Pulmonary venous hypertension (PVH) develops secondary to any left-sided heart disease associated with increased left atrial pressures. The classic hemodynamic profile in PVH is an elevated pulmonary artery pressure associated with an elevated pulmonary capillary wedge pressure and left ventricular enddiastolic pressure. There are two basic mechanisms in the pathophysiology of the disease: a passive component and a reactive component. In the passive form, pulmonary hypertension is a reflection of the passive downstream trans mission of elevated left heart pressures into the pulmonary vascular system. In the reactive form, a dysregulation of vascular smooth muscle tone and structural remodeling occur in the pulmonary vascular leading to elevated pulmonary arterial pressures considered “out of proportion” to the degree of left-sided heart disease. The main objective in the evaluation of PVH is to differentiate it from other forms of pulmonary. The mainstay treatment of PVH is directed at the cardiac dysfunction, rather than targeting the elevated pulmonary artery pressures alone.
|Title of host publication
|PanVascular Medicine, Second Edition
|Springer Berlin Heidelberg
|Number of pages
|Published - Jan 1 2015
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)