This can be attributed to the large individual night-to-night variability in levels of desaturation and amount of REM sleep which we have seen in such patients. Only one night (post acclimation) of sleep data was used to test these correlations in the present study. We in no way imply that one, two, or even three nights in the sleep lab are representative of the degree of desaturation present in the home setting. Because of EEG wiring and other manipulations for collecting data and the unfamiliar setting of the sleep laboratory, it is likely that the amount of REM sleep and the degree of desaturation only loosely approximate actual sleep events at home. other
These data are the first to indicate that there is a difference in cardiopulmonary hemodynamics between patients with chronic lung disease and NOD and those without NOD. The implications are important in establishing the clinical significance of transient NOD in such patients. First, there is no doubt that pulmonary hypertension is a progressive disease. Weitzenblum et al have demonstrated a 3.3 mm Hg increment in Ppa over 60 months in 32 untreated COPD patients whose initial Ppa was greater than 20 mm Hg. Second, Reid has recently summarized data in animals and man indicating that pulmonary hypertension initially associated with constriction (hypoxia) will ultimately result in histologic structural changes of either muscular hypertrophy or alveolar wall vessel destruction. This author indicates that by the time a patient develops symptoms of pulmonary hypertension (eg, cor pulmonale), efforts at reversing constriction will only be palliative. Finally, recent publications have demonstrated some degree of long-term improvement in pulmonary hemodynamics in patients with hypoxemic chronic lung disease treated with continuous home oxygen. The latter data taken in conjunction with improved survival in the NOTT and British Medical Research Council trial suggest that there is potential reversibility of abnormal cardiopulmonary hemodynamics as well as increased longevity with the use of supplemental oxygen. The question remains whether supplemental oxygen used to reverse the transient hypoxemia at night would improve pulmonary vascular resistance or delay the onset of pulmonary hypertension in transient desaturationbefore continuous daytime hypoxemia below 55 mm Hg develops. The results of this study support the need for continued examination of this question.
Category: Lung Disease
Tags: chronic lung disease, Pulmonary function, pulmonary vascular hemodynamics