From the archives of the AFIP - Pulmonary vasculature: Hypertension and infarction

Pulmonary hypertension is the hemodynamic consequence of vascular changes w ithin the precapillary (arterial) or postcapillary (venous) pulmonary circu lation. These changes may be idiopathic, as in primary pulmonary hypertensi on or pulmonary veno-occlusive disease, but more commonly they represent a secondary response to alterations in pulmonary blood flow. The pulmonary an d systemic bronchial circulations form broad anastomoses that largely preve nt infarction except in settings of markedly elevated pulmonary venous pres sure, underlying malignancy, or excessive embolic burden. Causes of precapi llary pulmonary hypertension include long-standing cardiac left-to-right sh unt, chronic thromboembolic disease, and widespread pulmonary embolism aris ing from intravascular malignant cells, parasites, or foreign materials. Th e classic radiologic features of precapillary pulmonary hypertension are ce ntral arterial enlargement, sharply pruned peripheral vascularity, and righ t-sided heart hypertrophy and chamber dilatation. Post-capillary pulmonary hypertension may develop secondary to focal venous constriction or to compr omised pulmonary venous drainage due to left atrial neoplasia, mitral steno sis, or left ventricular failure. Radiologic manifestations of postcapillar y pulmonary hypertension include prominent septal lines, small pleural effu sions, and occasionally air-space opacities. In addition, radiologic evalua tion of postcapillary pulmonary hypertension may demonstrate evidence of pu lmonary arterial hypertension, secondary to the retrograde transmission of elevated pulmonary venous pressure across the capillary bed.