In obesity-hypoventilation syndrome, awake alveolar hypoventilation appears to result from a combination of blunted ventilatory drive and increased mechanical load imposed upon the chest by obesity. Voluntary hyperventilation returns the PCO2 and the PO2 toward normal values, a correction not seen in lung diseases causing chronic respiratory failure, such as COPD. Diagnostic criteria include a BMI greater than 30, an arterial partial pressure of carbon dioxide greater than 45 mm Hg, and exclusion of other causes of alveolar hypoventilation. Most patients with obesity-hypoventilation syndrome also suffer from obstructive sleep apnea, which must be treated aggressively if identified as a comorbid disorder. Therapy of obesity-hypoventilation syndrome consists mainly of weight loss, which improves hypercapnia and hypoxemia as well as the ventilatory responses to hypoxia and hypercapnia. Avoidance of sedative-hypnotics, opioids, and alcohol is also recommended. NIPPV is helpful in many patients. Patients with obesity-hypoventilation syndrome have a higher risk of complications in the perioperative period, including respiratory failure, intubation, and heart failure. Recognition of these patients in the perioperative period is an important safety measure.
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