• Shahrokh Javaheri and Loretta A Simbartl.
• 1 Cincinnati Veterans Affairs Medical Center, Cincinnati, Ohio; and.
• Ann Am Thorac Soc. 2014 Jul 1;11(6):945-50.

RationaleAmong morbidly obese individuals, obstructive sleep apnea (OSA) is highly prevalent, with up to 20% suffering from hypoventilation syndrome. An increased diurnal PaCO2, the signature of obesity hypoventilation syndrome (OHS), implies diminished global ventilation, hence the term hypoventilation.ObjectivesWe hypothesized that hypercapnic patients with OSA have lower Ve than eucapnic patients with OSA.MethodsIn this prospective study we recorded respiratory variables to determine the pathophysiological mechanisms of steady-state diurnal hypercapnia of 12 consecutive hypercapnic and 20 consecutive eucapnic patients with OSA, matched for apnea-hypopnea index. Patients with any known causes of hypercapnia were not included.Measurements And Main ResultsComparing hypercapnic to eucapnic patients, the mean value (±SD) for PaCO2 (52 ± 5 vs. 40 ± 3 mm Hg) was significantly higher, and the mean PaO2 (59 ± 8 vs. 75 ± 10 mm Hg) was significantly lower, in the hypercapnic patients. Surprisingly, the mean values for [Formula: see text]e (12.2 ± 3.0 vs. 11.6 ± 2.0 L/min), alveolar ventilation, breathing rate, [Formula: see text]t, and dead space did not differ significantly. However, hypercapnic patients had a significantly greater CO2 production (336 ± 79 vs. 278 ± 58 ml/min), which was the main reason for hypercapnia. When adjusted for body surface area, the mean values for CO2 production were similar between the two groups.ConclusionsThese data emphasize the importance of weight loss, which could potentially reverse hypercapnic OSA to eucapnic OSA, hypothetically even in the absence of improvement in apnea-hypopnea index. In addition, reversal of hypercapnia should also improve oxygenation, both during sleep and while awake, minimizing hypoxia-induced organ dysfunction of OHS.

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