Trivial or very mild degrees of tricuspid regurgitation can frequently be present in normal individuals, and in the absence of abnormalities of the valvular structures or cardiac chambers, it should be regarded as a normal variant. Pathologic tricuspid regurgitation can be either congenital or acquired. Ebstein's anomaly is one of the important causes of congenital tricuspid regurgitation, and echocardiography plays a major role in the diagnosis and surgical planning. More commonly, however, tricuspid regurgitation is the result of right ventricular dilatation and/or dysfunction secondary to pulmonary hypertension or right ventricular infarction. Rheumatic heart disease (less frequently encountered in developed countries) and carcinoid heart disease result in thickening, restricted mobility, and/or malcoaptation of the leaflets, leading to incompetence of the valve. In patients with endocarditis, vegetations that tend to form on the atrial surface of the leaflets can lead to destruction of the leaflets and/or chordae, causing significant degrees of regurgitation in advanced cases. Annular dilatation can be seen in some cases of Marfan's syndrome, and tricuspid valve prolapse with or without associated mitral valve prolapse is another cause of tricuspid regurgitation. Occasionally, tumors such as right atrial myxomas can interfere with the normal coaptation of the leaflets, therefore causing regurgitation.
Two-dimensional examination of the tricuspid valve apparatus provides significant information regarding the underlying cause and mechanism of tricuspid regurgitation. The identification of anatomic abnormalities (eg, Ebstein's anomaly), abnormal masses, annular dilatation, and noncoaptation (see Figure 10–3) are all essential to make a correct diagnosis. Pacemaker wires or catheters passing through the tricuspid orifice are readily visualized (Figure 10–6), and although uncommonly encountered with the right-sided valves,4 TEE is highly sensitive for the detection of vegetations.5 Movement of any of the leaflets beyond the plane of the tricuspid annulus inside the right atrium indicates the presence of tricuspid prolapse (Figure 10–7).6 Additionally, in patients with tricuspid valve prolapse, the leaflets and chordae are usually redundant and myxomatous. Features characteristic of Ebstein's anomaly include apical displacement or “off-setting” of the hinge point attachment of the septal leaflet relative to that of the anterior mitral leaflet. A displacement index is easily produced by measuring the distance between the two hinge points and indexing to body surface area. This can be done in the midesophageal four-chamber view, and different angulations of the probe will help obtain the maximal difference. An indexed value greater than 8 mm/m squared7,8 or a nonindexed value of greater than 15 mm in children and 20 mm in adults,9 together with elongation of the anterior leaflet (the so-called “sail-like” or “curtain-like” appearance),10,11 tethering, and restricted leaflet motion,7 distinguish this congenital anomaly from other causes of tricuspid regurgitation. Additional echocardiographic features of Ebstein's anomaly include apical displacement of the other leaflets, absence or fenestration of any of the leaflets, and “atrialization” of a part of the right ventricle.
Midesophageal right ventricular inflow-outflow view showing a pulmonary artery catheter crossing the tricuspid valve and coursing through the outflow tract. (PA, pulmonary artery.)
Midesophageal four-chamber view of a patient with Marfan syndrome showing mild prolapse of the tricuspid leaflets (arrow).
Carcinoid heart disease in patients with carcinoid syndrome results from fibrous deposits on the endocardium of the right-sided valves and chambers. This leads to thickening and rigidity of the leaflets, with the valves fixed in an open position, and associated stenosis is common. Involvement of the left-sided valves should prompt a careful evaluation for right-to-left shunting.12 Thickening, shortening, and restricted mobility of the leaflets are all characteristics of rheumatic involvement of the valve. The presence of malcoaptation of the leaflets usually indicates severe regurgitation, as does a large tricuspid annulus (>2.1 cm/m2 of body surface area).13 Although measurement of the tricuspid annulus should be performed in multiple views during diastole, using the frame that shows maximal distance between the insertion points of the leaflets, the measurement from the transgastric right ventricular (RV) inflow view correlates best with surgical measures.14 Moreover, the dimensions of the right-sided chambers can provide clues to the severity of regurgitation. In contrast to mild regurgitation, chronic moderate and severe tricuspid regurgitation are usually associated with a dilated right atrium and ventricle. This is, however, not true in cases of acute moderate or severe tricuspid regurgitation where the chambers do not have time to remodel.
Color Doppler mapping can detect and provide a degree of quantification of the severity of tricuspid regurgitation. When applied, the multiplane angle should be changed and the probe tip manipulated in order to demonstrate the largest possible jet of regurgitation (Figure 10–8). Doppler principles similar to those used in the assessment of mitral regurgitation can be used to assess tricuspid regurgitation (Table 10–2). Measuring the vena contracta, which is the narrowest portion of the jet at the orifice of the valve, is easy to perform in the midesophageal four-chamber view; the cutoff for severe regurgitation is considered to be7 mm.15,16 In centrally directed regurgitation, measurement of the jet area can be helpful; an area of greater than 10 cm2 is indicative of severe insufficiency.16 Doppler parameters that indicate increased severity of tricuspid regurgitation include a tricuspid inflow velocity higher than 1 m/s, and a dense, triangular, and early-peaking continuous-wave (CW) Doppler signal of the tricuspid valve. The proximal isovelocity surface area (PISA) method can be applied for more quantitative assessment (Figure 10–9). A simplified approach has been suggested, whereby measuring the PISA radius at a Nyquist limit of about 28 cm/s can provide an estimate of the severity of the regurgitation; a radius of 5 mm or less usually identifies mild degrees, and a radius greater than 9 mm is found in severe cases.16
Transgastric right ventricular inflow view showing severe tricuspid regurgitation.
Table 10–2. Echocardiographic Findings in Tricuspid Regurgitation ||Download (.pdf)
Table 10–2. Echocardiographic Findings in Tricuspid Regurgitation
Can be normal
Malcoaptation ± flail
Can be normal
Dilated (unless acute)
Tricuspid annulus diameter
Area of the jet (cm2)a,b
Vena contracta width (mm)b
PISA radius (mm)c
CW Doppler signal
Soft and parabolic
Dense, variable contour
Dense, triangular with early peaking
Coronary sinus flow
Forward in systole
Hepatic venous flow
Modified midesophageal view showing flow acceleration and the proximal isovelocity surface area (PISA) contour.
In addition, severe tricuspid regurgitation is associated with systolic flow reversal in the hepatic veins and/or the coronary sinus, similar to what is seen in the pulmonary veins in the case of severe mitral regurgitation.
Hepatic Venous Flow Patterns
Imaging of the hepatic veins can be performed from the stomach by withdrawing the probe and rotating it to the right to visualize liver parenchyma in the transverse plane. The hepatic veins can be identified with the help of color Doppler (Figure 10–10) at a reduced Nyquist limit (<40 cm/s). Pulsed-wave (PW) Doppler is used to assess flow patterns in the largest hepatic vein identified. A normal flow pattern consists of larger systolic and smaller diastolic forward-flow waves. In addition, two flow-reversal waves may be noted: one in late diastole (which is the result of atrial contraction) and another in late systole. A blunted or reversed systolic wave is seen in patients with severe tricuspid regurgitation.17 Patients with elevated right atrial pressures or atrial fibrillation can exhibit blunting of the systolic wave.
Color Doppler visualization of hepatic venous flow (A). Normal hepatic vein Doppler profile (B) characterized by a small reversal of flow after atrial contraction (AR wave), an antegrade systolic phase during atrial filling from the superior and inferior vena cavae (S wave), a second small flow reversal at end-systole (V wave), and a second antegrade diastolic filling phase (D wave).
COronary SInus FLow PAtterns
PW Doppler sampling of the coronary sinus flow is best performed in the transverse view of the coronary sinus, obtained from the midesophageal four-chamber view by advancing the probe slightly and retroflexing it. This will visualize the coronary sinus in its long axis in the atrioventricular groove (Figure 10–11). In normal individuals with absent or mild degrees of tricuspid regurgitation, two negative waves are noted: a late systolic wave and a diastolic wave with higher velocity and longer duration. When severe tricuspid regurgitation is present, reversal of the systolic wave is seen. This finding has a high sensitivity and a good specificity for the detection of severe tricuspid regurgitation.18
Long-axis view of the coronary sinus. (CS, coronary sinus; LV, left ventricle; RV, right ventricle; RA, right atrium; SL, septal leaflet; PL, posterior leaflet of the tricuspid valve.)
Estimation of Systolic Pulmonary artery Pressure
Using CW Doppler, measurement of the peak tricuspid regurgitation jet velocity can be performed. Usually, the midesophageal right ventricular inflow-outflow view provides good alignment of the regurgitation jet with the Doppler signal. Localization of the jet is assisted by color Doppler flow mapping, and angulation of the probe with adjustment of the multiplane angle should be performed in order to identify the maximal velocity jet (Figure 10–12). Based on the simplified Bernoulli equation, the pressure gradient between the right ventricle and atrium is given by:
Pressure Gradient (mm Hg) = 4 × [Peak Regurgitant Velocity (m/s)]2
Continuous-wave Doppler measurement of the peak tricuspid regurgitation jet velocity from the midesophageal inflow-outflow view. Color Doppler is used to guide the placement of the CW Doppler cursor. In this patient, the peak systolic gradient across the tricuspid valve was 73 mm Hg, indicating significant pulmonary hypertension (there was no right ventricular outflow tract obstruction or pulmonary stenosis present).
When added to an estimate of the right atrial pressure, this gradient provides an approximation of the right ventricular systolic pressure, which in the absence of right ventricular outflow obstruction is equivalent to the systolic pulmonary artery pressure. Right atrial pressure is commonly assessed by examining the respirophasic changes in the diameter of the inferior vena cava (IVC) (Figure 10–13). A greater than 50% change in the diameter of the IVC with inspiration indicates a right atrial pressure of less than 10 mm Hg, while a less marked change is associated with a pressure that is above 10 mm Hg.19 This, however, is not reliable in patients on mechanical ventilation, or in those who do not mount a good inspiratory effort. In these patients, right atrial pressure can be assessed by examining the PW Doppler pattern of the hepatic veins, based on the following formula20:
Mean Right Atrial Pressure (mm Hg) = 21.6 − (24 × SFF)
where SFF is systolic filling fraction of the hepatic venous flow, which is obtained by dividing the hepatic vein systolic velocity-time integral (VTI) by the sum of systolic and diastolic VTIs. For the purpose of simplification, peak velocities can be used in lieu of VTIs.20 This method, however, has not been validated in patients with severe tricuspid regurgitation; instead, the right atrial pressure can be estimated in these patients at a constant of 20 mm Hg, especially in the presence of other indicators of elevated right atrial pressure (eg, significantly distended jugular veins).21
Significantly dilated vena cava (arrow), with spontaneous echocontrast, indicative of low flow. There were no respiratory variations in the diameter of the vessel, indicating elevated right atrial pressures.
More recently, Arthur et al22 found that measurement of the IVC diameter by TEE can provide an estimate of the central venous pressure (CVP) in mechanically ventilated patients. In their study, the IVC diameter was measured in the bicaval view (at 110°) at the level of the cavo-atrial junction and at the end of the T-wave of the electrocardiogram. The ventilator was turned off at time of the measurement to eliminate the effect of intrathoracic pressure changes. The linear regression–derived equation to calculate the CVP based on the IVC diameter [CVP = (IVC diameter − 4.004)/0.751] showed a good correlation with catheter-measured CVP. Based on their findings, we propose the following simplified formula for estimating the CVP based on the IVC diameter:
CVP (mm Hg) = 4/3 × [IVC diameter (mm) − 4]