About 5% of OSA patients have chronic alveolar hypoventilation with elevated arterial carbon dioxide tension while awake (

see Fig. 67-4). These patients have the so-called pickwickian or obesity-hypoventilation syndrome (OHS). They tend to be morbidly obese and have severe OSA with cor pulmonale and, in some cases, polycythemia. Although the pathophysiology of OHS remains poorly understood, daytime hypoventilation often resolves after effective treatment of the obstructive breathing events during sleep. Some OHS patients respond to nasal CPAP, but some require noninvasive mechanical ventilation, which provides augmented inspiratory pressure support.

Central sleep apnea (CSA) is not common. Central apneas result from an instability in the ventilatory control system. Congestive heart failure is the most common cause of CSA. Patients with neurologic disorders involving brain stem respiratory control centers may have CSA. The clinical sequelae of CSA are similar to those described for OSA. Supplemental oxygen, acetazolamide, or noninvasive nocturnal mechanical ventilation may help some patients.

Many patients with compromised pulmonary function (emphysema, kyphoscoliosis, respiratory muscle weakness) develop nocturnal oxygen desaturation from a combination of sleep-induced hypoventilation, reduced lung volumes, and ventilation-perfusion mismatching. These patients may benefit from assessment of the severity of nocturnal hypoventilation and the response to therapy. Therapy may involve optimizing pulmonary function, supplemental oxygen, or noninvasive nocturnal mechanical ventilation.

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