Thus, there was no basis on which to infer a difference in the structure of the pulmonary parenchyma. Differences between groups in variables marking hematopoietic effects of hypoxemia persisted. Hemoglobin and RBC mass per kilogram in the 13 matched NOD subjects remained nearly identical to values derived for the entire group of 36 and higher than those for the non-NOD subjects. The values for mean Pew and CO did not differ between groups. While the mean Ppa for the 13 matched NOD subjects did not differ significantly from the 13 non-NOD subjects (22.6 vs 20.4 mm Hg, respectively), PVR remained significantly higher (160 vs 102 dynes’sec’cm; p<0.0004) in the NOD group.
Hemodynamic changes during hypoxic and hyperoxic breathing for the 13 matched desaturators paralleled changes for the entire group (Fig 1, dashed-dotted line). Thus, despite similar daytime Pa02 levels and parameters of gas exchange, pulmonary hemodynamic (PVR) and hematopoietic (hemoglobin and RBC mass), measures of hypoxemia still differ between groups. This favors the hypothesis that nocturnal (and perhaps daytime) hypoxemia contributes to hemodynamic difference in these patients. review
Recurrent NOD may be an important factor in the development of the hemodynamic differences seen between the groups in this study. There are animal data supporting the concept that prolonged exposure to transient repetitive hypoxemia may lead to chronic pulmonary hypertension. As little as four hours per day of hypoxemia for 21 days elevated right ventricular pressures and weight in rats. In addition, studies in rats have shown right ventricular pressures remain elevated up to 16 hours after removal of an eight-hour transient hypoxic stimulus. It would be an oversimplification, however, to assume that 40 to 120 minutes (at most) per 24-hour period causes vascular smooth muscle hypertrophy through direct effects of vasoconstriction.
Category: Lung Disease
Tags: chronic lung disease, Pulmonary function, pulmonary vascular hemodynamics