Sleep-disordered breathing in COPD
- Peter C Gay, MD
Peter C Gay, MD
- Professor Of Medicine
- Mayo Medical School
- Section Editors
- James K Stoller, MD, MS
James K Stoller, MD, MS
- Section Editor — Chronic Obstructive Pulmonary Disease
- Jean Wall Bennett Professor of Medicine, Samson Global Leadership Academy Endowed Chair
- Cleveland Clinic Lerner College of Medicine
- Chairman, Education Institute, Cleveland Clinic
- Ronald D Chervin, MD, MS
Ronald D Chervin, MD, MS
- Editor-in-Chief — Sleep Medicine
- Section Editor — Pediatric Sleep Medicine
- Professor of Neurology
- University of Michigan
- Deputy Editors
- April F Eichler, MD, MPH
April F Eichler, MD, MPH
- Deputy Editor — Neurology and Sleep Medicine
- Assistant Professor of Neurology
- Harvard Medical School
- Helen Hollingsworth, MD
Helen Hollingsworth, MD
- Deputy Editor — Pulmonary, Critical Care, and Sleep Medicine
- Associate Professor of Medicine
- Boston University School of Medicine
Patients with chronic obstructive pulmonary disease (COPD) frequently suffer from nocturnal alterations in ventilation and gas exchange, which are generally unrelated to the development of bronchospasm or to changes in airway resistance [1,2]. The respiratory effects of sleep in patients with COPD, including a diagnostic approach to sleep-disordered breathing in this population, will be presented here. Treatment of sleep-disordered breathing in patients with COPD is discussed separately. (See "Treatment of sleep-disordered breathing in COPD".)
SLEEP AND VENTILATION IN COPD
Changes in chemoresponsiveness to CO2 and alterations in arterial PCO2 occur even in normal individuals during sleep, but these changes are accentuated in patients with COPD. In normal individuals, minute ventilation and ventilatory responsiveness to CO2 progressively decrease as the depth of sleep increases, with arterial PCO2 rising to a maximum during rapid eye movement (REM) sleep . However, this decrease in ventilation does not generally result in significant hypoxemia . (See "Control of ventilation".)
Nocturnal ventilatory drive is affected in a similar fashion, but to a larger extent, in patients with COPD compared to normal individuals. Thus, they experience a much greater decrease in the slope of the relationship between ventilation and PaCO2 during sleep, which can result in clinically significant alveolar hypoventilation with resulting hypoxemia [5-9].
The effect of sleep on minute ventilation and the pattern of breathing was demonstrated in five non-hypercapnic patients with hyperinflation due to severe emphysema (mean FEV1 1.1 L; awake SaO2 91 percent) . Patients were sleep-deprived and observed during wakefulness and while asleep in a body plethysmograph. Sleep did not reduce the breathing frequency or functional residual capacity (FRC), but minute ventilation fell by an average of 35 percent, a change that was accounted for entirely by a parallel decrease in tidal volume. Reduced respiratory neuromuscular output and increases in upper airway resistance contributed to these changes, and were progressive as the depth of sleep increased.
Oxygenation during sleep — Significant reductions in nocturnal oxygen saturation can occur in patients with COPD because of alveolar hypoventilation (as noted above), worsening of ventilation-perfusion mismatching, reduction of functional residual capacity, and increased upper airway resistance [7,8,10-13]. The changes are most profound during REM sleep, when reductions in PaO2 to levels as low as 20 mmHg have been reported .
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