Pressure Overload and Right Ventricular Failure: From Pathophysiology to Treatment

Abstract

Right ventricular failure (RVF) is often caused by increased afterload and disrupted coupling between the right ventricle (RV) and the pulmonary arteries (PAs). After a phase of adaptive hypertrophy, pressure-overloaded RVs evolve towards maladaptive hypertrophy and finally ventricular dilatation, with reduced stroke volume and systemic congestion. In this article, we review the concept of RV-PA coupling, which depicts the interaction between RV contractility and afterload, as well as the invasive and non-invasive techniques for its assessment. The current principles of RVF management based on pathophysiology and underlying etiology are subsequently discussed. Treatment strategies remain a challenge and range from fluid management and afterload reduction in moderate RVF to vasopressor therapy, inotropic support and, occasionally, mechanical circulatory support in severe RVF.

Keywords: adaptive hypertrophy; echocardiography; hemodynamics; maladaptive hypertrophy; pressure–volume loops; right heart failure; right ventricular failure; right ventricular–pulmonary artery coupling; therapy.

Figure 1

RV pressure–volume loops generated during progressive preload reduction (progressive occlusion of the inferior vena cava (IVC) with a balloon). The blue points indicate the maximal pressure/volume ratio (=end-systolic elastance, or E_es) of each loop, and the green line shows the linear regression of the relationship between volume and pressure at all E_es (end-systolic pressure–volume relationship) to assess contractility. Adapted with permission from Tello et al., BJP 2019, John Wiley and Sons (Hoboken, NJ, USA). [16] Copyright © 2019, John Wiley and Sons.

Figure 2

(A). RV pressure–volume loops model demonstrating stroke volume reduction with the increase in arterial elastance (E_a) (E_a1 > E_a2 > E_a3) at constant preload (unchanged end-diastolic volume) and constant contractility (linear relationship between all E_es); RV-PA coupling decreases from E_a1 to E_a3. (B). RV pressure–volume loops model with increasing contractility (E_es1 > E_es2 > E_es3) in response to increasing arterial elastance (E_a1 > E_a2 > E_a3). In this model, stroke volume increases, indicating better coupling with E_es3/Ea3 than with E_es1/E_a1. E_a = arterial elastance; EDV = end-diastolic volume; E_es = end-systolic elastance.

Figure 3

Pathophysiology of RV failure with pressure overload. Red frames indicate adverse events leading to RV failure. Green frames indicate adaptive events improving hemodynamics. Orange frames indicate maladaptive events leading to compensated RV failure. Red labels with white script indicate treatment targets in RV failure. SV, stroke volume; CO, cardiac output; RV, right ventricle; LV, left ventricle.