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Determinants of Daytime Hypercapnia in Obstructive Sleep Apnea : Is Obesity the Only One To Blame?

David Gozal, MD, FCCP
Author and Funding Information

Affiliations: Louisville, KY 
 ,  Professor Gozal is Vice-Chair for Research, and Director, Kosair Children’s Hospital Research Institute, Department of Pediatrics, University of Louisville.

Correspondence to: David Gozal, MD, FCCP, Kosair Children’s Hospital Research Institute, 570 S. Preston St, Suite 321, University of Louisville, Louisville, KY 40202



Chest. 2002;121(2):320-321. doi:10.1378/chest.121.2.320
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In contrast with COPD patients, patients with obstructive sleep apnea (OSA) have a priori normal respiratory mechanics and normal gas exchange during wakefulness. Increased upper airway resistance on sleep onset in OSA patients leads to intermittent or sustained alveolar hypoventilation during the night, but this process usually reverses within a short time after the patients wake up. However, about 30 to 40% of patients with OSA will continue to exhibit elevated Pco2 levels throughout the waking period, despite the absence of severe lung disease. In other words, OSA patients are at high risk for hypoventilation syndrome. Therefore, our primary gut feeling would be to attribute the daytime alveolar hypoventilation in patients with OSA to obesity, since it has been clearly implicated in the pathophysiology of OSA patients.14 Furthermore, we have now all become familiar with obesity hypoventilation syndrome (OHS), a complex condition that associates morbid obesity with severe daytime gas exchange abnormalities,5 such that we may have intuitively associated the daytime hypercapnia of OSA patients with obesity.

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