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This is an unpublished paper.

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Obesity hypoventilation syndrome (OHS) is a serious medical condition that remains undiagnosed in seriously ill hospitalized patients. Significant improvement of daytime hypercapnia can be achieved with positive airway pressure (PAP) therapy. Bi-level PAP is generally employed with the goal of improving ventilation. A 50-year-old woman with OHS and severe hypercapnia was successfully treated with an auto titrating continuous PAP (Auto-CPAP) device. The major role in the pathogenesis of daytime hypercapnia in patients with OHS, is the progressive accumulation of carbon dioxide (CO2) caused by repetitive obstructive events at night, which can be eliminated with the low cost approach of treating with Auto CPAP.


OHS, an interaction between sleep disordered breathing and obesity-related respiratory impairment leading to chronic daytime hypercapnia, remains under recognized and definitive treatment is often delayed.[1] Treatment of sleep disordered breathing with PAP therapy results in significant improvement of daytime hypercapnia.[2] Auto-CPAP is generally not recommended to treat obesity hypoventilation syndrome.[3,4] We present a patient with OHS and severe daytime hypercapnia who was successfully treated with Auto CPAP.

Case Presentation:

A fifty-year-old morbidly obese (BMI 52) non-smoking female with a history of hypertension and untreated obstructive sleep apnea (OSA) was admitted to the hospital with severe dyspnoea on exertion in July 2012. She was hypoxemic at admission. Arterial blood gas (ABG) on 2 liters of supplemental oxygen revealed a pH of 7.34, pCO2 of 88 mm Hg and a pO2 of 79 mm Hg. Serum bicarbonate level was elevated at 44mEq/L. Cardiac enzymes were normal. Brain natriuretic peptide (BNP) was elevated at 2161 pg/ml. D-dimer was normal. Chest x-ray was notable for prominence of main pulmonary artery, suggestive of pulmonary artery hypertension. EKG had non-specific changes. Echocardiogram revealed normal left ventricular systolic and diastolic function with mild pulmonary hypertension. Nuclear medicine stress test was normal. Computed tomography angiogram was normal.

Pulmonary/Sleep medicine was consulted, and a presumptive diagnosis of OHS was made given the patient's morbid obesity, previous history of OSA and hypoventilation on ABG. She was placed on CPAP at 10 cm water pressure in the hospital and demonstrated significant clinical improvement with relief of shortness of breath. Supplemental oxygen requirements improved from as high as 4 liters per minute via nasal cannula to 2 liters per minutes.