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Obesity Hypoventilation Syndrome as a Spectrum of Respiratory Disturbances During Sleep^*

^* From the Division of Pulmonary and Critical Care Medicine, Bellevue Hospital Chest Service, Department of Medicine, New York University School of Medicine, New York, NY.

Correspondence to: Kenneth I. Berger, MD, FCCP, Department of Medicine, NYU Medical Center, 550 First Ave, New York, NY 10016; e-mail: kenneth.berger{at}med.nyu.edu

Objective: To identify the spectrum of respiratory disturbances during sleep in patients with obesity hypoventilation syndrome (OHS) and to examine the response of hypercapnia to treatment of the specific ventilatory sleep disturbances.

Designs and methods: Twenty-three patients with chronic awake hypercapnia (mean [± SD] PaCO₂, 55 ± 6 mm Hg) and a respiratory sleep disorder were retrospectively identified. Nocturnal polysomnography testing was performed, and flow limitation (FL) was identified from the inspiratory flow-time contour. Obstructive hypoventilation was inferred from sustained FL coupled with O₂ desaturation that was corrected with treatment of the upper airway obstruction. Central hypoventilation was inferred from sustained O₂ desaturation that persisted after the correction of the upper airway obstruction. Treatment was initiated, and follow-up awake PaCO₂ measurements were obtained (follow-up range, 4 days to 7 years).

Results: A variable number of obstructive sleep apneas/hypopneas (ie, obstructive sleep apnea-hypopnea syndrome [OSAHS]) were noted (range, 9 to 167 events per hour of sleep). Of 23 patients, 11 demonstrated upper airway obstruction alone (apnea-hypopnea/FL) and 12 demonstrated central sleep hypoventilation syndrome (SHVS) in addition to a variable number of OSAHS. Treatment aimed at correcting the specific ventilatory abnormalities resulted in correction of the chronic hypercapnia in all compliant patients (compliant patients: pretreatment, 57 ± 6 mm Hg vs post-treatment, 41 ± 4 mm Hg [p < 0.001]; noncompliant patients: pretreatment, 52 ± 6 mm Hg vs post-treatment, 51 ± 3 mm Hg; [difference not significant]).

Conclusions: This study demonstrates that OHS encompasses a variety of distinct pathophysiologic disturbances that cannot be distinguished clinically at presentation. Sustained obstructive hypoventilation due to partial upper airway obstruction was demonstrated as an additional mechanism for OHS that is not easily classified as SHVS or OSAHS.

Key Words: blood • carbon dioxide • hypercapnia • physiopathology • respiration • sleep apnea syndromes

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