Factors affecting regional pulmonary blood flow in left heart valvular disease

The base to apex distribution of blood flow per unit of lung volume was assessed by pulmonary scintigraphy in 99 patients with rheumatic heart disease. The prevalent valvular lesion was mitral stenosis in 56, mitral regurgitation in 14, aortic stenosis in 11 and aortic insufficiency in 18. Each patient underwent hemodynamic assessment by cardiac catheterization within a few days of scintigraphic study. Some hemodynamic parameters were then correlated with the ratio between upper and lower third of lung scan (U:L ratio) taken as a numerical index of the base to apex distribution of lung blood flow. The U:L ratio had a positive correlation coefficient with the mean pulmonary wedge pressure (MPWP) but the dispersion of individual data was wide. Dividing the patients into groups according to the level of MPWP and to the location of U:L ratio either above or below the regression line, variance analysis showed that a highly significant part of this dispersion can be accounted for by pulmonary vascular resistance (PVR). The same conclusion was reached using different statistical approaches. These findings suggest that inversion of pulmonary blood flow is not only associated with elevation of MPWP and increase of vascular resistance in the dependent lung zones but also with a rise in the general PVR. Furthermore, the cardiothoracic ratio, as index of the heart size relative to the chest cage and, therefore, of the parenchymal compression in the lower lung zones, also proved statistically and at the individual level responsible at least in part for this dispersion. Considering these multiple influences on the regional distribution of lung blood flow in these cardiac patients, a very close correlation between U:L ratio and MPWP is not to be expected. Consequently, an estimate of MPWP from U:L ratio is open to great uncertainties. Furthermore, our data show that, at the same level of MPWP, U:L ratio is higher when PVR is higher. This observation means that PVR increases and pulmonary perfusion inversion develops to some extent independently from the actual value of MPWP. We then suggest that water filtration in the lung interstitium may be ruled out as a factor responsible per se for these changes and can only be retained as a mechanism initiating them. We postulate that functional and pathologic changes in the lung vessels and interstitium may develop on the basis of a different individual response to a given stimulus. © 1974.