Volume overload and the right heart

Right ventricular (RV) volume overload can be seen as an isolated or predominant abnormality in the presence of right-sided valvular (tricuspid and/or pulmonary) regurgitation, or in pre-tricuspid systemic-to-pulmonary shunts (atrial septal defect and/or partial anomalous pulmonary vein drainage). From a macroscopic and functional perspective, compensated RV volume overload is typically characterized by RV dilatation and hypertrophy (normal free wall thickness but increased mass), preserved RV ejection fraction, and predominantly diastolic septal flattening resulting in left ventricular (LV) underfilling and reductions in LV diastolic volume with preserved or mildly reduced LV ejection fraction. The molecular biology of RV volume overload and the mechanisms eliciting the transition from a compensated to decompensated state are not well characterized and may resemble to some extent those in RV pressure overload, which has been much more extensively studied. Isolated RV volume overload has a remarkably benign clinical course when compared with pressure overload, and may be well tolerated with no symptoms for decades. However, there is extensive evidence that eventually decompensation does occur, with development of severe RV dilatation and systolic dysfunction as well as right-heart failure, which are associated with increased morbi-mortality. If the patient is symptomatic, percutaneous or surgical repair of the underlying cause of RV volume overload is indicated. In the absence of symptoms, monitoring the development and degree of RV dilatation and/or systolic dysfunction with serial imaging plays an important role in triggering these interventions, because late repair may lead to irreversible changes in RV performance and impaired clinical outcomes.