Right Ventricular Hypertrophy

Excerpt

Right ventricular hypertrophy (RVH) is an abnormal enlargement or pathologic increase in the right ventricular muscle mass as a maladaptive response to chronic pressure overload. RVH most commonly arises from chronic, severe lung disease. The right ventricle is considerably smaller than the left in the normal heart, producing electrical forces largely obscured by the larger left ventricle. By comparison, RVH leads to right axis deviation (RAD) and reversal of the normal R wave progression in the precordial leads. Pulmonary hypertension of any cause and tricuspid valve conditions, commonly regurgitation, often lead to right ventricular impairment.

Anatomy of the Right Ventricle

The right ventricle's complex geometry poses function assessment challenges. A thorough evaluation necessitates diverse imaging planes and acoustic windows due to the differences between the structures and functions of the right and left ventricles. These ventricles originate from separate embryonic origins. The left ventricle arises from the heart tube, whereas the right ventricle derives from the anterior heart field.

The right ventricle comprises inflow (sinus) and outflow (conus) regions, separated by a muscular ridge, the crista supraventricularis. The inflow region includes the tricuspid valve, chordae or papillary muscles, and right ventricular body. The right ventricle's free wall forms its boundaries, extending from the anterior and posterior aspects of the interventricular septum. The standard septal curvature forms a convexity toward the right ventricular cavity and imparts a crescent shape to the ventricle when cross-sectioned. The right ventricle's interior surface is heavily trabeculated. This feature, along with the moderator band and more apical insertion of the tricuspid valve's annulus, imparts key morphologic differences distinguishing the right from the left ventricle on echocardiography. The infundibulum is the right ventricle's smooth, funnel-shaped outflow portion ending at the pulmonic valve.

A standard RV free-wall thickness of 0.3 to 0.5 cm imparts a greater distensibility and larger cavity volumes in the right than the left ventricle due to lower end-diastolic filling pressures. Thus, the right ventricle's ejection fraction is typically 35% to 45%—less than the left ventricle's 55% to 65%—though both chambers generate identical stroke volumes.

Physiology of Right Ventricle

Preload, afterload, and intrinsic contractility abnormalities can cause ventricular dysfunction. Muscle fiber orientation variations in the right ventricle determine its symmetrical shortening in the longitudinal and radial planes. Longitudinal shortening contributes significantly more to ejection than in the left ventricle. The pronounced right ventricle shortening along the longitudinal axis facilitates systolic function measurement using straightforward techniques that avoid geometric assumptions or meticulous endocardial definition, addressing limitations in noninvasive assessment.

Key features distinguishing right from left ventricular physiology include a 2-layered muscle (instead of 3), resulting in longitudinal shortening, heightened sensitivity to pressure overload (as opposed to volume overload seen the left ventricular dysfunction), lower energy requirements for maintaining stroke volume, greater reliance (50%) on direct oxygen extraction from intraventricular blood rather than coronary blood flow, shorter action potential duration, and greater density of adrenergic and cholinergic receptors compared to the left ventricle. The predominantly longitudinal shortening leads to longitudinal motion instead of the wringing torsional motion observed in the left ventricle. Due to its thinner wall, the right ventricle is more susceptible to minor changes in pulmonary vascular resistance (PVR). Chronic pressure overload can induce RVH, ultimately progressing to right ventricular failure if left untreated.