Version May 2024
INTRODUCTION — The right ventricle (RV) has historically received less attention than its counterpart on the left side of the heart, yet there is a substantial body of evidence showing that RV size and function are equally important for the prognosis of patients with various forms of cardiovascular disease. RV dysfunction is associated with excess morbidity and mortality in patients with chronic left-sided heart failure, acute myocardial infarction (with or without RV infarction), pulmonary embolism, pulmonary arterial hypertension, and congenital heart disease [1-3]. Advances in noninvasive imaging of the RV, particularly with echocardiography, have yielded insights into the pathophysiology of this complex and once elusive chamber.
In an attempt to standardize the echocardiographic evaluation of the right heart, the American Society of Echocardiography and European Association of Cardiovascular Imaging published guidelines and reference values [4,5]. This topic will review the echocardiographic assessment of the right-sided heart chambers, specifically the right atrium (RA) and RV. The echocardiographic assessment of right-sided heart valves is presented separately. (See "Echocardiographic evaluation of the tricuspid valve" and "Echocardiographic evaluation of the pulmonic valve and pulmonary artery".)
RIGHT VENTRICULAR ANATOMY AND PHYSIOLOGY — The RA transmits and pumps blood across the tricuspid valve into the RV, which then ejects the stroke volume through the pulmonic valve and into the main pulmonary artery. In the absence of shunt, forward stroke volume of the right heart is obligately equal to that of the left.
The right heart differs from the left in terms of anatomy and physiology. The RV loosely resembles a pyramid and is composed of three portions: the inlet, the body, and the outflow tract. Contraction is generated by a deep layer of longitudinal fibers that result in longitudinal (base to apex) shortening, and a superficial layer of circumferential fibers that result in inward thickening (movie 1) [6]. The RV lacks a third layer of spiral fibers as seen in the left ventricle (LV).
The RV end-diastolic volume is slightly larger than that of the LV, and as a result has a slightly lower ejection fraction to generate the same stroke volume. RV ejection is accomplished with a mass that is approximately one-fifth that of the LV. Accordingly, the RV is well suited as a volume pump, but is prone to failure when faced with an acute pressure challenge.
These anatomic and physiologic features, coupled with the less accessible retrosternal position of the RV, have resulted in many challenges in the noninvasive evaluation of RV size and function by echocardiography.
CHAMBER SIZE AND WALL THICKNESS — Certain descriptive features may raise the suspicion of RV enlargement (as examples, the RV cavity appearing "larger than" the LV in the apical four-chamber view, or the RV being "apex-forming"). However, given the complex and multifaceted configuration of the RV, all available echocardiographic views should be reviewed, and quantitative measures of RV and RA size and function should be reported as part of a comprehensive echocardiographic assessment (table 1). (See 'Right atrial size' below and 'Right ventricular size' below.)
Right atrial size — Emerging data have suggested that RA enlargement is an important prognostic marker for patients with cardiovascular disease, which should be routinely measured in the echocardiography lab (table 1). The significance of RA size is illustrated by the following examples:
●In a meta-analysis of 12 studies comprising 1085 patients with pulmonary arterial hypertension followed for an average of 9 to 60 months, each 5-unit increment in RA area was associated with a 50 percent increase in hazard of mortality [7].
●In a study of 192 patients with chronic systolic heart failure followed for an average of 36 months, RA volume indexed to body surface area (BSA) was found to be predictive of mortality, need for heart transplantation, or hospitalization for heart failure; an association that persisted after adjusting for age, right and left ventricular systolic function, and B-type natriuretic peptide [8].
●RA enlargement is a risk factor for development of atrial fibrillation or flutter, caused by atrial wall remodeling ("atriopathy") and associated electrophysiologic perturbations [9,10]. Furthermore, chronic atrial fibrillation or flutter is a risk factor for progression of RA enlargement, leading to annular dilation and functional tricuspid regurgitation [11].
RA area — RA area is measured by planimetry of the RA cavity in the apical four-chamber view at end-systole (when the RA cavity is at its largest) (image 1). When tracing the endocardial contour, the area below the tricuspid annular plane, the superior and inferior venae cavae, and the RA appendage should be excluded. The normal reference limit (table 1) for RA area is ≤18.5 cm2 [4]. Of note, RA volume (see below) has supplanted RA area as the preferred measure.
RA linear dimensions — RA linear dimensions are also measured in the apical four-chamber view at end-systole (image 1). The normal reference limit for RA major-axis dimension (superior-inferior, from the center of the tricuspid annular plane to the uppermost aspect of the RA wall) is ≤5.3 cm; for RA minor-axis dimension (left-right, from the interatrial septum to the rightmost aspect of the RA wall), it is ≤4.4 cm [4].
RA volume — RA volume is measured by planimetry of the RA cavity in a single-plane apical four-chamber view at end-systole (when the RA cavity is at its largest) and extrapolated to a volumetric estimate using Simpson’s method or the area-length formula. Like the left atrium, RA volume should be indexed to the patient’s BSA, with the normal reference limit for RA volume index using Simpson’s method being <33 mL/m2 (or <35 mL/m2 in males and <31 mL/m2 in females) [12].
To minimize geometric assumptions and achieve greater accuracy, RA volume can be measured by planimetry of consecutive short-axis slices in a three-dimensional (3D) volumetric acquisition using the method of discs. For technical reasons, two-dimensional (2D) area-length measurements are approximately 10 percent larger and 3D volumetric measurements are up to 30 percent larger than 2D Simpson’s estimates, depending on the study.
Right ventricular size — RV enlargement may be caused by states of acute or chronic pressure overload, chronic volume overload, or intrinsic myocardial pathology (table 2), often indicating severe and/or advanced disease with a relatively poor prognosis.
●In patients with moderate-to-severe chronic pulmonary disease, the basal diameter of the RV (measured at end-diastole and indexed to BSA) was readily obtained in 92 percent of patients and was the most significant predictor of mortality over a follow-up period of 16 months [13].
●In a large registry of patients with acute pulmonary embolism, relative RV enlargement as suggested by an RV to LV end-diastolic diameter ratio ≥0.9 was predictive of in-hospital mortality and has been useful in identifying which patients require more aggressive therapy [14].
●In patients with repaired tetralogy of Fallot and free pulmonary regurgitation, RV end-diastolic volume index is vigilantly monitored to determine the timing of pulmonary valve replacement. Volumetric measurements can be obtained by 3D echocardiography [15] or, preferably, by cardiovascular magnetic resonance (CMR) imaging, given its superior accuracy and sensitivity to serial changes [16]. (See "Tetralogy of Fallot (TOF): Long-term complications and follow-up after repair", section on 'Tests' and "Tetralogy of Fallot (TOF): Long-term complications and follow-up after repair", section on 'Indications'.)
RV area — Due to the complex shape of the RV, there is no single representative 2D measure of RV size, and any given measure has modest correlation with actual RV volume as measured by CMR or ex vivo, especially when the RV cavity is dilated [17].
The area of the body and apex of the RV is measured by planimetry of the RV cavity in the apical four-chamber view at end-diastole (when the RV cavity is at its largest) (image 2). When tracing the endocardial contour, care must be taken to trace along the true border of the RV wall rather than the prominent trabeculations or moderator band (image 3). The normal reference limit for RV end-diastolic area is ≤24 cm2 in males and ≤20 cm2 in females [5].
Two common sources of error, resulting in underestimation of RV area, are:
●Tracing too far into the RV cavity along the border of the noncompacted RV trabeculations (image 3).
●Accidentally excluding the apex of the RV by tracing the inferior border along the moderator band rather than the true apex (image 3).
RV linear dimensions — RV linear dimensions are measured in the apical four-chamber view, ideally using the RV-focused view, at end-diastole (image 2). The normal reference limit (table 1) for RV basal dimension (maximal diameter in the basal one-third of the RV) is ≤4.1 cm [5]. The normal reference limit for RV basal dimension indexed to BSA is ≤2.1 cm/m2. The RV basal dimension is recommended as the preferred standard basic measure of RV size to be reported, unless 3D volumes are reported.
Two common sources of error with the measurement of RV linear dimensions are (figure 1 and image 3):
●Acquiring a nonoptimized four-chamber view that results in underestimation of RV size.
●Acquiring and making measurements on the RV-modified apical four-chamber view (as opposed to the RV-focused apical four-chamber view) that results in overestimation of RV size.
Therefore, it is critical to obtain a well-aligned RV-focused apical four-chamber view (movie 2). This is accomplished by ensuring that the transducer is positioned over the apex of the heart (and not over the body of the RV as in the RV-modified apical four-chamber view), tilted to bring the entire RV into the imaging sector, and rotated until the maximal RV dimension is in-plane [18].
RVOT dimension — The proximal RV outflow tract (RVOT) dimension is measured from the RVOT anteriorly to the aortic root posteriorly; it can be measured in the parasternal long-axis or parasternal short-axis view (image 4) and the normal reference limits (table 1) are ≤3.3 and ≤3.5 cm, respectively [4]. The distal RVOT diameter, commonly used in the calculation of RV stroke volume, is measured just proximal to the insertion of the pulmonary valve leaflets in the parasternal short-axis view (image 4) and the normal reference limit is ≤2.7 cm [4].
RV volume — 2D estimates of RV volume are not recommended due to their inherent geometric assumptions and lack of full representation of the different RV regions (often resulting in substantial underestimation of true RV volume). 3D measures of RV volume overcome these limitations and can be obtained using one of two preferred approaches (see "Three-dimensional echocardiography", section on 'Assessment of right ventricular volumes'):
●Method of discs – Starting with a full volume acquisition of the RV, the user manually traces the endocardial border of the RV in a series of consecutive short-axis slices or orthogonal long-axis slices. The software algorithm segments the RV into contiguous discs of fixed height (usually 10 mm) from base to apex, and sums the volumes of the contiguous discs to calculate a global RV volume.
●3D surface modeling – Also starting with a full volume acquisition of the RV, the user manually identifies specified RV landmarks or contours and the proprietary software algorithm proceeds to fit a 3D model and calculate global and regional RV volumes (image 5). This approach is popular due to its ease and speed of use, close correlation with CMR [19,20], and availability of normative data.
3D measures of RV volume and ejection fraction are endorsed by the American Society of Echocardiography and European Association of Cardiovascular Imaging [5] in laboratories with suitable equipment and expertise [21]. The normal reference limits for 3D-derived RV end-diastolic volume index are ≤87 mL/m2 in males and ≤74 mL/m2 in females. On average, 3D echocardiography-derived RV volumes, especially when enhanced by contrast, are closely correlate with the CMR reference standard [22]. However, at the individual patient level, there is wider variability between 3D echocardiography and CMR-derived RV volumes such that the two modalities are not interchangeable. When monitoring serial changes in RV volumes, there is lower reliability with 3D echocardiography to detect changes of less than 15 percent [23].
Wall thickness — RV hypertrophy is recognized by inspecting the wall of the RVOT in the parasternal views, the RV free wall in the apical four-chamber view, and the RV inferolateral/diaphragmatic wall in the subcostal view. Generally, the RV free wall in diastole is approximately 3 to 4 mm thick; if it exceeds 5 mm, it is considered hypertrophied (image 6) [24,25].
RV wall thickness, when inspected or measured in the subcostal view, allows differentiation of the wall thickness from cavity trabeculations [26]. Contrast enhancement of M-mode or two-dimensional images can aid in measuring wall thickness [27,28]. Due to measurement variability, regardless of the method used, it should be noted that RV thickness by echocardiography has low sensitivity and specificity for identifying true RV hypertrophy.
INTERVENTRICULAR SEPTAL SHAPE — A D-shaped LV cavity (also referred to as a flattened interventricular septum) in systole (particularly end-systole) suggests RV pressure overload, whereas a D-shaped LV cavity in diastole suggests RV volume overload (image 7). An LV eccentricity index (defined as the ratio of the two perpendicular minor-axis diameters, one of which bisects and is perpendicular to the interventricular septum) has been measured at end-diastole and end-systole to identify interventricular septal deformation in patients with RV volume and/or pressure overload [29].
RIGHT VENTRICULAR FUNCTION — The predominant motion of the RV is longitudinal shortening, visible as systolic descent of the basal portion of the free wall toward the apex. A secondary motion is radial thickening, visible (albeit less readily) as systolic thickening of the myocardium. Unlike the LV, circumferential shortening is negligible in the RV, owing to its lack of circumferential fibers. The quantitative echocardiographic parameters used to measure RV systolic function reflect longitudinal motion, longitudinal motion plus free wall and septal inwards motion, or global RV performance.
Tricuspid annular plane systolic excursion — Tricuspid annular plane systolic excursion (TAPSE), sometimes referred to as tricuspid annular motion (TAM), reflects longitudinal shortening of the RV. TAPSE is measured in the apical four-chamber view by placing an M-mode cursor on the lateral tricuspid annulus and measuring the peak distance travelled by this reference point during systole (image 8). A greater distance travelled during systole implies greater RV systolic function, with the normal reference limit (table 1) being a TAPSE of ≥1.7 cm [5,30,31].
The primary limitation of TAPSE is that it only represents one component of RV motion within one single segment of RV myocardium. The RV may be frankly dysfunctional despite relatively preserved TAPSE, as in some cases of severe pulmonary arterial hypertension (movie 3). Alternatively, the RV function may be globally preserved despite significantly reduced TAPSE, as seen after cardiac surgery [32,33]. Another potential limitation of TAPSE is that it is directly proportional to and, hence, influenced by RV size [34].
Two common sources of error with TAPSE are:
●Not placing the M-mode cursor parallel to the plane of longitudinal motion, which results in angle-dependent underestimation of TAPSE.
●Incorrectly measuring the magnitude of displacement from the M-mode image.
These issues aside, TAPSE remains one of the most widely used measures of RV systolic function since it is easily obtained and has been shown to have robust diagnostic and prognostic value in several disease states.
●In patients with precapillary pulmonary hypertension (PH), TAPSE has been shown to correlate with CMR-derived RV ejection fraction (RVEF) and predict long-term mortality [1,35].
●In patients presenting with inferior myocardial infarction, a reduced TAPSE was found to be an indicator of RV infarction even when no RV regional wall motion abnormalities could be identified [36].
●In three separate series of patients with chronic left-sided systolic heart failure, up to 50 percent of patients were found to have a reduced TAPSE, a finding that was associated with a significant increase in long-term mortality [37-39].
●In a meta-analysis of patients undergoing transcatheter aortic valve replacement, a reduced TAPSE as well as a reduced tricuspid annular velocity (S') and fractional area change (FAC) were independent risk factors for post-procedural mortality [40]. (See 'Tricuspid annular velocity' below and 'Fractional area change' below.)
Tricuspid annular velocity — Akin to TAPSE, which reflects the longitudinal displacement of the tricuspid annulus during systole, S' reflects the longitudinal velocity of the tricuspid annulus during systole. S' is measured in the apical four-chamber view by placing a tissue Doppler cursor on the lateral tricuspid annulus and measuring the peak velocity of this point during systole (image 9). Care should be taken to measure the peak of the ejection waveform and not the earlier isovolumetric contraction waveform. A greater velocity during systole implies greater RV systolic function, with the normal reference limit (table 1) being an S' of ≥9.5 cm/s. Both pulsed tissue Doppler and color-coded tissue Doppler can be used to measure S', although the color-coded method yields mean velocities that are usually slightly lower [41]. The ultrasound transducer may be slightly tilted to optimize the alignment of the Doppler cursor with the plane of RV longitudinal motion.
The advantages and limitations are the same as TAPSE: S' is simple to perform and has prognostic data, yet it is angle-dependent and only represents the longitudinal annular component of RV contraction.
S' has been shown to correlate with CMR-derived RVEF [42,43] and predict outcomes in patients with PH [44,45], inferior myocardial infarction [36,46], chronic heart failure [47,48], and arrhythmogenic RV cardiomyopathy (ARVC) [49,50].
Fractional area change — FAC is the percent change in RV area in the apical four-chamber view from diastole to systole, a two-dimensional surrogate for ejection fraction, and thereby reflects the systolic function of the inflow and apical portions of the RV (since the outflow portion is not seen in this view). FAC is not limited to one type of motion, but rather encompasses longitudinal shortening as well as radial thickening and the contribution of the interventricular septum. It is measured by manually tracing the contour of the RV at end-diastole (when the RV cavity is at its largest) and at end-systole (when the RV cavity is at its smallest) (image 10). The FAC is calculated as follows:
FAC = [(end-diastolic RV area – end-systolic RV area) / end-diastolic RV area] x 100
The normal reference limit (table 1) for FAC is ≥35 percent [4]. The primary challenge and main limitation of FAC is the accurate identification and tracing of the true RV endocardial border rather than the prominent trabeculations and muscle bands (image 3). (See 'RV area' above.)
FAC appears to be an excellent compromise between efficiency of use and global representation of RV systolic function. Compared with other two-dimensional measures of RV systolic function such as TAPSE and S’, FAC was found to correlate best with the reference standard of CMR-derived RVEF (R = 0.80) [51].
●In substudies from the SAVE and VALIANT trials, 416 and 522 patients with acute myocardial infarction and evidence of LV dysfunction underwent complete echocardiographic assessment [52,53]. Four independent predictors of subsequent all-cause mortality were identified: age, Killip classification, LV ejection fraction, and FAC; with FAC <35 percent carrying an adjusted hazard ratio of 3.56 (95% CI 1.07-11.90).
●In the Multidisciplinary Study of Right Ventricular Dysplasia, FAC was found to be significantly reduced in probands compared with normal controls [54]. The revised ARVC Task Force Criteria list FAC ≤33 percent as a major diagnostic criterion and FAC 34 to 40 percent as a minor criterion (no other 2D echocardiographic measures of function were endorsed) [55].
Myocardial performance index — Myocardial performance index (MPI), also referred to as RV index of myocardial performance (RIMP) or RV Tei index, reflects both the systolic and diastolic function of the RV [56]. Contrary to the TAPSE, S’, and FAC, the MPI is based on time intervals and is independent of chamber geometry and contraction pattern. The MPI was once thought to also be independent of loading conditions, although this has subsequently proven to be false [57].
The MPI is derived by calculating the ratio of isovolumetric time over ejection time as follows:
MPI = (isovolumetric relaxation time + isovolumetric contraction time) / ejection time = (tricuspid closure-to-opening time – ejection time) / ejection time
Lower values indicate superior function since the healthy RV should theoretically spend a lower relative proportion of time in an isovolumetric state and a greater proportion ejecting blood.
The MPI can be measured in one of two ways (image 11 and image 12). For both methods of measuring MPI, the expertise of the observer is crucial since the time intervals being measured are often difficult to delineate, and small variations can lead to substantial differences in the final calculated value [4].
●Pulsed Doppler method – The ejection time is derived from the pulsed wave Doppler tracing of the distal RV outflow tract; the tricuspid-closure-opening time is derived from the pulsed wave Doppler tracing of the tricuspid inflow (time from end of the A wave to the onset of the following E wave) or the continuous wave Doppler tracing of the tricuspid regurgitation jet (time from the beginning to the end of the holosystolic jet); and the total isovolumetric time is derived from the difference between the tricuspid-closure-opening time and the ejection time (image 12). The normal reference limit for the pulsed Doppler MPI is ≤0.43.
●Tissue Doppler method – The ejection time, tricuspid-closure-opening time, and total isovolumetric time are all derived from the pulsed tissue Doppler tracing of the lateral tricuspid annulus (image 11). The normal reference limit for the tissue Doppler MPI is ≤0.54. This method has the distinct advantage of being measured from a single acquisition in a single heartbeat.
MPI is particularly well suited to two clinical scenarios: First, since MPI is often affected before other functional parameters, it is a more sensitive parameter to evaluate subclinical or early RV dysfunction. Second, since MPI is nongeometric in nature and relies solely on time intervals to derive a measure of RV function, it is useful to evaluate an RV which is oddly shaped or poorly visualized.
Similar to TAPSE, S', and FAC, MPI appears to have prognostic value in a variety of clinical conditions [58-65] and has been used to predict response to therapy in patients with pulmonary arterial hypertension or chronic thromboembolic disease [66,67]. In patients scheduled to undergo coronary artery bypass or aortic valve replacement surgery, abnormal RV MPI was found to be a risk factor for postoperative mortality and major morbidity [2,68,69].
RV ejection fraction by 3D — RVEF is calculated as
(end-diastolic volume - end-systolic volume) / end-diastolic RV volume
with volumes measured from a 3D acquisition. Given adequate image quality, 3D-derived RVEF using either the method of discs or surface modeling is the most accurate echocardiographic measure of global RV systolic function. The prognostic value of 3D-derived RVEF has emerged as one of the foremost predictors of adverse events, as illustrated by the following studies:
●In a study of 151 patients with chronic thromboembolic PH, 3D-derived RVEF was the echocardiographic parameter most predictive of mortality and major morbidity [70].
●In a study of 446 patients with various cardiovascular diseases, 3D-derived RVEF was an echocardiographic parameter predictive of four-year cardiac mortality in a multivariable model [71].
A study of 507 normal subjects has provided reference values for males and females [72], which was subsequently validated and partitioned in a study of 858 patients [73].
●Normal 3D-RVEF – ≥45 percent, associated with very low risk of cardiac mortality
●Mildly reduced 3D-RVEF – 40 to 45 percent
●Moderately reduced 3D-RVEF – 30 to 40 percent
●Severely reduced 3D-RVEF – <30 percent, associated with high risk of cardiac mortality
To reduce the time and variability associated with 3D echocardiographic measurements, machine learning algorithms with and without operator adjustment are undergoing development and testing [74].
Strain imaging by 2D — Strain is defined as the percent change in myocardial deformation (predominantly longitudinal shortening in the case of the RV). Strain should be measured by the speckle-tracking (non-angle-dependent) approach [75,76]. Potential pitfalls include technical challenges in image acquisition and analysis (need for high frame rates, high signal-to-noise, minimal image dropout, experienced observers for reproducible measurements) as well as inter-vendor variability.
Contemporary speckle-tracking algorithms have enhanced reproducibility and are beginning to yield clinically relevant observations:
●In a large cohort of 575 patients with pulmonary arterial hypertension, free wall longitudinal strain by 2D speckle tracking was predictive of functional capacity and 18-month mortality [77].
●In 200 patients with heart failure and seemingly normal RV systolic function (TAPSE >16 mm), a substantial proportion of patients was found to have abnormal RV free wall strain indicative of subclinical RV dysfunction, which was in turn predictive of death and hospitalization [78].
●To identify signs of RV infarction in patients presenting with acute myocardial infarction, RV free wall strain was superior to conventional echocardiographic parameters [79].
The normal reference limit for speckle-tracking strain of the RV is -23 percent (with more negative values indicating better function). Of note, the three segments of the RV free wall may be reported as an average free wall strain or as separate indicators of regional function for the base, midbody, and RV apex [80].
Diastolic function — Diastolic function of the RV, although infrequently considered, can be assessed by echocardiography in a fashion similar to the LV using pulsed wave Doppler interrogation of the trans-tricuspid inflow, tissue Doppler interrogation of the lateral tricuspid annulus, speckle-tracking interrogation of the RV free wall, and evaluation of RA pressure (RAP) using inferior vena cava size and collapsibility and hepatic vein flow pattern.
●Impaired relaxation – E/A ratio less than 0.8 or e'/a' ratio less than 0.5.
●Pseudonormal filling – E/A ratio of 0.8 to 2.1 or e'/a' ratio of 0.5 to 1.9, combined with evidence of elevated RAP (particularly a dilated or noncollapsing inferior vena cava or an increased E/e′ ratio greater than 6).
●Restrictive filling – E/A ratio greater than 2.1 or e'/a' ratio greater than 1.9, with deceleration time less than 120 msec and evidence of elevated RA pressure.
A more detailed description of RV diastolic function assessment is included in the 2010 American Society of Echocardiography right heart guidelines [4].
HEMODYNAMICS — In addition to the anatomic and functional parameters, the comprehensive echocardiographic examination provides an assessment of right heart hemodynamics. Integration of these three components (anatomy, function, and hemodynamics) is vital to enable the clinician to understand and delineate the pathophysiology at hand.
RA pressure — Estimation of RA pressure (RAP) is clinically relevant in many circumstances:
●As an indicator of volume status and responsiveness to fluid challenge in critically ill patients
●As a diagnostic sign in patients with suspected cardiac tamponade or other pericardial syndromes
●As a prognostic sign in patients with pulmonary arterial hypertension [81]
●As part of the echocardiographic estimation of pulmonary artery pressure
RAP is most commonly estimated based on the diameter and degree of collapse of the inferior vena cava (IVC) imaged from the subcostal view during quiet inspiration and during rapid inspiration ("sniff") (movie 4) [4,82,83]. Overly forceful inspiration should be discouraged, as this can cause translation of the IVC out of the imaging plane. RAP is typically estimated as follows (table 3):
●Normal RAP (3 mmHg) – IVC diameter ≤2.1 cm and collapse during sniff >50 percent.
●Intermediate RAP (8 mmHg) – IVC diameter ≤2.1 cm and collapse during sniff <50 percent or IVC diameter >2.1 cm and collapse during sniff >50 percent.
●Elevated RAP (15 mmHg) – IVC diameter >2.1 cm and collapse during sniff <50 percent.
The interpreter, however, may upgrade or downgrade the intermediate RAP value based on secondary indices that suggest either normal or elevated RAP, such as RA enlargement, RV hypertrophy, diastolic predominance in the hepatic veins, restrictive filling pattern in the transtricuspid inflow, or tricuspid E/e' >6 [84-86], although the incremental yield of considering these secondary indices appears to be modest [87]. The simplified combination of a plethoric IVC diameter and a dilated RA volume index ≥35 mL/m2 achieved 88 percent accuracy to predict elevated RA pressure ≥10 mmHg in one study [88]. In some subjects with markedly elevated RAP, the "elevated" category of 15 mmHg may be an underestimate, and this should be considered in certain clinical scenarios. In mechanical ventilated subjects, the use of IVC size and collapse to estimate RAP is less reliable but may still be of value in certain circumstances [89].
The IVC is occasionally dilated in healthy young subjects and in athletes, in which case the IVC size can be reassessed in the left lateral decubitus position and ancillary signs of elevated RAP can be verified (hepatic vein flow pattern showing diastolic predominance [ie, diastolic wave velocity >systolic wave velocity]). If the IVC appears plethoric and there is no suggestion of right heart pathology, positioning the patient in the left lateral decubitus position may cause the IVC to collapse normally with inspiration and may be interpreted as normal RAP. Moreover, in healthy subjects with smaller body surface areas (defined as 1.61 m2 or less), some investigators have suggested that the normal reference limit for IVC diameter be reduced to ≤1.7 cm (as opposed to ≤2.1 cm) [90].
Pulmonary artery pressure
Estimation of pulmonary artery systolic pressure — Estimation of pulmonary artery pressure (PAP) is an important component of the echocardiographic study, particularly in the evaluation of dyspnea. The simplified Bernoulli equation, ΔP = 4V2, estimates the pressure drop between two chambers (ΔP) based on the peak velocity (V) in the presence of turbulent flow. Thus, the gradient estimated by the peak tricuspid regurgitation velocity (TRV) measured by continuous wave Doppler is equal to the systolic pressure in the RV (RVSP) minus the systolic pressure in the RA (RAP). RVSP is equivalent to pulmonary artery systolic pressure (PASP) in the absence of an RV outflow gradient (such as with pulmonic stenosis). This equation is re-arranged to yield [91]:
PASP ≈ RVSP = 4(peak TRV2) + RAP
Careful acquisition and interpretation of Doppler TRV and RAP data are crucial. While some studies have documented a strong correlation between echocardiographic estimates and right heart catheterization measurements of PASP [91-94], other studies have found wide limits of agreement [95-98]. The main causes of discrepant findings are inaccurate RAP estimation and suboptimal Doppler TR signal quality and interpretation. When the TR signal is of high quality and interpreted by expert readers, the area under the curve for the diagnosis of pulmonary hypertension (PH) reaches 0.97 [92]. When the TR signal is not reliably interpretable, ancillary parameters (such as eccentricity index and non-TR-dependent estimators of PAP) may be used to infer a possible diagnosis of PH. (See 'Interventricular septal shape' above and 'Other measures of pulmonary artery pressure' below.)
The following steps along with interpretation by an expert are suggested to optimize the accuracy of RVSP and PASP estimation [92]:
●Examine the TR jet in multiple views (parasternal RV inflow, parasternal short-axis, RV-modified apical four-chamber, and subcostal views; the last particularly when the TR jet is highly medially directed) and measure the peak TRV using the Doppler spectral recording from the position most closely aligned with the jet. As with all Doppler measurements, it is critical to minimize the angle of incidence of the cursor to the flow (to <40°) to avoid underestimating TRV.
●Adjust the sweep speed between 75 and 150 mm/sec, depending upon the heart rate.
●When measuring peak TRV in a patient with an arrhythmia, avoid nonrepresentative beats. For example, avoid using a post-premature ventricular contraction beat. For patients with atrial fibrillation, use the third beat after two consecutive equal RR intervals or an average of at least five heartbeats.
●Optimize the signal-to-noise ratio by carefully adjusting the Doppler gain to avoid over- or underestimation of maximal velocities (image 13).
●Measure the peak TRV only if the signal is interpretable (with a complete or partial envelope).
●Measure the peak TR velocity using the modal frequency (image 13).
●Use intravenous microbubble agitated saline or commercial ultrasound contrast agent (off-label use) as needed to enhance the signal-to-noise ratio for the Doppler TR spectral recording.
●Integrate RA size, hepatic vein Doppler tracings, and tricuspid E/e' along with IVC size and collapsibility to estimate RAP, and avoid translational motion when assessing the IVC. (See 'RA pressure' above.)
In general, echocardiographically estimated PASP exceeding 35 mmHg in younger adults or 40 mmHg in older adults (≥60 years of age) is considered elevated. PASP rises slightly with increasing age and body surface area [99] and during exercise. Stress echocardiography may be indicated in certain cases to diagnose exercise-induced PH [100,101].
The 2022 European Society of Cardiology/European Respiratory Society guidelines for the diagnosis and treatment of PH recommend comprehensive echocardiography as a pivotal test to assess diagnostic probability and prognostic risk [102].
Echocardiographic parameters for probability of PH are summarized as follows [102]:
●High probability of PH – The probability of PH is deemed to be high if TRV is >3.4 m/s or if TRV is 2.9 to 3.4 m/s with one or more secondary indices: RV/LV basal diameter ratio >1.0, LV eccentricity index >1.1, tricuspid annular plane systolic excursion (TAPSE)/PASP <0.55 mm/mmHg, RV outflow tract (RVOT) acceleration time <105 ms or midsystolic notching, early diastolic pulmonic regurgitation velocity >2.2 m/s, pulmonary artery diameter >25 mm, estimated RAP ≥15 mmHg, or RA area >18 cm2.
●Intermediate probability of PH – The probability of PH is deemed to be intermediate if TRV is 2.9 to 3.4 m/s and secondary indices are absent or if TRV is ≤2.8 m/s and secondary indices are present.
●Low probability of PH – The probability of PH is deemed to be low if TRV is ≤2.8 m/s and secondary indices are absent.
The following echocardiographic variables are combined with other clinical findings to estimate one-year mortality risk in pulmonary arterial hypertension [102]:
●High – The risk is deemed to be high (>20 percent) if there is a moderate or large pericardial effusion, TAPSE/PASP is <0.19 mm/mmHg, or RA area is >26 cm2.
●Intermediate – The risk is deemed to be intermediate (5 to 20 percent) if there is a minimal pericardial effusion, TAPSE/PASP is 0.19 to 0.32 mm/mmHg, or RA area is 18 to 26 cm2.
●Low – The risk is deemed to be low if there is no pericardial effusion, RA area is <18 cm2, and TASPE/PASP is >0.32 mm/mmHg.
Invasive right heart catheterization is often indicated to confirm the diagnosis of PH, especially when echocardiographic parameters are technically suboptimal, pulmonary arterial hypertension or chronic thromboembolic PH are suspected, or hemodynamic parameters are required to clarify the etiology and support treatment decisions. (See "Pulmonary artery catheterization: Indications, contraindications, and complications in adults" and "Pulmonary artery catheterization: Interpretation of hemodynamic values and waveforms in adults" and "Clinical features and diagnosis of pulmonary hypertension of unclear etiology in adults".)
Other measures of pulmonary artery pressure — Echocardiography can also be used to estimate mean and diastolic pulmonary artery pressures, using either the tricuspid or pulmonary regurgitation velocity, or the acceleration time (time to reach peak velocity in the distal RVOT flow tracing measured by pulsed wave Doppler), as follows:
●Mean PAP = 4V2early PR velocity + RAP
●Mean PAP = 79 – [(0.45)(Acceleration time)] [103,104]
●Mean PAP = VTI of the TR jet + RAP [105]
●Mean PAP = 0.61 x PASP + 2 [106]
●Systolic PAP = 10[(-0.004)(Acceleration time) + 2.1] [107]
●Diastolic PAP = 4V2end PR velocity + RAP
These values may be reported in patients with right heart pathology, or may be used as surrogate measures of PAP when there is no adequate TR signal to estimate PASP. Furthermore, the combination of acceleration time ≤60 msec and PASP ≤60 mmHg, termed the 60/60 sign, has been proposed as an echocardiographic sign to identify patients with acute pulmonary embolism [108].
Pulmonary vascular resistance — The determinants of pressure are flow and resistance, according to the formula P = QR, where pressure (P) is equal to the product of flow (Q) and resistance (R). Pathological elevations in PASP (P) are generally caused by increased pulmonary vascular resistance (R) secondary to embolic occlusion, endothelial proliferation, or vasoconstriction; or increased pulmonary arterial flow (Q) secondary to high-output states or shunts. By using a measure of flow (velocity time integral [VTI] of the RVOT) and a measure of pressure (TRV), a simple regression formula can be used to estimate pulmonary vascular resistance (PVR) [109]:
PVR = [(TRV / RVOT VTI) x 10] + 0.16
This yields a value in Wood units (WU), and maintains a good correlation with invasively measured PVR up to approximately 8 WU [110]. A subsequent refinement showed that
PVR = [(TRV2 / RVOT VTI) x 5.19] – 0.4
performed better, especially when PVR exceeded 6 WU [111]. This measure has not been validated for clinical use or to prognosticate patients and should not replace invasive hemodynamic measurements. It may be useful, however, to screen for PH related to high flow states or in athletes, both at rest and with exercise. Of note, using the principles elaborated above, when the RV fails, and the stroke volume decreases, one may observe a fall in PASP.
Pulmonary arterial right ventricular uncoupling — When faced with progressive elevations in PASP, the RV hypertrophies to normalize its wall stress and hence maintain a balanced quotient of afterload-to-contractility, termed RV-PA coupling. If PASP continues to rise, this adaptive mechanism is exhausted, and the RV dilates to maintain a sufficient stroke volume, eventually causing myocardial fibrosis to limit its expansion. Thus, increasing afterload due to rising PASP and exhaustion of compensatory hypertrophy is coupled with decreasing contractility due to overstretching and fibrosis of the myocardium, termed RV-PA uncoupling.
The gold standard for assessing RV-PA uncoupling is pressure-volume loops from invasive right heart catheterization, although there has been interest in deriving noninvasive surrogates. TAPSE/PASP is the ratio of TAPSE, reflective of RV systolic function, to PASP, reflective of RV afterload [112]. Reduced TAPSE/PASP, usually defined at a cutoff of ≤0.35 mm/mmHg (or, previously, ≤0.55), has been associated with mortality and major morbidity in patients with PH, TR, and heart failure [113]. Some studies have challenged the validity of TAPSE/PASP, arguing that TAPSE alone is more predictive of invasively-measured RV-PA uncoupling and similarly predictive of adverse outcomes [114].
Other findings — There are several other ancillary findings that should be used to assess for RV overload. A D-shaped LV cavity in systole suggests RV pressure overload (image 7). Midsystolic notching of the RVOT pulsed wave Doppler flow signal or pulmonary valve M-mode signal suggests increased PVR (image 14) [115,116]. This finding reflects a prominent reflected wave, and has been used to refine estimates of PVR using the formula:
PVR = (PASP / RVOT VTI) + 3
if a midsystolic notching of the RVOT is present [117].
In addition, when assessing for increased PASP or PVR, corroborative signs of right-sided dilation and dysfunction should be sought (table 4). (See 'Chamber size and wall thickness' above and 'Interventricular septal shape' above and 'Right ventricular function' above.)
CONDITIONS ASSOCIATED WITH RIGHT VENTRICULAR PATHOLOGY — The RV can be pathologically abnormal in response to a number of situations and conditions, many of which have characteristics that permit echocardiographic differentiation (table 5). RV pathology can be due to volume or pressure overload from a variety of etiologies (eg, valvular disease, congenital heart disease, etc). In addition, primary myopathic processes or tumors can result in RV pathology. Complete discussions of the following conditions are presented separately:
Conditions associated with RV volume overload
●Atrial septal defect. (See "Management of atrial septal defects in adults".)
●Valvular regurgitation (tricuspid or pulmonic regurgitation). (See "Etiology, clinical features, and evaluation of tricuspid regurgitation" and "Management and prognosis of tricuspid regurgitation" and "Echocardiographic evaluation of the pulmonic valve and pulmonary artery", section on 'Pulmonic valve regurgitation'.)
Conditions associated with RV pressure overload
●Pulmonary arterial hypertension (idiopathic, heritable, drug-induced, HIV, connective tissue diseases).
●Acute or chronic thromboembolic disease. (See "Epidemiology and pathogenesis of acute pulmonary embolism in adults", section on 'Clinical presentation, evaluation, and diagnosis' and "Epidemiology, pathogenesis, clinical manifestations and diagnosis of chronic thromboembolic pulmonary hypertension" and "Chronic thromboembolic pulmonary hypertension: Initial management and evaluation for pulmonary artery thromboendarterectomy".)
●Pulmonary hypertension due to left heart diseases (eg, systolic dysfunction, diastolic dysfunction, valvular heart disease). (See "Pathophysiology of cardiogenic pulmonary edema", section on 'Predisposing conditions'.)
●Pulmonary hypertension due to lung diseases and/or hypoxemia. (See "Pulmonary hypertension due to lung disease and/or hypoxemia (group 3 pulmonary hypertension): Treatment and prognosis".)
●Pulmonary valve or supra-valvular stenosis. (See "Clinical manifestations and diagnosis of pulmonic stenosis in adults", section on 'Supravalvular pulmonic stenosis'.)
●RV outflow obstruction. (See "Clinical manifestations and diagnosis of pulmonic stenosis in adults" and "Tetralogy of Fallot (TOF): Pathophysiology, clinical features, and diagnosis".)
Cardiomyopathic conditions associated with RV pathology
●RV ischemia or infarction. (See "Right ventricular myocardial infarction".)
●Dilated cardiomyopathy. (See "Determining the etiology and severity of heart failure or cardiomyopathy" and "Echocardiographic recognition of cardiomyopathies", section on 'Right ventricle'.)
●Arrhythmogenic RV cardiomyopathy. (See "Arrhythmogenic right ventricular cardiomyopathy: Anatomy, histology, and clinical manifestations".)
●Endomyocardial fibrosis. (See "Endomyocardial fibrosis".)
●Other cardiomyopathies affecting the RV and the LV (eg, cardiac amyloidosis, stress-induced cardiomyopathy). (See "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy" and "Cardiac amyloidosis: Epidemiology, clinical manifestations, and diagnosis".)
Tumors involving the RV
●Cardiac myxomas (see "Cardiac tumors", section on 'Myxomas') and other primary cardiac tumors (eg, sarcomas, fibromas, rhabdomyomas). (See "Cardiac tumors".)
●Metastatic lesions (eg, melanoma, renal cell carcinoma). (See "Cardiac tumors", section on 'Secondary cardiac tumors' and "Clinical manifestations, evaluation, and staging of renal cell carcinoma".)
SUMMARY AND RECOMMENDATIONS
●Role of right heart assessment – Assessment of the right heart is a critical component of every echocardiographic study. Measurement of chamber dimensions, evaluation of right ventricle (RV) systolic function, and estimation of hemodynamic parameters (eg, right atrial [RA] pressure, systolic pulmonary artery pressure [PASP]) should be routinely performed. (table 1)
●Core right heart parameters – When feasible, the following core measurements (table 1) should be reported in all studies (with additional measurements performed and reported as clinically indicated):
•Right ventricle
-RV size – RV basal diameter from the RV-focused apical four-chamber view (normal ≤4.1 cm), or, if feasible, RV volume from a three-dimensional (3D) acquisition. (See 'Right ventricular size' above.)
-RV function – RV systolic function is assessed using at least one quantitative parameter: tricuspid annular plane systolic excursion (TAPSE; normal ≥1.7 cm), tricuspid annular velocity (S') (normal ≥9.5 cm/s), fractional area change (FAC; normal ≥35 percent), myocardial performance index (MPI; normal ≤0.43 by pulsed Doppler or ≤0.55 by tissue Doppler). In addition, 3D-derived RV ejection fraction (RVEF) is recommended when suitable technology and expertise is available. (See 'Right ventricular function' above.)
•Right atrium
-RA volume – RA volume is assessed from the apical four-chamber view using the single-plane Simpson's method. (See 'Right atrial size' above.)
-RA pressure – RA pressure is estimated from the inferior vena cava size and collapse (3, 8, 15 mmHg). (See 'RA pressure' above.)
•Pressures – PASP from the tricuspid regurgitation velocity (TRV) and estimated RA pressure (table 3). (See 'Pulmonary artery pressure' above and 'RA pressure' above.)
ACKNOWLEDGMENT — The UpToDate editorial staff thank Nelson B Schiller, MD, FACC, FRCP, FASE, Bryan Ristow, MD, FACC, FASE, FACP, Xiushui Ren, MD, and Warren Manning, MD, who contributed to earlier versions of this topic review.
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