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Obesity can have detrimental effects on respiratory function, and it may lead to chronic hypoventilation in some patients. Why some obese patients develop OHS while others breathe normally remains speculative. Contributing factors may include the restrictive pulmonary function defect, increased work of breathing and CO2 production, and altered central respiratory control.- Some available data support a possible role for airway obstruction in the pathogenesis of diurnal hypercapnia in certain patients with OHS and SAS, although this finding has not been confirmed in other studies. We think that most authors would exclude patients with significant COPD from the diagnosis of OHS, and, in this article, we have only considered those patients who did not have an obstructive ventilatory defect, as measured by spirometry. On the other hand, OHS and SAS have frequently been associated,2 and it is not fully understood whether there is a role for SAS in the pathogenesis of the hypercapnia of OHS patients. Some authors have proposed to not include SAS patients in the entity of OHS, because sleep apnea can sometimes induce hypercapnia per se, even in nonobese patients. However, we agree with most authors in not considering SAS as an exclusionary criterion for the diagnosis of OHS.2″ There is a subgroup of patients with SAS and OHS who have persistent nonapneic desaturation on polysomnography even after the elimination of occlusive apneas with nasal CPAP therapy. Despite a reduction in the resistive load against which the ventilatory pump must work by nasal CPAP therapy, hypoxemia and hypercapnia often persist during sleep and wakefulness in those patients. To avoid the confounding effect of hypoventilation as a consequence of SAS, we chose to include in this study only patients with severe respiratory failure because, in this subset of patients, it seems unlikely that upper airway obstruction could be the dominant mechanism of hypoventilation.

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