One could postulate additional periods other than nocturnal desaturation or an intermediate step active even when Sa02 is at baseline. Eicosanoids including arachidonic acid, leukotrienes, thromboxanes, and prostaglandins are potent vasoconstrictors and may be elaborated by aggregated platelets or leukocytes. Perhaps transient hypoxemia induces deposition of platelets in the pulmonary arteriolar endothelium which leads to release of one or more of the above mediators and smooth muscle hypertrophy. One study has demonstrated decreased platelet survival in hypoxemic COPD patients and correction of survival with supplemental oxygen.
Alternatively, transient decreases in Sa02 may not be limited to sleep. Continuous monitoring of Sa02 in the awake patient may demonstrate that substantial decreases in Sa02 occur during coughing, micturation, defecation, eating, and exercise. fully
Based upon the present data, a gradual decline in daytime Pa02 cannot be ruled out as a factor contributing to the elevated Ppa. However, to our knowledge, a daytime Pa02 in the range of 60 to 70 mm Hg has not been associated with increased hemoglobin or RBC mass. It is doubtful that elevated levels of carboxyhemoglobin contributed to this difference because the same proportion (about two thirds) of subjects in both groups were smokers at the time of study. Previous authors have demonstrated some correlation between daytime Sa02 and Ppa in groups of COPD patients which include those with severe awake hypoxemia. However, studies restricted to patients who are not severely hypoxemic (Sa02>90 percent) do not demonstrate this correlation. Using linear regression, we were unable to show a substantial correlation between the average daytime Pa02 and Ppa in this group of patients. However, we were also unable to show a substantial correlation between various parameters of NOD and the level of daytime pulmonary hypertension.
Category: Lung Disease
Tags: chronic lung disease, Pulmonary function, pulmonary vascular hemodynamics