Echocardiographic Planes and Right-Sided Heart Structures

The right ventricle (RV) is located anterior to the left ventricle (LV) and is positioned just behind the sternum. When viewed anteriorly, the right ventricular cavity appears triangular in shape; however, it takes a crescentic shape in cross section. This anatomic orientation means that no single acoustic window allows visualization of the whole of the RV, so multiple transducer positions must be used. Standard echocardiography of the right side of the heart includes use of the parasternal (long-axis, right ventricular inflow, short-axis) (see Videos 1 and 2), apical (four-chamber) (see Video 3 ) and (modified four-chamber), and subcostal acoustic windows (see Video 4), generating a report that includes a qualitative description of right-sided heart anatomy and function, with at least one measurement of right atrial and right ventricular size, and a quantitative assessment of right ventricular function (Table 14-1). The venous inflow to the right side of the heart comprises the coronary sinus, superior vena cava, and inferior vena cava. The venous inflow is easily visualized from the parasternal acoustic window, in the right ventricular inflow view (Figure 14-1, A, and Video 5) and from the parasternal acoustic window, in the right ventricular inflow view (see Figure 14-1, B, and Video 4). The right atrium, tricuspid valve, and RV (inlet, free wall, apex, and infundibulum) are seen from the parasternal short axis (see Figure 14-1, C) and modified apical four-chamber views (see Figure 14-1, D). The tricuspid valve comprises septal, anterosuperior, and posterior leaflets, attached by chordae tendineae to papillary muscles located within the septum and lateral walls of the RV. Unlike with the aortic and mitral valves, it is not possible to see all three leaflets of the tricuspid valve from any single two-dimensional view—the septal and anterosuperior leaflets are seen in the apical four-chamber view, with the posterior and anterosuperior leaflets seen in the right ventricular inflow view. The pulmonary valve consists of three cusps without subvalvular apparatus and, along with the main pulmonary artery and proximal branch pulmonary arteries, is best seen on the parasternal short axis (see Figure 14-1, C, and Video 6) and rotated subcostal views. Normal ranges for right ventricular and right atrial size have been derived from normal healthy populations. An important point in this context is that these measures are not indexed to body surface area, so reported values may lose discriminatory power in assessment of these structures at either end of the normal distribution curve for size.

Table 14-1 Normal Limits for Recommended Measurements of Right-Sided Heart Structure and Function

A, velocity of active ventricular filling (see Figure 14-3, A); E, velocity of passive right ventricular filling (see Figure 14-3, A); E′, a tissue Doppler measurement of the motion of the lateral tricuspid valve annulus during early diastole (see Figure 14-2, B); PLAX, parasternal long axis; RV, right ventricle; RVOT, right ventricular outflow tract; RA, right atrium; TV, tricuspid valve.

Data from Rudski L, Lai W, Afilalo J, et al: Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography, J Am Soc Echocardiogr 23:685–713, 2010.

Figure 14-1 Echocardiographic views. A, Tilted right ventricular inflow view; B, subcostal view; C, parasternal short axis view; D, apical four-chamber view. AV, aortic valve; IAS, interatrial septum; IVC, inferior vena cava; LA, left atrium; LV, left ventricle; PA, pulmonary artery; PAb, pulmonary artery bifurcation; PV, pulmonary valve; RA, right atrium; RV, right ventricle; RVD1, right ventricular basal diameter; RVOTp, right ventricular outflow tract proximal diameter; RVw, site of measurement of right ventricular wall thickness; TV, anterosuperior (TVas), posterior (TVp), and tricuspid valve with septal (TVs) leaflets.

Assessment of Right Ventricular Function by Echocardiography

The orientation of the myocardial fibers within the right ventricular wall is different from that within the LV, leading to three definable modes of contraction. First, the right ventricular contraction is sequential and peristaltic, from inlet to infundibulum, and results in longitudinal shortening, which is the main driver behind right ventricular stroke volume. Second, the right ventricular free wall is observed to move inwards toward the interventricular septum (IVS), contributing to stroke volume through a bellows-like effect. Third, twist or torsion of the RV is less important than in the LV but arises predominantly from contraction against the insertion points of the RV into the septum. Although longitudinal (rather than radial) shortening is most important, the IVS contributes between 20% to 40% of right ventricular stroke volume. Echocardiographic evaluation of right ventricular function is complicated, because volumetric assessment of the RV (using end-diastolic and end-systolic volumes to calculate an ejection fraction) cannot be performed without advanced three-dimensional techniques. Visual assessment of right ventricular function may provide an initial qualitative evaluation of the function of the right side of the heart but suffers from interstudy variability of up to 15%; however, one or more of the following quantitative measurements should be incorporated.

Tricuspid Annular Plane Systolic Excursion

Tricuspid annular plane systolic excursion (TAPSE) is measured using M-mode echocardiography in the apical four-chamber view to generate an image that illustrates the systolic longitudinal displacement of the lateral tricuspid annulus toward the apex (Figure 14-2, A). Because the septal attachment of the tricuspid annulus is relatively fixed, the major component of longitudinal systolic motion occurs at this point. The greater the displacement, the better is right ventricular function—a value less than 16 mm is considered abnormal. TAPSE correlates closely with right ventricular ejection fraction (RVEF) measured by radionuclide angiography, the “gold standard” modality for assessment of right ventricular function. TAPSE is simple to perform, with reproducible results, and is less dependent on optimal image quality than other measurements. It does not require complex calculations (the result obtained may be multiplied by 3.2 to give a value for RVEF, if desired) and can predict likelihood of death among patients with pulmonary arterial hypertension (PAH). However, TAPSE makes the assumption that displacement of a single segment represents function of the entire RV, which does not apply in the presence of regional dysfunction, particularly that affecting the septum. TAPSE is afterload dependent and falls with increasing severity of PAH.

Figure 14-2 Assessment of right ventricular systolic function by various modalities: A, tricuspid annular plane systolic excursion (TAPSE); B, S′ wave measurement by tissue Doppler imaging; C, myocardial performance index (MPI), or Tei index, calculated as isovolumetric relaxation time (IVRT) plus isovolumetric contraction time (IVCT) divided by ventricular ejection time (ET), or a/b − a; D, fractional area change (FAC)—here, from 9.6 cm² to 4.9 cm² = 49%. E/E′ is calculated as follows: peak velocity of pulsed-wave Doppler E wave (measured at the tips of the tricuspid valve; see Figure 14-3, A) divided by peak velocity of the E′ wave (measured using tissue Doppler imaging at the lateral tricuspid valve annulus).

Right Ventricular Diastolic Function

Diastolic function, which reflects the relaxation and filling of the RV, can be a useful early marker predicting deterioration in right ventricular function and may be of prognostic utility in patients with a number of acute and chronic respiratory conditions, although further data are needed. The parameters used for assessment of right ventricular diastolic function are essentially the same as those used in left ventricular diastolic assessment, including pulsed-wave Doppler-derived transtricuspid E/A ratio, tissue Doppler–derived E/E′ ratio, IVRT, and right atrial size (Figure 14-3, A). IVRT is a tissue Doppler measurement of the time taken for the right ventricle to relax, which is made at the basal right ventricular free wall. This relaxation period occurs after pulmonary valve closure (end of the S′ wave) and before tricuspid valve opening (beginning of the E′ wave) (see Figure 14-2, C). A prolonged IVRT (longer than 75 ms) may represent impaired myocardial relaxation and can be highly suggestive of PAH. Diastolic measurements should be acquired in end-expiration, and interpretation of the results should take account of the age of the patient (see Table 14-1). One additional important finding is the presence of late antegrade flow measured by pulsed-wave Doppler midway between the pulmonary valve leaflets and the pulmonary artery bifurcation, which is a sign of restrictive right ventricular filling and is associated with a poor prognosis.

Figure 14-3 A, Pulsed-wave Doppler assessment of tricuspid valve inflow from the apical four-chamber view. E wave velocity reflects passive ventricular filling, whereas A wave velocity represents ventricular filling secondary to atrial systole. B and C, Flattening of the interventricular septum (arrow). D1, minor axis dimension perpendicular to and bisecting septum; D2, minor axis dimension parallel to the septum. Eccentricity index (EI) is calculated as D2/D1. Normal EI value is 1.0; EI greater than 1.0 at end-diastole is indicative of volume overload of right ventricle, whereas EI greater than 1.0 at end-systole is indicative of pressure overload.

Hemodynamic Assessment of the Right side of the Heart By Echocardiography

In health, the right side of the heart ejects blood into a low-resistance, highly distensible pulmonary vascular bed. The RV is thin-walled and more compliant than the LV (so it adapts well to increases in volume) but demonstrates heightened sensitivity to change in afterload (so it adapts poorly to increases in pulmonary vascular resistance). The LV and RV interact with one another during systole, and this ventricular interdependence is mediated mainly by the motion of the IVS. Both changes in volume (preload) or pressure (afterload) within the right side of the heart will have an impact on the motion of the IVS. Under normal conditions, the higher intracavity pressure in the LV, as compared with that in the RV, helps to maintain a circular shape of the LV when imaged in cross section (see Video 2). Pressure loading of the RV results in a “flattening” of the IVS during systole, creating a more D-shaped left ventricular cavity. Volume loading of the RV results in a “flattening” of the IVS during diastole (see Figure 14-3, B and C; see also Video 7 ). This is an important marker of loading conditions within the RV, which can be measured by calculating the “eccentricity index” of the LV in the parasternal short-axis view (i.e., the ratio of the anterior-posterior dimension to septal-lateral dimension of the left ventricular cavity).

A number of direct parameters can be used for hemodynamic assessment of the right ventricular and pulmonary circulations, the most common being measurement of right ventricular systolic pressure (RVSP) estimated from the velocity of the jet of the tricuspid regurgitation (Figure 14-4, A and B, and Video 8). Using the simplified Bernoulli equation,

Figure 14-4 Hemodynamic measurements in echocardiography. A, Color flow Doppler imaging demonstrating tricuspid regurgitation (TR), with blood being ejected back into the right atrium. B, Continuous-wave Doppler interrogation of the regurgitant jet. Point 1 denotes peak jet velocity, which measures 3.6 m/s in this example. C, M-mode assessment of the inferior vena cava (IVC) from the subcostal acoustic window. The IVC can be seen to collapse with short sharp inspiration, decreasing in size from 1.94 cm to 0.648 cm in this example. Right atrial pressure can be estimated by assessing the diameter of the IVC at rest and then recording the change in size in response to inspiration: normal IVC diameter (i.e., less than 1.5 cm) with full collapse, 0 to 5 mm Hg; IVC diameter 1.5 to 2.5 cm with greater than 50% collapse, 5 to 10 mm Hg; IVC diameter 1.5 to 2.5 cm with less than 50% collapse, 10 to 15 mm Hg; IVC diameter greater than 2.5 with less than 50% collapse, 15 to 20 mm Hg; and IVC diameter greater than 2.5 cm with no change, 20 mm Hg or greater. D, Echocardiographic determination of diastolic and mean pulmonary artery pressure (PAP) by continuous-wave Doppler assessment of the signal generated by pulmonary regurgitation (PR). Point 1 indicates the maximal velocity of the jet of pulmonary regurgitation at the beginning of diastole. Mean PAP can be calculated as 4 × (early pulmonary regurgitation jet velocity)² + estimated right atrial pressure. Point 2 indicates the pulmonary regurgitant jet velocity at end-diastole, with diastolic PAP calculated as 4 × (end pulmonary regurgitant jet velocity)² + estimated right atrial pressure.

where v = maximal velocity of the jet of tricuspid regurgitation (in m/s) and right atrial pressure is estimated from resting inferior vena cava diameter taking into account the degree of inspiratory collapse (see Figure 14-4, C, and Video 9 ). In the absence of a gradient across the pulmonary valve or RVOT, RVSP equals the systolic pulmonary artery pressure (PAP). Care must be taken to ensure that this measurement is made with an adequate Doppler signal; if the signal is not clear, it can be improved with the injection of an agitated mixture of blood, saline, and air for contrast. The measurement should be made several times, and the highest velocity obtained used in calculation. A normal value for a peak tricuspid regurgitation signal is less than 2.6 m/s (equivalent to a pressure of 27 mm Hg + right atrial pressure), but this value increases with age and with increasing body mass index. This method may underestimate RVSP when severe tricuspid regurgitation is present.

The simplified Bernoulli equation also can be used to estimate diastolic PAP from the end-diastolic velocity of the pulmonary regurgitant jet: diastolic PAP = 4v² + right atrial pressure (see Figure 14-4, D), where v = terminal velocity of the regurgitant jet (in m/s). Mean PAP can then be calculated using a standard formula: mean PAP = 1/3 systolic PAP + 2/3 diastolic PAP. It also can be estimated directly from the early peak of the regurgitant jet velocity: mean PAP = 4v² (v = early maximal velocity of the regurgitant jet [in m/s]) plus right atrial pressure (see Figure 14-4, D). Echocardiography also can deliver measurements of pulmonary vascular resistance, pulmonary capillary wedge pressure, and pulmonary capacitance, although these are not in routine use. These measurements provide important insights into right ventricular and pulmonary hemodynamic status, although any conclusions should be based not only on a single hemodynamic parameter, such as jet velocity in tricuspid regurgitation, but also in the context of a full assessment of right ventricular and right atrial size, shape, and function.

Right ventricular adaptation to disease is complex and depends on many factors. The most important factors appear to be the type and severity of myocardial stress, the time course of the disease (acute or chronic), and the time of onset of the disease process (young age or adult years). The remodeling of the right side of the heart produces classic anatomic and hemodynamic characteristics that are used by echocardiographers to diagnose and assess prognosis in specific disease states, as discussed next.

Echocardiography in Evaluation of Specific Disease States

Acute Right-Sided Heart Failure

Acute right ventricular dysfunction may occur as a consequence of various disease processes, which include ischemic heart disease, myocarditis, and pulmonary embolism. Among patients presenting with suspected acute pulmonary embolism, neither TTE nor TEE have sufficient sensitivity to be used as the primary imaging modality for diagnosis but may provide useful supportive data and can identify those persons at high risk for adverse outcomes. Typically, the abrupt vascular obstruction sets up a cascade of adverse hemodynamic effects that not only exert strain on the RV but also may impair left ventricular function and coronary artery perfusion (Figure 14-5).

Figure 14-5 The vicious circle of detrimental pathophysiologic events that may occur in the setting of acute vascular obstruction, such as with acute pulmonary embolism. CO, cardiac output; IVS, interventricular septum; RV, right ventricle; RVEDP, right ventricular end-diastolic pressure.

Although echocardiography may be normal in up to 50% of patients with confirmed pulmonary embolism, sensitivity is increased with increasing hemodynamic compromise from the event. Typical echocardiographic findings include dilatation of the RV with reduced thickening of the free wall, flattening of the IVS in systole, dilatation of the right atrium due to elevated right ventricular end-diastolic pressure, paradoxical atrial septal motion due to high right atrial pressure, which also is associated with dilatation of the inferior vena cava, and loss of respiratory variation. Hemodynamic measurements altered by acute pulmonary embolism include increased jet velocity in tricuspid regurgitation (more than 2.7 m/s) and reduction in TAPSE and S′, together with shortened RVOT acceleration time. Rarely, thrombus may be seen in the right side of the heart or pulmonary artery. The McConnell sign, consisting of hypokinesis of the mid–free wall in the presence of normal apical wall motion, is reported to be 77% sensitive and 94% specific for acute pulmonary embolism.

In the setting of acute pulmonary embolism, the presence of right ventricular dysfunction and/or elevated PAP has been shown to predict poor outcome. Consequently, using echocardiography early in the assessment of patients with acute hemodynamic instability may assist with rapid detection of these high-risk features and may identify a cohort of subjects who may benefit from more aggressive management, perhaps involving the use of thrombolysis. An important point in this context is that these changes occur in patients with acute pulmonary embolism who have no preexisting thromboembolism or PAH, in which case the effect of chronic pressure overload on the RV modifies the appearance of the right side of the heart.

Pericardial Effusion and Tamponade

The pericardium consists of a monolayer of mesothelial cells that directly overlie the epicardial fat (visceral layer) and reflects back upon itself to form a second (parietal) layer. In health, the pericardium contains a small volume (15 to 35 mL) of plasma ultrafiltrate, which acts as a lubricant. Under physiologic conditions of low stress, the pericardium is elastic, but under higher stress, it has the tensile strength of rubber and becomes stiff and resistant to stretch. This transition in mechanical properties occurs close to the upper limit of normal pericardial volume. As the pericardial reserve volume is exceeded, pressure within the pericardium increases rapidly. This rise in pressure is dependent not only on the volume but also on the rate of accumulation, which explains why large pericardial effusions may cause no hemodynamic compromise if they have developed slowly, whereas very small volumes can cause hemodynamic collapse if the ultrafiltrate accumulated rapidly. Under conditions in which pericardial pressure rises, the mechanical properties of the pericardium become an important determinant of right atrial and right ventricular filling, and cardiac function may be adversely affected, with loss of normal ventricular interdependence.

Pericardial effusion is detected easily by TTE and is distinguished from pleural fluid by its presence anterior to the descending aorta in the parasternal long-axis view (Figure 14-6 and Video 13 ). Pericardial fluid almost never overlaps the left atrium and usually collects behind the right atrium and then the RV and extends to the lateral wall of the LV. This localization obviously depends on patient position, but the effusion can be a focal process with a localized accumulation of fluid—for example, after cardiothoracic surgery. Assessing the size of a pericardial effusion is important for prognostication: The larger the collection, the worse the outcome. The presence of even a small pericardial effusion, however, is a marker for increased risk of death.

Figure 14-6 A large pericardial effusion, viewed from the parasternal long-axis (PLAX) (A) and apical four-chamber (B) acoustic windows. In A, the effusion can be seen to lie anterior to the descending thoracic aorta (DA), thereby differentiating it from a left-sided pleural effusion, which usually is seen to extend posteriorly to the descending aorta. In this example, the effusion extends alongside the left atrium (LA), which is unusual. In B, the right atrium (RA) is seen to collapse during diastole (arrow), which may be a feature of significantly increased intrapericardial pressure and may be an early sign of tamponade.

Although cardiac tamponade remains a clinical diagnosis, certain echocardiographic features are often used to confirm the presence of a hemodynamically significant pericardial collection. As the pericardial pressure increases, the first effect is for ventricular interdependence to be exaggerated—this means that respiratory variation in tricuspid valve inflow measured at the tips of the valve on pulsed-wave Doppler imaging is exaggerated at the expense of mitral valve inflow. On inspiration, for example, tricuspid valve inflow velocity and volume increase, whereas mitral valve inflow velocity and volume decrease. As pressure rises further and diastolic filling of the heart is impaired, the chambers of the heart start to “collapse” in order of intracavity pressure—first the right atrium, then the RV, and subsequently the left atrium (see Videos 14 and 15; see also Video 13 ). Abnormal posterior motion of the anterior right ventricular free wall during diastole seen in the parasternal long-axis view should prompt urgent review, with consideration of pericardiocentesis. TTE can then play a vital role in guiding percutaneous needle aspiration, or drain insertion, which may rapidly alleviate symptoms. Echocardiography-guided aspiration has a high procedural success rate and carries a risk of major complications of only 1% to 2%.

Conclusions

Traditionally, the right side of the heart has often been ignored relative to the LV, but right ventricular function is well recognized to play a vital role in determining clinical outcome in both acute and chronic respiratory disease. Careful qualitative and quantitative examination of the right side of the heart with echocardiography can provide valuable data to assist in diagnosis, guiding treatment, and establishing prognosis in patients with cardiorespiratory disease. Echocardiography provides this information cheaply and at no risk to the patient. Those clinicians limiting their understanding of echocardiography to the reading of report conclusions may be limiting the care that they are providing to their patients. When interpreting echocardiographic reports, however, clinicians should pay particular attention to the quality of the data presented to them, because acquisition of good-quality images can be challenging, especially in patients with respiratory disease.

Acknowledgments

With thanks to Jenny Green, Echocardiographer, University Hospitals Birmingham, The New Queen Elizabeth Hospital Birmingham, and Kam Rai, Lead Echocardiographer, University Hospitals Coventry and Warwickshire NHS Trust, United Kingdom.