Right Ventricular Hypertrophy

Excerpt

Right ventricular hypertrophy (RVH) is an abnormal enlargement or pathologic increase in muscle mass of the right ventricle in response to pressure overload, most commonly due to severe lung disease. The right ventricle is considerably smaller than the left ventricle and produces electrical forces that are largely obscured by those generated by the larger left ventricle.

Size and function of the right ventricle are adversely affected by the following:

1. Pulmonary hypertension with or without left ventricular dysfunction

2. Conditions that affect the tricuspid valve leading to significant tricuspid regurgitation (TR)

Anatomy and Physiology

The right ventricle is composed of inflow (sinus) and outflow (conus) regions, separated by a muscular ridge, the crista supraventricularis. The inflow region includes the tricuspid valve (TV), the chordae/papillary muscles as well as the body of the RV. The RV body boundaries are formed by the RV free wall, extending from the interventricular septum's anterior and posterior aspects. The standard septal curvature convexes toward the RV cavity and imparts a crescent shape to the right ventricle when cross-sectioned. The RV's interior surface is heavily trabeculated; this feature along with the moderator band and more apical insertion of the TV-annulus impart key morphologic differences that distinguish the RV from the LV by echocardiography. In contrast, the infundibulum is a smooth, funnel-shaped outflow portion of the RV that ends at the pulmonic valve. Thus, the RV has a complex geometry, with traditional RV free-wall thickness of 0.3-0.5 cm, imparting greater distensibility and larger cavity volumes in the RV versus the LV, despite lower end-diastolic filling pressures. This translates to an RVEF that is typically 35% to 45% (versus 55% to 65% in the LV) yet generates the identical SV as the LV.

Changes in preload, afterload, and intrinsic contractility of the ventricle influence the systolic function of the RV, like the LV. Differences in RV muscle fiber orientation dictate that the body of the RV shortens symmetrically in the longitudinal and radial planes; thus, longitudinal shortening accounts for a much larger proportion of RV ejection than in the LV. The relatively conspicuous RV shortening along the longitudinal axis can measure RV systolic function using uncomplicated techniques that do not require geometric assumptions or meticulous endocardial definition, both being known limitations to the noninvasive assessment of RV systolic function.