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The Physiologic Basis of Right Ventricular Echocardiography
The right ventricle (RV), which had been deemed the forgotten ventricle, is now recognized as a central player in cardiovascular function. Its physiology, shape, function, and coronary blood flow are complex and impose impediments to noninvasive imaging. This chapter reviews the physiology of the RV and describes echocardiographic, functional, and structural correlates.
The RV was first described as more than a passive conduit in 1616 by Sir William Harveyin, who recognized that the “right ventricle may be said to be made for the sake of transmitting blood through the lungs, not for nourishing them.” In the following centuries, studies focused on the left ventricle (LV) overshadowed studies of the RV. It was not until the 1970s when the RV became fully recognized as a key player in cardiovascular disease states, such as heart failure and pulmonary hypertension. In the final decades of the 20th century, standard two-dimensional (2D) transthoracic echocardiographic (TTE) imaging of the RV became a mainstay for its evaluation. Recently, advances in imaging modalities such as three-dimensional (3D) TTE have improved detection and characterization of RV pathophysiologic states.
Evaluation of the RV by echocardiography relies on knowledge of its anatomy and physiology and involves characterization of wall thickness, shape, ventricular cavity size, and regional and global contractile function. A complete RV examination includes both qualitative and quantitative parameters, including RV size, right atrial (RA) size, RV systolic function, and pulmonary hemodynamics.
Structure And Anatomy Of The Right Ventricle
The location of the right ventricle in the thorax as the most anterior cardiac structure places it retrosternally and in the near field of the ultrasound beam, thus limiting optimal echocardiographic imaging windows and resolution ( Fig. 28.1 , top right ). Several anatomic features distinguish the RV from the LV ( Table 28.1 ). These include (1) relative apical displacement of the tricuspid valve (TV) compared with the mitral valve (MV), (2) the presence of bands and coarse apical trabeculations, (3) the presence of more than three papillary muscles, and (4) a trileaflet TV with septal papillary muscle attachments.
Table 28.1
Comparison of Normal Right Ventricular and Left Ventricular Parameters
Adapted from Haddad F, et al: Right ventricular function in cardiovascular disease, part I: anatomy, physiology, aging, and functional assessment of the right ventricle, Circulation 117:1436–1448, 2008.
| Right Ventricle a | Left Ventricle a | |
|---|---|---|
| Structure | Thin compacta, heavily trabeculated cavity | Thicker compacta |
| Shape | Crescentic with triangular base | Truncated ellipse |
| End-diastolic volume | 75 ± 13 (49–101) | 66 ± 12 (44–89) |
| Mass, g/m 2 | 26 ± 5 (17–34) | 87 ± 12 (64–109) |
| Wall thickness, mm | 2–5 | 7–11 |
| Ventricular pressures, mm Hg | ||
| Systolic | 25 (15–30) | 130 (90–140) |
| Diastolic | 4 (1–7) | 8 (5–12) |
| RVEF, % | > 40-45 | > 50 |
| Ventricular elastance (Emax), mm Hg | 1.30 ± 0.84 | 5.48 ± 1.23 |
| Afterload resistance, WU | 0.88 (0.25–1.63) | 13.75 (8.75–20) |
| Stroke work index, g/m 2 per beat | 8 ± 2 | 50 ± 20 |
| Major vector of contraction | Longitudinal | Circumferential and longitudinal |
RVEF , Right ventricular ejection fraction.
Anatomically, the RV may be separated into three unique components: (1) the RV inlet, which consists of the TV, chordae tendineae, and papillary muscles (PMs); (2) the RV body, which is made up of the highly trabeculated apical myocardium; and (3) the smooth outlet conus (also known as the infundibulum). The positioning of the RV places its body as the most rightward cardiac structure and the end of the outflow tract as the most leftward. Therefore, a single 2D sector does not encompass the entire ventricle. The anterior location and thin walls of the RV mandate the use of the transducer with the highest available carrier frequency that permits adequate penetration. Most often, the use of higher frequencies, which are optimal for RV imaging, are less successful in imaging the left ventricle. Therefore, the RV tends to be imaged at suboptimal resolution (see Fig. 28.1 , top right ).
The RV inlet can be best imaged in the RV inflow (RVI) view (see Fig. 28.1 left, third from top ), which allows for visualization of the tricuspid annular plane and can be useful in identifying congenital lesions involving the annulus and the TV; these include prolapse, vegetations, and Ebstein anomaly. In most 2D TTE tomographic planes, only two of three of the TV leaflets are visualized, and multiple views are needed to adequately image all leaflets. In the RVI view, the anterior and either septal or posterior leaflets are best visualized, whereas the apical four-chamber (A4C) view (see Fig. 28.1 right, second from top ) allows observation and characterization of the anterior and septal leaflets.
The RV body can be fully imaged on 2D TTE. From a segmental point of view, it is also useful to divide the chamber into its respective anatomic walls (anterior, lateral, inferior, basal mid, and apical). This anatomic classification allows for localization of RV pathologic states, such as occlusion of the right coronary artery, which can result in localized right ventricular infarction ( Fig. 28.2 ). The thin but variable thickness of the walls is an additional factor in segmental susceptibility to ischemia and infarction. In the standard A4C view of the body of the RV, the basal wall, lateral wall (also known as the free wall), and apical segments are readily visualized, whereas the RVI view (see Fig. 28.1 left, third from top ) allows for visualization of the inferior wall of the RV and the anterior and posterior leaflets of the TV. The parasternal short-axis (PSAX) view at the base of the heart allows visualization of the right ventricular outflow tract (RVOT), along with the anterior and lateral cusps of the pulmonic valve (PV) (see Fig. 28.1 , left, third from bottom ).
Similar to the division of its walls, the trabeculations of the ventricle are subdivided into three anatomically distinct bands: parietal, septomarginal, and moderator. The crista supraventricularis (CSV) consists of the parietal band and the infundibular septum, and the septomarginal band is continuous with the moderator band ( Fig. 28.3 ). The CSV is an important anatomic marker of RV dimensions that also serves multiple other functions, including narrowing of the TV annulus during systole.
Unlike the LV, where the MV and aortic valve (AV) are in fibrous continuity, the TV and PV are anatomically separated by the ventriculoinfundibular fold, which creates a spatial boundary that may have physiologic significance. For example, endovascular infections can spread directly from the mitral to aortic valves (or vice versa), but this is much less common on the right side because of the presence of ventriculoinfundibular fold. The moderator band, when particularly complex, may also connote RV dysplasia.
The geometry of the right ventricle is also complex. Unlike the ellipsoid LV, the RV is triangular when viewed from the side and crescentic when viewed in cross section (see Fig. 28.1 , top right, and Table 28.1 ). This complex three-dimensional shape complicates the echocardiographic quantitation of RV size and ejection fraction (EF). Importantly, only the compact muscle layers of the ventricle should be included in this measurement, and the trabecular layer should be systematically excluded. Because the infundibulum can account for 25% to 30% of RV volume, awareness of its absence should attend the analysis of measurements of the RV body. Owing to the complex geometry of the RV when qualitatively evaluating RV size by 2D TTE, multiple complementary views should be considered before suggesting RV enlargement ( Fig. 28.4 ). Note that the image of the body of the RV in the four-chamber view often includes an outpouching that is a normal anatomic structure known as the acute margin of the heart . The American Society of Echocardiography (ASE) reference limits for normal RV linear dimensions in the A4C view are basal RV diameter, 2.5 to 4.1 cm; mid-RV diameter, 1.9 to 3.5 cm; and base-to-apex length, 5.9 to 8.3 cm. The normal RVOT proximal diameter is 2.1 to 3.5 cm, and the distal diameter is 1.7 to 2.7 cm. The normal end-diastolic areas indexed to body surface area for men and women are 5 cm/m 2 to 12.6 cm/m 2 and 4.5 to 11.5 cm/m 2 , respectively. The normal end-systolic areas indexed to body surface area for men and women are 2 to 7.4 cm/m 2 and 1.6 to 6.4 cm/m 2 , respectively. The normal end-diastolic volumes indexed to body surface area for men and women are 35 to 87 mL/m 2 and 32 to 74 mL/m 2 , respectively. The normal end-systolic volumes indexed to body surface area for men and women are 10 to 44 mL/m 2 and 8 to 36 mL/m 2 , respectively. ,
Echocardiographic measures of RV size are significantly different in men and women, as demonstrated in a study using 2D and 3D. In one study, the authors found that RV end-diastolic volume using 3D echocardiography was larger in men than women (129 ± 25 mL vs 102 ± 33 mL P < .01). , In our lab, we performed 3D measurements of the RV on 29 normal participants without known cardiovascular disease and found these to be more rational volumes as they are more similar to the LV volumes. Fig. 28.5 demonstrates how we measured RV volumes in our cohort. Given the irregular shape of the RV, 3D volume measurements may become the method of choice. We found the normal RV volume in a healthy cohort of adults was 100 ± 22 mL (52 ± 10 mL/m 2 ). In women, the volume was 79 ± 13 mL (45 ± 7 mL/m 2 ), and in men, the volume was 107 ± 20 mL (54 ± 10 mL/m 2 ) ( Table 28.2 ).
Table 28.2
Right Ventricular Three-Dimensional Volume and Strain (Two- and Three-Dimensional) in Our Normal Cohort
Data from the Research Cardiology Physiology Laboratory of the Health eHeart Study, Cardiovascular Research Institute, University of California-San Francisco, CA.
| All ( n = 29) | Women ( n = 7) | Men ( n = 22) | |
|---|---|---|---|
| 3D RV end-diastolic volume | 100 ± 22 | 79 ± 13 | 107 ± 20 |
| 3D RV end-systolic volume | 50 ± 18 | 45 ± 13 | 52 ± 19 |
| 3D RV end-diastolic volume index | 52 ± 10 | 45 ± 7 | 54 ± 10 |
| 3D RV end-systolic volume index | 26 ± 10 | 25 ± 6 | 27 ± 11 |
| 3D RV septal wall strain | 20 ± 7 | 20 ± 5 | 20 ± 8 |
| 3D RV free-wall strain | 28 ± 9 | 26 ± 6 | 28 ± 10 |
| 2D RV septal wall strain | 16 ± 3 | 16 ± 3 | 15 ± 3 |
| 2D RV free-wall strain | 28 ± 4 | 29 ± 3 | 28 ± 4 |
RV, Right ventricular.
In addition to RV function and dimensions, measurement of RV mass also poses a clinical challenge. The RV mass is one-sixth that of the LV, but its volume is larger, and the mass is asymmetrically distributed. RV wall thickness can be measured in diastole, from the subcostal view (using either M-mode or 2D TTE) or in the left parasternal view. Agitated saline or microbubble contrast may be helpful in measuring wall thickness by distinguishing the compact from the trabecular muscle. Standard practice calls for using RV free-wall thickness greater than 5 mm to define RV hypertrophy, but quantification of total RV mass has not been satisfactorily performed with 2D TTE. During normal loading conditions, the RV retains its crescentic shape. However, in the setting of pressure or volume overload because of ventricular interdependence, the RV may hypertrophy and become more circular or spheroid, whereas the LV may assume a crescentic shape. Such geometric transformations may alter the mathematical assumptions that are used in normally shaped hearts to extrapolate EF from linear dimensions to become particularly inaccurate once ventricular remodeling has occurred. 2D biplane measurements from apical views continue to provide accurate information about volume and function in this setting. A summary of some of the aforementioned challenges to assessing the right ventricle by transthoracic echocardiography are listed in Box 28.1 .
Box 28.1
Limitations of Two-Dimensional Echocardiographic Assessment of the Right Ventricle
RV, Right ventricular.
-
Anterior retrosternal position
-
Complex asymmetric shape
-
Poor demarcation of the RV endocardial border because of a heavily trabeculated inner contour
-
Difficult to image all portions of the RV in perpendicular views; separate inflow and outflow portions require visualization from separate views
-
Asymmetric distribution of RV mass
-
Load dependency
Right Ventricular Hemodynamics
As with the LV, RV function is based on preload, contractility, and afterload, and each of these will be sequentially discussed in the following sections.
Right Ventricular Preload
The RV has a thin wall and operates at low filling pressure, making it very sensitive to changes in preload. Physiologically, this sensitivity becomes apparent during exaggerated respiration or when pericardial restraint is increased. For this reason, the free wall of the RV, in the absence of pulmonary hypertension, collapses during states of cardiac tamponade. This collapse is in proportion to the elevation in intrapericardial pressure and is respirophasic, reflecting increased sensitivity to the waxing and waning of caval filling. This is in turn dictated by the respiratory cycling of the thoracic pump as it overcomes or succumbs to inflow obstruction imposed by elevated intrapericardial pressures. The LV has a thick wall and higher filling pressure, so it resists collapse from elevated intrapericardial pressures during early tamponade. As tamponade worsens, however, transmural pressure rises, and the LA may also phasically collapse.
Right Ventricular Contractility
A discussion of the contraction of the RV and its hemodynamic correlates is informed by considering the myocyte configuration unique to this thin-walled ventricle. There are two layers of muscle fibers in the RV wall (superficial and deep) with a complex overlapping pattern that forms a 3D network. The superficial muscle layer is parallel to the atrioventricular groove and the right coronary artery, whereas the deep fibers are longitudinally aligned from the base to the apex. The superficial RV fibers are continuous with those of the LV, resulting in continuity between the ventricles. The functional consequences of this continuous layer include coordination of the RV and LV, ventricular interdependence, and traction on the RV free wall caused by LV contraction.
Although the normal RV operates at lower pressure than the LV, the ventricles are connected in series, and their effective stroke volume must be equal. Many factors maintain this equality, including the pericardium (so-called fifth chamber), the interatrial and interventricular septa, and great veins and pulmonary veins (Dr. John Tyberg, personal communication). For echocardiographers, the motion and position of the interatrial septa during respiration is one among many examples of how small pressure and volume changes in the atria during the respiratory cycle are constantly modulating interventricular output.
The contraction of the RV occurs in a sequential fashion, beginning with the trabeculations and ending with the contraction of the conus, about 25 to 50 milliseconds apart. , During RV systole, the free wall moves inward, then the long axis shortens, and the base descends toward the apex. Because of the deeper longitudinal fibers, the RV shortens longitudinally more than it shortens horizontally, , which is different from the LV. A higher surface area–to-volume ratio of the RV allows for less inward motion than the LV for same volume ejected. In addition, bulging of the ventricular septum into the right ventricular cavity contributes to ejection.
The fiber orientation of the RV musculature makes the longitudinal vector of its contraction the most important; this is appreciated in real-time imaging by the highly visible descent of the RV base (also known as the movement of the tricuspid annulus toward the apex) that occurs during systole. This motion is best appreciated in the apical and subcostal views of the RV.
A first step in evaluating right ventricular contractile function is visual inspection of the real-time 2D echocardiogram. Because the wall of the RV is thin, careful adjustments of instrument gain and settings and judicious selection of transducers may be needed to accurately detect RV inward systolic motion or wall thickening. In addition, the RV is extremely sensitive to loading conditions. For example, a high pulmonary vascular resistance (afterload) may affect contractility and EF of the RV much more than it would impact the LV. Given that the RV and LV stroke volumes are identical in the absence of a shunt, a decrease in RV stroke volume may significantly decrease the preload of the LV ( Table 28.3 ), thus diminishing its volume and obscuring preexisting pathology as well as diminishing cardiac output. Therefore, it is important to note comprehensive RV hemodynamics in any complete echocardiographic assessment.
Table 28.3
Echocardiographic Measurements in Normal Control Participants and Patients With Cor Pulmonale Demonstrate the Reversal in Right and Left Heart Ratios With Chronic Pressure Overload
Modified with permission from Himelman RB, et al: Improved recognition of cor pulmonale in patients with severe chronic obstructive pulmonary disease, Am J Med 84:891–898, 1988.
| Control Participants | Cor Pulmonale | |
|---|---|---|
| Right ventricle/left ventricle | 0.6 ± 7 | 1.1 ± 0.6 |
| Right atrium/left atrium | 0.8 ± 0.3 | 1.3 ± 0.7 |
Pressure–volume loops are particularly helpful for understanding the complex interplay of RV hemodynamics as they contribute to RV function. The slope of the end-systolic pressure–volume relationship is defined as the elastance. Elastance is a measure that is relatively independent of load and therefore a reliable index of contractility. The end-systolic volume index of the LV, an expression of elastance, is a relatively load-independent indicator of LV function and offers independent prognostic information about adverse cardiovascular outcomes such as mortality and heart failure in patients with coronary artery disease. , However, because of geometric constraints, RV end-systolic volume is difficult to measure accurately by 2D TTE, and a noninvasive expression of its elastance is not readily available. Hopefully, future research in this area, particularly with 3D volumes of the RV, will provide this potentially valuable clinical information ( Fig. 28.6 ).
Right ventricular stroke work index (SWI), a combined expression of the pressure and volume work done by the right ventricle, is another useful parameter. It can be calculated by subtracting right atrial pressure from mean pulmonary artery pressure and multiplying this difference by stroke volume index. Because of the difference in structure and contractile properties of the LV and RV, their relative stroke work indices are quite different, whereby the RV SWI is only approximately 15% of LV SWI.
Right Ventricular Afterload
The RV has heightened sensitivity to increased afterload for several reasons: (1) coronary flow is more vulnerable, and increases in pressure can readily lead to RV ischemia (see the discussion of RV perfusion later); and (2) the RV has a thin wall, so wall stress, which is estimated by Laplace law (and is inversely proportional to twice wall thickness), increases more rapidly with pressure increase than in the LV. Normally, the resting peak systolic pulmonary pressure achieved by the RV is less than 30 mm Hg, but this value varies by age and cardiac output. With exercise, the pulmonary pressure may rise as high as 40 mm Hg in unconditioned normal individuals and as high as 55 mm Hg in athletes or persons older than age 65 years. Characteristically, normal systolic pulmonary pressure rises slowly through grades of cardiac output that attend increasing exercise levels. Rapid increases in pressure are more characteristic of a pathologic response. Thus, the healthy RV has considerable reserve as long as the pressure load increases slowly and is not accompanied by elevated pulmonary vascular resistance. Abrupt increases in pulmonary pressures are poorly tolerated by the thin-walled RV because the wall stress increases rapidly. Examples of situations in which this intolerance is manifest are acute pulmonary embolism and the abrupt dilation of a transplanted heart when the recipient has underlying elevated pulmonary vascular resistance. Deterioration of RV function in these circumstances is accompanied by rapid dilatation of the chamber and by a sudden drop in contractile function. One feature of pulmonary embolism that affords insight into the vulnerability of normal RV function is the segmental loss of RV midwall function that is said to be a diagnostic feature of major pulmonary embolism. We theorize that an abrupt rise in pulmonary pressure and subsequent oxygen demand of the RV myocardium is likely to cause midwall ischemia because the timing of right coronary flow is, contrary to left coronary flow, systolic dominant. An acute elevation of RV wall stress may markedly impair right coronary blood flow, especially at the midwall. The rise in troponin and the location of the wall motion in acute pulmonary embolism appear to support this pathophysiologic explanation.
The use of Doppler to determine pulmonary artery pressure is a mainstay of current echocardiography practice. The first step is the demonstration of tricuspid regurgitation by color-flow Doppler in the A4C view ( Fig. 28.7 ). Then the continuous wave beam is placed across the jet, and the peak velocity is used to calculate the peak gradient between the right atrium and right ventricle with the Bernoulli equation: peak gradient (mm Hg) = 4 × peak velocity. Provided that there is no pulmonary stenosis, this gradient added to the RA pressure is equal to peak systolic pulmonary artery pressure. RA pressure is determined by the respiratory behavior of the inferior vena cava (IVC). An alternative method of estimating RA pressure has been published by the ASE and is as follows. For an IVC diameter of 2.1 cm or less that collapses more than 50% with a sniff, a normal RA pressure of 3 mm Hg is assigned. For an IVC diameter of at least 2.1 cm that collapses less than 50% with a sniff, an elevated RA pressure of 15 mm Hg is assigned. In cases in which the IVC diameter and collapse do not fit this paradigm, an intermediate value of 8 mm Hg is assigned. Additional information to validate RA pressure may be obtained from Doppler imaging of the hepatic vein. Normal RA pressure (<5 mm Hg) is assumed if the hepatic vein is systolic dominant, and low RA pressure (2 mm Hg or negative) is assumed if flow is continuous. If the IVC is not visualized, skilled sonographers may image the superior vena cava (SVC) and obtain the flow profile of pulsed-wave Doppler (PWD), seeking the same flow patterns seen in the hepatic vein. Another method of judging RA pressure is to observe the curvature and respiratory responses of the interatrial septum. The chamber with the higher pressure will dictate the curvature. Usually, when the septum is bidirectional, the pressure in both chambers is low.
In addition to peak systolic pressure, it is useful to measure end-diastolic pulmonary regurgitation (EDPR) gradient and then add it to RA pressure, which provides a direct correlate of PA diastolic pressure (an indirect correlate of left ventricular end-diastolic pressure [LVEDP]). The gradient, as a standalone measurement without RA pressure, suggests abnormal hemodynamics when it is greater than 5 mm Hg. Mean PA pressure may be calculated by three methods. First, mean pressure can be calculated from the peak (opening) PR gradient + RA when this measurement is available. Second, planimetry of the TR signal + RA provides a validated estimate of mean pulmonary pressure. Third, the formula used for calculating mean arterial systolic pressure {mean pressure = [systole + (2 × diastole)]/3} may be applied if diastolic pressure from EDPR is available. Resistance may also be estimated from the simple ratio of peak TR velocity to PA velocity time integral. Use of noninvasive pulmonary vascular resistance (PVR) prevents mistaking elevated pulmonary pressure that is caused by increased flow for pressure that is mediated by elevated resistance. Central to understanding hemodynamics of the right side of the heart is PA velocity time integral, or stroke distance, as an indicator of cardiac output. In individuals with high blood flow, such as patients with sickle cell disease or end-stage liver disease, a high stroke distance with borderline elevated PA pressure indicates normal PVR. Conversely, a very low stroke distance (velocity time integral well below 17 cm) may be a sign of markedly increased PVR even when pulmonary artery systolic pressure (PASP) is only mildly elevated.
Overall, despite the hemodynamic sensitivity of the RV to acute changes in preload, contractility, and afterload, the RV is highly adaptable and can even take on the role of the systemic ventricle if needed. , We care for a patient in his eighth decade with L-transposition and a systemically functioning subaortic right ventricle with normal resting hemodynamics and above average formally measured exercise tolerance.
Quantitative Assessment Of Right Ventricular Function
Despite the complexity of the RV anatomy and assessing the RV size, there are options for global quantitation of RV function. These include RVEF and fractional area shortening from the four-chamber view of RV body, tricuspid annular plane systolic excursion (TAPSE) ( Fig. 28.8A ), and RV dP/dt from the acceleration of the tricuspid regurgitation signal, RV index of myocardial performance (RIMP, the Tei) index and Doppler tissue imaging (DTI) ( Fig. 28.8B ) may also describe the systolic velocity of the tricuspid annulus (S′), and RV strain.
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