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The right ventricle (RV) is a very unique chamber whose importance has been neglected in the past; hence, it is frequently given the name the “forgotten ventricle.” For many years, primary emphasis was placed on left ventricular (LV) physiology, thus overshadowing the study of the RV. In recent years more efforts have been made to describe and quantify RV function using transesophageal echocardiography (TEE) in ways useful to clinicians.1,2 Such efforts have been limited by the nongeometric, asymmetric shape of the chamber; its sequential contraction pattern; and the obscuring effect of epicardial fat on RV wall motion and thickness.

The RV is anatomically divided into two components: its inflow (sinus) and outflow (conus) portions, reflecting its dual embryonic origin. The inflow accommodates the tricuspid valve and extends toward the apex to include the trabeculated, posteroinferior segments, whereas the outflow portion, or infundibulum, accounting for up to 25% of the total right ventricular volume, is usually free of trabeculations and includes the anterosuperior segments, ending with the pulmonic valve. A muscular band, the crista supraventricularis, divides the inflow and outflow portions and is made up of the infundibular septum and the parietal band. A second set of intracavitary muscular bands, the septal and the moderator bands, is present in the right ventricle. The moderator band extends from the base of the anterior papillary muscle to the ventricular septum and should not be mistaken for a thrombus or intracavitary mass (see Chapter 6).35

Ventricular systolic ejection of the RV is in a peristaltic manner different from the twisting and rotational motions that predominate on the left side. Right ventricular contraction is sequential, beginning with the inlet portion contracting toward the apex and ending with the infundibulum. The ejection phase begins earlier and lasts longer, and the velocity profile is characterized by a lower and delayed peak.68 Ventricular interdependence is also a feature to be remembered in assessing RV (or LV) function. It is a term used to describe the dysfunction of one ventricle secondary to a disorder of the other, through direct mechanical interactions mainly due to the involvement of the interventricular septum and the constraint of the pericardium. Under normal conditions, the septum is concave toward the LV during the entire cycle. With RV pressure or volume overload, the interventricular septum (IVS) flattens or displaces toward the LV, impairing compliance and filling.9,10 Ventricular interdependence is not only diastolic but also systolic, mediated primarily by the interventricular septum. Animal studies have shown that approximately 20% to 40% of the RV systolic pressure and volume outflow of the RV results from LV contraction.9


Although the vast majority of information about the RV can be obtained from a small number of images, the chamber's complexity defies standardized description or ...

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