Nocturnal oxyhemoglobin desaturation (NOD) associated with rapid-eye-movement (REM) sleep is described in patients with COPD, interstitial lung disease, and various diseases of the chest wall.’ This nocturnal fall in saturation (Sa02) is believed to result from a combination of hypoventilation and gas exchange abnormalities. It is accompanied by transient elevation of pulmonary artery pressure and may be reversed with the use of supplemental oxygen. Such repetitive desaturations have been proposed as a cause of chronic pulmonary hypertension. At this time however, there is neither evidence that REM sleep related NOD causes chronic pulmonary hypertension nor that the two are even associated. other
This is an important clinical question because of the demonstrated benefits of home oxygen in prolonging life and improving pulmonary hemodynamics in hypoxemic COPD patients. In most patients with NOD and daytime hypoxemia (Pa02<55 mm Hg), nocturnal hypoxemia will be adequately treated when home supplemental oxygen is prescribed. However, possible benefit from supplemental oxygen during sleep for patients with chronic lung disease and NOD, but daytime PaOz levels above that traditionally used to prescribe home oxygen remains an intriguing possibility. One question to be asked is whether or not end organ evidence of chronic hypoxemia is associated with recurrent NOD. To answer this, we examined a variety of laboratory and cardiopulmonary variables including supine hemodynamics in a group of patients with lung disease and a daytime Pa02>60 mm Hg who showed REM sleep NOD. We compared these to data from an equivalent group of patients with similar symptoms and pulmonary dysfunction (spirometry, plethsmography, carbon monoxide diffusion) but without evidence of NOD on polysomnographic sleep study.
Category: Lung Disease
Tags: chronic lung disease, Pulmonary function, pulmonary vascular hemodynamics