The control of breathing in patients with chronic obstructive pulmonary disease (COPD) follows the same basic principles as in normal subjects, both awake and asleep, with an expected lower feedback response during sleep.
This impacts nocturnal gas exchange and sleep quality most profoundly in patients with more severe COPD, as multiple factors come into play. Hypoventilation causes the most important gas-exchange alteration in COPD patients, leading to hypercapnia and hypoxemia, especially during rapid-eye-movement sleep, when marked respiratory muscle atonia occurs.
The hypoxia leads to increased arousals, sleep disruption, pulmonary hypertension, and higher mortality. The primary mechanisms for this include decreased ventilatory responsiveness to hypercapnia, reduced respiratory muscle output, and marked increases in upper airway resistance.
In the presence of more profound daytime hypercapnia, polysomnography should be considered (over nocturnal pulse oximetry) to rule out other co-existing sleep-related breathing disorders such as obstructive sleep apnea (overlap syndrome) and obesity hypoventilation syndrome.
Present consensus guidelines provide insight into the proper use of oxygen, continuous positive airway pressure, and nocturnal noninvasive positive-pressure ventilation for those conditions, but several issues remain contentious.
In order to provide optimal therapy to patients, the clinician must take into account certain reimbursement and implementation-process obstacles and the guidelines for treatment and coverage criteria.