Pulmonary Venous Hypertension and Edema

Abstract

Cardiogenic edema can be characterized in three phases: pulmonary venous hypertension, interstitial edema, and alveolar edema, each with different radiographic findings. Radiographic and clinical findings must be correlated to achieve an accurate diagnosis of pulmonary edema, as other causes of interstitial and airspace opacities can have overlapping appearances. Comparison with prior radiographs is extremely useful. Clinical information and the time course of findings should be considered to avoid misinterpretation. In the acute setting, pulmonary hemorrhage and diffuse pneumonia may manifest with bilateral perihilar consolidation and interstitial thickening. In the chronic setting, fibrosing interstitial lung disease may manifest with progressive basilar reticular opacities. Brain-type natriuretic peptide (BNP) is produced by cardiac myocytes. Serum levels are elevated in cardiogenic edema and can be used to support a suspected diagnosis of pulmonary edema at imaging. Although BNP can also be elevated in a variety of lung diseases, low BNP levels suggest a diagnosis other than cardiogenic pulmonary edema. Pulmonary edema is often diagnosed and monitored through noninvasive means, including BNP monitoring, clinical assessment, and imaging studies, rather than pulmonary artery catheterization. Treatment of cardiogenic edema usually involves medical therapy (inotropic agents and preload/afterload reduction) and ventilation support to improve oxygenation. Supportive devices such as intra-aortic balloon pumps can be used to stabilize patients with severe heart failure.