Right Ventricular-Pulmonary Vascular Interactions

Abstract

Accurate and comprehensive evaluation of right ventricular (RV)-pulmonary vascular (PV) interactions is critical to the assessment of cardiopulmonary function, dysfunction, and failure. Here, we review methods of quantifying RV-PV interactions and experimental results from clinical trials as well as large- and small-animal models based on pressure-volume analysis. We conclude by outlining critical gaps in knowledge that should drive future studies.

FIGURE 1.

Schematic of the relationship between supply and demand of right ventricular-pulmonary vascular unit Schematic of pressure and flow supply vs. demand showing the main contributors of right ventricular-pulmonary interactions including supply-side determinants: right ventricular dimensions and geometry, myocyte mechanics, and right ventricular preload; and demand-side determinants: pulmonary vascular compliance, which is dependent on transmission and modulation of pressure waves through large and small pulmonary arteries and pulmonary vascular resistance, which is dependent mostly on small arterial caliber and tone. Heart rate and left ventricular function are not shown.

FIGURE 2.

Elastances derived from pressure-volume loops Pressure-volume loops showing the calculation of effective arterial elastance and end-systolic elastance by decreasing preload such as by inferior vena cava occlusion.

FIGURE 3.

Methods for approximating ventricular vascular coupling in clinical studies Comparison of the single-beat method (A) and the volume method (B) for the approximation of ventricular vascular coupling (VVC).

FIGURE 4.

Evolution of right ventricular response to PAH Changes in idealized pressure-volume loops with increases in afterload and RV dilatation (A) and representative pressure-volume loops (B) from mice with PAH and RV dilatation via chronic hypoxia (Hy) and hypoxia+sugen (HySu) acute decreases in preload to obtain E_es.