The right ventricle (RV) is built to accommodate a large range in venous return and pump the blood through the pulmonary circulation. Left heart disease and several forms of pulmonary disease may lead to a tremendous increase in RV afterload (pulmonary hypertension). The RV adapts by hypertrophy and increasing contractility. However, when this adaptation falls short, the RV dilates and output declines. An unmet increase in oxygen demand, altered metabolism, fibrosis, neurohormonal dysregulation, inflammation and stiffening of the heart are implicated in the transition to right heart failure. This article describes the complex interplay between all these factors.
|Title of host publication||Reference Module in Biomedical Sciences|
|Publication status||Published - 2020|