What are the long-term consequences of elevations in PVP?

Pulmonary hypertension. The typical pathologic change associated with left-heart-related pulmonary hypertension is medial thickening due to vascular smooth muscle hypertrophy and/or hyperplasia. Pulmonary parenchymal abnormalities may also be seen, especially in advanced mitral stenosis. These include alveolar wall thickening, fibrosis, hemosiderosis, and even parenchymal calcification.

Can other classes of cardiac disease alter the pulmonary vasculature?

Congenital heart disease with left-to-right shunting will affect the pulmonary vasculature by causing large increases in pulmonary blood volume and flow. These diseases include atrial septal defects, ventricular septal defects, patent ductus arteriosus, and anomalous pulmonary venous return. The increased flow seen with these lesions may ultimately cause pulmonary hypertension. Ultimately, patients may develop pulmonary vascular resistance sufficiently high that shunt flow equalizes or reverses to right-to-left (Eisenmenger’s syndrome).

What are the pleural manifestations of cardiac disease?

Normally, a thin layer of fluid exists between the visceral and parietal pleura. Net filtration is favored by Starling forces into the pleural space from the parietal pleura, but the visceral pleura absorbs the fluid to prevent its accumulation. However, increased hydrostatic pressure as in heart failure results in a transudative pleural effusion. The parietal pleura is supplied by the systemic circulation, so any increase in systemic venous pressure, as occurs in right-heart failure, promotes increased fluid formation. The visceral pleural is supplied by the pulmonary circulation, so any increase in pulmonary pressure, as in left heart failure, impedes fluid resorption.

Effusions from heart failure are usually bilateral, but when unilateral, they occur more frequently on the right side.

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