The right ventricle is located anterior to and wraps around the left ventricle. The entrance to the right ventricle is defined by the tricuspid annulus and the tricuspid valve leaflets. The exit is the right ventricular outflow tract and the pulmonary valve. In cross-sectional views, it has a crescent shape. In the apical four-chamber view of the echocardiogram, the right ventricle has a triangular shape. Anatomically from the anterior view with the free wall is removed, it resembles a check mark with the tricuspid valve at the entrance and the pulmonary valve at the exit. When the heart is viewed on chest x-ray, the right margin of the heart forms an acute angle with the diaphragm resulting in this region being called the acute margin of the heart. The acute marginal branches of the right coronary artery lie in this anatomic area. In contrast to the prolate ellipse shape of the left ventricle, the overall shape of the right ventricle defies traditional geometry.

In general, the right ventricle can be divided into three anatomic regions: the inlet, apical, and outlet regions. The inlet region consists of the tricuspid valve and its apparatus. The apical region of the right ventricle has several heavy trabeculations including the apically located moderator band and the septomarginal band. These prominent trabeculations are thick and distinguish the right ventricle from the less trabeculated left ventricle. The third region or outflow region is less trabeculated and leads to the pulmonary valve. From the frontal view, the outflow region of the right ventricle crosses the midline and situates itself to the left of the left ventricular outflow tract. This results in the left and right circulations crossing each other in the frontal plane—a feature that is not present in some congenital abnormalities such as transposition of the great arteries.

The interventricular septum is a part of all three regions of the right ventricle. It supports the apical region, the tricuspid valve apparatus, and the outlet region. It gives rise to papillary muscles and trabeculations and supports the outlet region. The interventricular septum is muscular except for the membranous portion of the septum. The membranous septum usually gives rise to the septal leaflet of the tricuspid valve. The upper regions of the interventricular septum support the pulmonary valve. The left side of the septum relates to the right cusp area of the aortic valve.

The right ventricle has two layers of myocardium in contrast to the left, which has three. The thin-walled right ventricle has an outer, subepicardial circumferential layer and an inner subendocardial longitudinal layer. The shape of the right ventricle and the muscle fiber arrangement make remodeling a challenge. These factors are especially important in clinical situations such as pulmonary hypertension and transposition of the great vessels in which the right ventricle faces pressures that can be in the systemic range.

The blood supply of the right ventricle consists of a conus branch, acute marginal branches, and, to a small degree, the posterior descending. The conus branch supplies the right ventricular outflow tract area and may continue and supply some of the interventricular septum. The acute marginal branches supply the free wall of the right ventricle. The posterior descending coronary artery supplies the surface of the right ventricle close to the interventricular groove. A proximal occlusion of the right coronary artery before the conus branch and the acute marginal branches can result in the serious right ventricular infarction syndrome in which there are high central venous pressures and low cardiac output.¹

Parameters used for measurement:

Evaluation of diastolic function of the right ventricle is similar to that of the left ventricle. Pulse wave analysis of the tricuspid inflow velocity profile sampled at the tips of the tricuspid leaflets produces E and A waves. Tissue Doppler analysis of the lateral tricuspid annular velocities also offers analysis of e′ and a′ values. Similar patterns to those on the left allow for identification of abnormal relaxation, pseudonormal filling, and restrictive filling. Usually, abnormal findings of these patterns are associated with significant findings in functional class and other findings such as a dilated right atrium, dilated inferior vena cava, hepatic vein flow abnormalities, and elevated pressures on the right.

Parameters that indicate abnormal relaxation include E/A ratio of <0.8 or e′/a′ <0.5. E/A ratio of 0.8 to 2.1 or e′/a′ of 0.5 to 1.9 suggests high filling pressures. E/e′ < 6 or diastolic flow predominance in the hepatic veins suggests pseudonormal filling, and E/A > 2.1 and e′/a′ > 1.9 and an abbreviated deceleration time <120 ms along with diastolic integrate flow in the pulmonary artery suggests restrictive filling.⁴

The right ventricle is designed to function by generating volume and not pressure. Abnormalities that result in pressure overload result in remodeling of the right ventricle in response to the imposed load. As the right ventricle changes shape, distorts the interventricular septum, and dilates the tricuspid annulus, coaptation of the tricuspid valve is compromised and tricuspid regurgitation results.

Elevations of right ventricular systolic pressure can occur in several clinical settings. Individuals with chronic obstructive lung disease, idiopathic pulmonary hypertension, pulmonary embolism, and systemic diseases such as systemic sclerosis and many others can result in elevations in pressures in the right ventricle and the pulmonary artery. Much interest has been present in recent years in measuring and estimating these pressures associated especially since a host of novel drugs are available to alter pulmonary vascular resistance.

The importance of carefully separating out primary elevations of pulmonary artery pressure from secondary elevations has become important. Elevations in left ventricular filling pressure or pulmonary artery wedge pressure >15 mm Hg changes the target of treatment from the pulmonary circulation to the left ventricle and the systemic circulation. Once this issue has been eliminated, focus can be directed to the pulmonary vasculature at rest and sometimes with exercise.

Echocardiography and right heart catheterization have played a major role in the diagnosis of pulmonary hypertension and in the treatment and follow-up of interventions. Measurements of the tricuspid regurgitation jet velocity along with estimation of right atrial pressure offer a noninvasive approach for estimation of right ventricular systolic pressure. Direct measurement of these pressures with Swan-Ganz catheters offers objective information for diagnosis and treatment of these conditions. Many standards have been set, but currently mean pulmonary artery pressures at rest of >25 mm Hg and mean pulmonary artery pressures with exercise >30 mm Hg define pulmonary hypertension. This assumes pulmonary capillary wedge pressure is <15 mm Hg. Pulmonary arterial resistance as measured in Wood units normally should be <2 units. Generally when pulmonary hypertension is present, the pulmonary vascular resistance is >3 Wood units. These standards have been outlined in recent publications.⁵,⁶

Examples of alterations of the right ventricle and estimations of right ventricular systolic pressure as estimated by echocardiography and Doppler techniques are illustrated in the following pages. It should be noted that in the absence of right ventricular outflow obstruction, pulmonary valve stenosis or stenosis within the pulmonary arteries right ventricular systolic pressure is the same as pulmonary artery systolic pressure.⁷