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Chest, Vol 103, 1325-1329, Copyright © 1993 by American College of Chest Physicians
ARTICLES |
AR Gold, AR Schwartz, RA Wise and PL Smith
Department of Medicine, Johns Hopkins Sleep Disorders Center, Francis Scott Key Medical Center, Johns Hopkins School of Medicine, Baltimore.
To determine whether moderately obese, normocapnic, sleep apnea patients are distinguished from normal obese individuals by differences in waking pulmonary function and respiratory chemosensitivity, we compared the waking pulmonary function, hypercapnic, and hypoxic ventilatory responses of 35 nonhypercapnic sleep apnea patients (32 men and 3 women) with those of 17 age-, sex-, weight-, and obesity-matched nonapneic control subjects (16 men and 1 woman). The waking ventilatory response to hypercapnia was lower among sleep apnea patients (mean +/- SD, 2.05 +/- 1.29 L/min/mm Hg) than control subjects (3.02 +/- 2.05 L/min/mm Hg, p < 0.05). Patients with sleep apnea demonstrated a higher waking PaCO2 (40.4 +/- 2.9 vs 37.0 +/- 2.7 mm Hg, p < 0.001), and a lower waking PaO2 (81.4 +/- 11.7 vs 89.7 +/- 10.4 mm Hg, p < 0.03). The waking hypoxic ventilatory response, however, was not significantly different between the groups. Moreover, control subjects had a higher total lung capacity than sleep apnea patients (6.99 +/- 1.12 L and 6.27 +/- 1.09 L, respectively, p < 0.05). The lower hypercapnic ventilatory response, higher waking PaCO2, and lower total lung capacity in the sleep apnea patients resemble the pattern observed in patients with pickwickian syndrome. This suggests that disturbances in pulmonary function and ventilatory control in moderately obese sleep apnea patients are intermediate along a continuum from normal obesity to the pickwickian syndrome.
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