Pulmonary Vascular Hemodynamics in Chronic Lung Disease Patients: Discussion

Pulmonary Vascular Hemodynamics in Chronic Lung Disease Patients: DiscussionThe goal of this study was to determine whether there were differences in parameters of cardiopulmonary function between two subsets of patients with chronic lung disease. Since the predominant lung disease pattern was obstructive, FEV! was chosen as a parameter for matching groups. Numerous studies show that in obstructive lung disease, FEVi correlates with clinical symptomatology, survival, and to some degree, pulmonary hemodynamics.

Patients who had restrictive components along with their obstructive disease were not excluded as patients from the study because NOD has been demonstrated in patients with pure restrictive disease as well as COPD. However, by smoking history, symptoms, and spirometry, the predominant disease was chronic airway obstruction in 35 of 36 NOD subjects and all nonNOD subjects. Because blood gas values, pulmonary function studied, and mechanism of pulmonary hemodynamic abnormalities may differ between chronic obstructive and restrictive diseases, all variables in those subjects with COPD alone vs those with COPD and evidence of restriction were examined to be sure these were not disparate populations. The group with pure obstruction (n = 24) did not vary from the group with COPD and restriction (n = 12) with respect to body morphometry, blood gas values, hemoglobin, Deo percent predicted, or any of the hemodynamic variables. The 12 “restrictive component” patients did have a slightly higher FEV! (1.58 vs 1.2 L, p<0.04), and FEV/FVC ratio (0.60 vs 0.40, p<0.005). itat on
Both NOD and non-NOD groups had daytime awake Pa02 levels above 60 mm Hg and were separated only by the presence NOD. However, distinct differences in oxygenation emerged. The daytime resting Pa02 was about 12 mm Hg higher in the non-NOD group. This appears to be due to a more significant disturbance in gas exchange in the NOD subjects based upon lack of evidence of hypoventilation (Table 1), a wider P(A-a)02 and a lower a/A ratio in that group. The Deo values did not differ significantly between groups. This similarity in parameters of pulmonary dysfunction (other than gas exchange) between the two groups agrees with previous observations. Furthermore, the difference in resting gas exchange may indicate a greater propensity to desatu-rate during REM sleep. Proposed mechanisms of NOD include acute deterioration of gas exchange as a contributing factor.

Category: Lung Disease

Tags: chronic lung disease, Pulmonary function, pulmonary vascular hemodynamics