The right ventricle: anatomy, physiology and clinical imaging

Not long ago the right ventricle (RV) was considered an “unnecessary” part of the normal circulation. While factually correct—ablation or replacement of the RV free wall can be well tolerated by experimental animals without reduction in cardiac output, and many surgical algorithms for congenital heart diseases culminate in a circulation devoid of a sub-pulmonary ventricle, a Fontan procedure, for example—it is clear that such circulations are far from normal. Furthermore, recent studies consistently demonstrate a central role for RV dysfunction in the prognosis and outcomes for a wide variety of acquired and congenital cardiac conditions. Consequently there has been a renewed interest in the singular role of the RV, as well as its influence on global function via biventricular interactions. In this review, we will discuss some of the challenges encountered in the measurement of RV volume and function in the context of the RV’s unique anatomic structure and physiology. The role of both ventricles is to propel blood forward in the circulation. To enable this mechanical role, ventricular function is intimately related to ventricular structure. However, the two ventricles differ. Morphologically, the RV is distinguished from the left ventricle (LV) by having coarser trabeculae, a moderator band, and a lack of fibrous continuity between its inlet and outflow valves. In the RV the pulmonary valve sits on a freestanding muscular infundibulum and the crista supraventricularis courses between it and the tricuspid valve to aid free wall contraction toward the interventricular septum. Because it normally operates at a lower pressure than the LV, the RV has a thinner wall. Its septal contour is indented by the dominant LV, producing a shape that is difficult to model geometrically (fig 1). Figure 1 Three dimensional reconstructions of the right ventricle (RV) illustrating its complex shape in a normal subject (A). RV remodelling in diseased hearts can result in profound shape change, as in this patient (B) with dilated RV due to severe pulmonary regurgitation following repair of tetralogy of Fallot. The mesh surface is the left ventricle. LV, left ventricle; P, pulmonary valve; RV, right ventricle; T, tricuspid valve. See Sheehan and Bolson14 for explanation of reconstruction method. Nearly all studies of ventricular fibre structure were performed on the LV.1 Dissection studies showed that its fibres course …