Obesity hypoventilation syndrome: prevalence and predictors in patients with obstructive sleep apnea

Abstract

Patients with obesity hypoventilation syndrome (OHS) have a lower quality of life, more healthcare expenses, a greater risk of pulmonary hypertension, and a higher mortality compared to eucapnic patients with obstructive sleep apnea (OSA). Despite significant morbidity and mortality associated with OHS, it is often unrecognized and treatment is frequently delayed. The objective of this observational study was to determine the prevalence of OHS in patients with OSA seen at the sleep disorders clinic of a large public urban hospital serving predominantly minority population and to identify clinical--not mechanistic--predictors that should prompt clinicians to measure arterial blood gases. In the first stage, we randomly selected 180 patients referred to our sleep disorders clinic between 2000 and 2004 for suspicion of OSA. From this retrospective random sample we calculated the prevalence of OHS in patients with OSA and identified independent clinical predictors using logistic regression. In the second stage, we prospectively validated these predictors in a sample of 410 consecutive patients referred to the sleep disorders clinic for suspicion of OSA between 2005 and 2006. The prevalence of OHS in patients with OSA was 30% in the retrospective random sample and 20% in the prospective sample. Three variables independently predicted OHS in both samples: serum bicarbonate level (p < 0.001), apnea-hypopnea index (p = 0.006), and lowest oxygen saturation during sleep (p < 0.001). Due to the serious morbidity associated with OHS, we selected a highly sensitive threshold of serum bicarbonate level. A threshold of 27 mEq/l had a sensitivity of 92% and a specificity of 50%. Only 3% of patients with a serum bicarbonate level <27 mEq/l had hypercapnia compared to 50% with a serum bicarbonate > or =27 mEq/l. In conclusion, OHS is common in severe OSA. A normal serum bicarbonate level excludes hypercapnia and an elevated serum bicarbonate level should prompt clinicians to measure arterial blood gases.

Pulmonary function in the morbidly obese

“…The diagnosis of COPD was determined from a physician diagnosis recorded in the chart. The diagnosis of obesity hypoventilation syndrome (OHS) was inferred by the presence of resting hypoxemia (partial pressure arterial oxygen <70 mm Hg) and/or resting hypercarbia (partial pressure of carbon dioxide ≥45 mm Hg) in the setting of a BMI >30 kg/m 2 according to previously recommended diagnostic criteria [9–11]. …”

Upper Airway Mechanics

“…However, it does not appear that obesity is the only determinant of hypoventilation as only a minority of morbidly obese patients develop chronic hypercapnia [100, 101]. …”

“…This acute hypercapnia causes a small increase in serum bicarbonate level that is not corrected before the next sleep period if the time constant of bicarbonate excretion is longer than that of CO 2 . The elevated bicarbonate level blunts the ventilatory response to CO 2 from its initial value by reducing the change in hydrogen ions for a given change in CO 2 and would ultimately result in a higher wake CO 2 level [100, 117]. …”

Characteristics of Patients With the “Malignant Obesity Hypoventilation Syndrome” Admitted to an ICU

“…6 The incidence of OHS increases significantly as the prevalence of obesity increases, with a reported prevalence of between 10% and 20% in outpatients presenting to sleep clinics and 30% in hospitalized obese patients. [6][7][8][9][10] The syndrome is postulated to result from complex interactions between impaired respiratory mechanics, abnormal central ventilatory control, sleep-disordered breathing, and neurohormonal (leptin resistance) and endocrine aberrancies (insulin resistance, low progesterone). 6 It is likely that the vast majority of patients with OHS remain undiagnosed.…”