Right ventricular function in pulmonary hypertension: physiological concepts

Abstract

The symptoms of pulmonary hypertension are explained by a decrease in cardiac output caused by an afterload-induced right ventricular (RV) failure. However, the standard haemodynamic evaluation of pulmonary hypertension, with measurements of mean pulmonary vascular pressures and cardiac output, does not capture the determinants of RV function. Right ventricular afterload can be measured either as a hydraulic load calculated from spectral analysis of pulmonary artery pressure and flow waves, or as a maximal wall tension estimated from instantaneous ventricular pressure, volume, and wall thickness measurements. The adequacy of ventricular adaptation to afterload can be assessed by a measurement of the matching of systolic function to arterial elastance. The difficulty in measuring instantaneous RV volume is overcome using a single-beat method, which derives a systolic pressure–volume relationship from instantaneous RV pressure and an integration of pulmonary arterial flow. On such a pressure–volume curve, it is easy to determine graphically end-systolic elastance ( E es, end-systolic pressure on end-systolic volume), as a load-independent measure of contractility, and arterial elastance ( E a, end-systolic pressure on stroke volume), as a measure of afterload. The optimal value of the E es/ E a ratio, compatible with flow output at a minimal energy cost, is between 1 and 2. Patients with severe pulmonary hypertension present with a decreased elastance ratio, in spite of an adaptative increase in systolic function, which underscores that RV failure in the face of increased afterload is a relative notion. Further studies are needed to confirm that right ventriculo-arterial decoupling accounts for a decreased aerobic exercise capacity by a limitation of cardiac output adaptation to peripheral demand.