Rationale: Among 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.
Objectives: We hypothesized that hypercapnic patients with OSA have lower Ve than eucapnic patients with OSA.
Methods: In 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 results: Comparing 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.
Conclusions: These 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.
Keywords: CO2 retention; hypoxia; metabolic rate; morbid obesity; weight loss.