Pulmonary vascular resistance in emphysema.

To assess the hemodynamic effects of pulmonary microvasculature disruption in emphysema, we examined resting pulmonary hemodynamics and lung function in 12 carefully identified patients with type A chronic obstructive pulmonary disease. Individuals with respiratory muscle weakness and intercurrent infection were excluded. Standard spirometry, helium dilution lung volumes, and single-breath carbon monoxide diffusing capacity (DCOSB) were obtained within 24 h of right heart catheterization. Resistance to pulmonary blood flow was assessed using the difference between pulmonary arterial (PA) diastolic and mean wedge pressures, and expressed as the pulmonary diastolic gradient (PDG). Mean FEV1/FVC was 51 +/- 8 percent, RV/TLC was 48 +/- 11 percent, DCOSB percent predicted was 62 +/- 29 percent, PaO2 was 72 +/- 11 mm Hg (FIO2, 0.21), and PaCO2 was 39 +/- 5 mm Hg. Mean PDG was 5 +/- 3 mm Hg (normal < or = 3 mm Hg) with normal PA pressures, indicating mildly elevated resistance to pulmonary blood flow. The PDG correlated most closely with DCOSB, rising in curvilinear fashion as DCOSB fell (r = -0.869, p < 0.001). These observations were compared with our previous report of analogous findings in patients with chronic, diffuse interstitial lung disease (ILD). In that group, PDG also increased curvilinearly as DCOSB fell (r = -0.839, p < 0.001). Subjects with FVC greater than 50 percent predicted had elevated PDG with normal pressures, while those with FVC less than 50 percent had pulmonary hypertension. The regression of PDG on DCOSB was strikingly similar to emphysema, although the slope in emphysema was less than that in ILD (p < 0.001). These observations suggest that elevated pulmonary vascular resistance in emphysema stems from disruption of the microcirculation in a fashion similar to that encountered in mild-moderate ILD. However, the magnitude of increase is not sufficient to generate resting pulmonary hypertension in the absence of disturbed gas exchange.