The normal thickness of the RV lateral wall measures less than 5 mm at end-diastole (1,2,3). RV hypertrophy is present when the RV lateral wall thickness exceeds 5 mm, indicating RV systolic pressure overload from elevated PA pressure, chronic pulmonary thromboembolism, RVOTO, or pulmonic stenosis (PS) (4). The inferior or lateral walls of the RV are the preferred locations for measurement since, in contrast to the anterior wall, they are not invested with as much epicardial fat that must be excluded from RV wall thickness measurement (5). The inferior wall of the RV is best assessed in TG views performed at 0°, whereas the RV lateral wall is best measured in the ME four-chamber view. Because the RV wall is thinner and more
trabeculated than the LV wall, precise measurements are more difficult to obtain. In patients with chronic cor pulmonale, the RV wall thickness may exceed 10 mm while intracavitary trabecular patterns become more prominent, particularly at the apex. Certain conditions are associated with RV wall thinning, such as RV myocardium infarction, Uhl syndrome, or arrhythmogenic RV cardiomyopathy. In the latter condition, the aneurysms occur most commonly in the anterior infundibulum, basal inferior wall, and apex. There are no accepted echocardiographic criteria to define an abnormally thin RV wall (3,6).

RV dimension is best estimated at end-diastole from an ME four-chamber view (Fig. 14.4). Care should be taken to obtain RV-focused image demonstrating its maximal diameter without foreshortening. This can be accomplished by making sure that the crux and apex of the heart are in view. Diameter >41 mm at the base and >35 mm at the midlevel indicates RV dilation. Similarly, longitudinal dimension, from the apex to tricuspid annulus, >86 mm indicates RV enlargement (2,3). RV dilation may be seen with RV volume or pressure overload. Normally, the RV end-diastolic cross-sectional area is approximately 60% of the area of the LV. As the RV dilates, its shape changes from triangular to round. In addition, the cardiac apex, which should be made up solely of the LV, may be equally shared between the ventricles or even dominated by the RV, indicating significant RV dilation. With mild RV dilation, the RV area is >70% of the LV area on two-dimensional (2D) imaging. With moderate RV dilation, the RV area may equal the LV area, and with severe RV enlargement, the RV area exceeds that of the LV (7).

The analysis of interventricular septum may provide useful insights into RV pathology. Examination of interventricular septal motion can help distinguish RV volume overload from RV pressure overload. Normally, the interventricular septum functions as part of the LV and maintains a concave shape on the LV side throughout the cardiac cycle. As the RV dilates or becomes hypertrophic the septum flattens and paradoxical septal motion develops. Normally in systole, inward and outward motion of all the walls of the LV will be seen in systole and then in diastole. If there is an opposite motion of the interventricular wall during diastole, the term paradoxical motion is used. It can be seen in an ME four-chamber view or the TG midpapillary view. The eccentricity index, a measure of septal curvature, represents the ratio of the LV minor axis diameter (parallel to the septum) to its perpendicular axis. In normal subjects, the index is essentially one both at enddiastole and end-systole (Fig. 14.5 A,B). Acquired pressure overload situations such as pulmonary hypertension or pulmonary stenosis displace the interventricular septum toward the LV at end-diastole leading to a D-shaped LV with eccentricity index <1. The septal displacement reflects the pressure gradient between the two ventricles. In early stages of RV volume overload diastolic pressure in RV exceeds that in the LV thus pushing the septum toward LV cavity in diastole only (Fig. 14.5 C,D). With severe RV pressure overload, the LV exhibits a D shape in both diastole and systole (Fig. 14.5 E,F) (1,8).

Volumetric evaluation is commonly estimated by the right ventricular fractional area change (RVFAC) defined as (end-diastolic area – end-systolic area) / end-diastolic area × 100 assessed from the ME fourchamber view. Diagnosis of RV dysfunction is made by RVFAC <35% and its severity can be described as mild, moderate, or severe for values of 25% to 35%, 18% to 25%, and ≤18%, respectively (Fig. 14.6) (1). A limitation of this approach is that RVFAC does not examine contribution of the RV outflow tract that corresponds to approximately 20% of the ejected RV volume.

Tissue Doppler peak velocity at the tricuspid annulus (S’) (Fig. 14.9) <9.5 cm/s is a sign of RV dysfunction as it represents the basal RV lateral wall function. RV acceleration during isovolumic acceleration (IVA) is also measured by TDI at the lateral tricuspid annulus. RVIVA is defined as the peak isovolumic myocardial velocity divided by time to peak velocity. This parameter is rate dependent and appears to be less load dependent than RVMPI. Value <2.2 m/s² is considered to be related to RV dysfunction.

Early- and late-filling wave velocities (E- and A-wave, respectively) and E deceleration time recorded by PWD in the TTF and the lateral tricuspid annulus velocity during early filling (E’) recorded by TDI allows diastolic categorization of RV function. A tricuspid E/A ratio <0.8 suggests impaired relaxation, a tricuspid E/A ratio of 0.8 to 2.1 with an E/E’ ratio >6 or diastolic flow predominance in the hepatic veins suggests pseudonormal filling, and a tricuspid E/A ratio >2.1 with a deceleration time <120 ms suggests restrictive filling (see Fig. 14.10) (11).

Deformation indices such as strain and strain rate have been shown to be useful parameters for estimating RV global and regional systolic function (2). Longitudinal strain is a percentage of systolic shortening of the RV lateral wall that should be measured in the RV-focused ME four-chamber view. This measurement is still dependent on RV loading conditions, RV size and shape. Peak global longitudinal strain of the RV lateral wall (also termed RV free wall strain in the literature) has been shown to be more sensitive and specific for detection of RV systolic dysfunction than other evaluation modalities (12). It has also been reported to have prognostic value in various disease states such as heart failure, acute myocardial infarction, pulmonary hypertension, and amyloidosis and to predict RV failure after LV assist device implantation. Current reference values have been published (2). Global longitudinal RV lateral wall strain >-20% is likely abnormal.

Three-dimensional (3D) echocardiographic RVEF is a global measure of RV systolic function and performance. This newer modality has been extensively validated against cardiovascular magnetic resonance (CMR) (2). It has been described as being of particular value in patients after cardiac surgery when conventional indices of RV function are generally reduced and no longer a real representation of the overall RV performance. The limitations of the 3D RVEF are load dependency, interventricular changes affecting septal motion (RV pacing), poor acoustic windows, and irregular rhythms. Keeping this in mind, the latest American Society of Echocardiography (ASE) guidelines on Chamber quantification published in 2015 recommend 3D RVEF as a method to quantify RV systolic function. An RVEF of <45% reflects abnormal RV systolic function. Limitation of 3D RVEF is that it is not available on real time in the most current TEE platform.

Examination of flow velocity patterns during phases of the cardiac cycle with PWD can contribute useful information about RV function. Normal hepatic flow is directed away from the liver to the RA and fluctuates during the cardiac cycle (Fig. 14.11C).

Normal hepatic venous flow patterns have four phasic components: AR corresponding to atrial reversal, S corresponding to ventricular contraction, translation of the tricuspid annulus toward RV apex, and D corresponding to early ventricular filling. Initial forward flow during systole is associated with atrial relaxation and apical movement of the TV during RV systole and corresponds to the x-descent in atrial pressure measurements. Subsequent diastolic flow, associated with early ventricular filling, corresponds to the y-descent. Two small retrograde hemodynamic waves are often detectable, corresponding to atrial contraction at enddiastole (A) and at end-systole a small V-wave corresponding to the end-systolic phase prior to the y-descent.

Systolic flow is usually of higher velocity than diastolic flow. This correlates with the x-descent being normally more important than the y-descent. This is due to the downward motion of the tricuspid annulus during ventricular systole resulting in a rapid filling of the RA. In patients with RV dysfunction, decreased

TAPSE and/or TR during ventricular systole lead to a reduction of the velocity in systole (S) and to a systolic-to-diastolic ratio less than 1 (S/D <1) as shown in Figure 14.11H. In severe RV failure or TR, the S-wave appears to be completely reversed with backward flow in the hepatic veins during systole rendering negative systolic-to-diastolic ratio (S/D <0) as shown in Figure 14.11M (18).

Flow in the portal or splenic veins can be assessed using TEE (16) but more easily with transthoracic echocardiography (TTE). The splenic vein is a direct tributary of the portal vein and thus its assessment could provide the same information. Imaging of the portal vein is accomplished by means of a TG short-axis cut of the liver by turning the probe on the right side of the patient. A multiplane angle rotation of 90° to 120° leads to a craniocaudal plane of the liver. The portal vein is usually within a few centimeters of the transducer and the inferior vena cava (IVC) is usually not included in the same 2D view (Fig. 14.12). Alternatively, assessment of splenic vein flow can also be done with TG scanning. This view can be obtained by turning the probe to the left side of the body and by performing a multiplane angle rotation of 90°. This will bring the view close to the splenic hilum. In this view, venous blood will travel in the direction of the probe and the velocities measured during Doppler examination will be positive (Fig. 14.13A-C). An alternative view can be obtained. With the probe toward the posterior aspect of the body, the electronic rotation angle is maintained at 0°. From this position, the splenic vein is located anterior to the descending aorta. From this view, the venous flow will be traveling away from the probe and the Doppler signal produced will exhibit negative velocities (Fig. 14.13D-F). The success rate for portal flow assessment using TEE has
not been systematically studied but is believed to be as good or better than portal flow assessment based on clinical experience.