Radiographics 2000 Mar-Apr;20(2):491-524; quiz 530-1, 532
From the archives of the AFIP: pulmonary vasculature: hypertension and
infarction.
Frazier AA, Galvin JR, Franks TJ, Rosado-De-Christenson ML.
Pulmonary hypertension is the hemodynamic consequence of vascular changes within
the precapillary (arterial) or postcapillary (venous) pulmonary circulation.
These changes may be idiopathic, as in primary pulmonary hypertension or
pulmonary veno-occlusive disease, but more commonly they represent a secondary
response to alterations in pulmonary blood flow. The pulmonary and systemic
bronchial circulations form broad anastomoses that largely prevent infarction
except in settings of markedly elevated pulmonary venous pressure, underlying
malignancy, or excessive embolic burden. Causes of precapillary pulmonary
hypertension include long-standing cardiac left-to-right shunt, chronic
thromboembolic disease, and widespread pulmonary embolism arising from
intravascular malignant cells, parasites, or foreign materials. The classic
radiologic features of precapillary pulmonary hypertension are central arterial
enlargement, sharply pruned peripheral vascularity, and right-sided heart
hypertrophy and chamber dilatation. Postcapillary pulmonary hypertension may
develop secondary to focal venous constriction or to compromised pulmonary
venous drainage due to left atrial neoplasia, mitral stenosis, or left
ventricular failure. Radiologic manifestations of postcapillary pulmonary
hypertension include prominent septal lines, small pleural effusions, and
occasionally air-space opacities. In addition, radiologic evaluation of
postcapillary pulmonary hypertension may demonstrate evidence of pulmonary
arterial hypertension, secondary to the retrograde transmission of elevated
pulmonary venous pressure across the capillary bed.
