PG, Wynne JW. The origins of cor pulmonale: A hypothesis. Chest 1979;75:109-110. This editorial suggests that nocturnal hypoxemia and resultant hypoxemic pulmonary vasoconstriction indicate early stages of pulmonary hypertension in COPD.

Catterall JR, Douglas NJ, Calverley PMA, et al. Transient hypoxemia during sleep in chronic obstructive pulmonary disease is not a sleep apnea syndrome. Am Rev Respir Dis 1983;128:24-29. This articles gives evidence that nocturnal hypoxemia is usually caused by factors other than sleep apnea.

Flenley DC. Sleep in chronic lung disease. Clin Chest Med 1986;6:652-658. An overlap syndrome of concurrent nocturnal hypoxemia in COPD and sleep apnea is discussed here.

Fletcher EC, Donner CF, Midgren B, et al. Survival in COPD patients with a daytime PaO2 >60 Torr with and without nocturnal oxyhemoglobin desaturation (NOD). Chest 1992;101:649-655. This study shows the adverse prognosis of patients with isolated nocturnal oxygen desaturation compared with patients who do not have nocturnal oxygen desaturation.

Fletcher EC, Luckett RA, Goodnight-White S, et al. A double-blind trial of nocturnal supplemental oxygen for sleep desaturation in patients with chronic obstructive pulmonary disease and a daytime PaO2 above 60 Torr. Am Rev Respir Dis 1992;145:1070-1076. A favorable effect of nocturnal oxygen administration on survival in nocturnal desaturations is suggested by this study.