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Figure 13-85: A. Pulmonic stenosis. The pulmonic valve leaflet is thickened and echo-reflective (arrow). RA = right atrium; LA = left atrium; AO = aorta; PA = pulmonary artery; RV = right ventricle. B. Doppler interrogation reveals increased flow velocity (4 m/s) through the valve orifice.

Although severe pulmonic regurgitation (PR) is rare, mild PR is common and appears as a flame shaped flow disturbance in the right ventricular outflow tract (RVOT) in diastole.345 Many individuals have trivial PR on color Doppler examination; this is a physiologic, normal variant Fig. 13-86). Hemodynamically significant PR is uncommon; when present, it is usually due to congenital heart disease, valvular tumors, endocarditis, or carcinoid heart disease (Chap. 59). The echocardiographic grading of PR is semiquantitative, based on the density of the CW envelope, area of the color Doppler jet, and width of the jet at the valve.346,347 The PR pressure half-time by CW Doppler may be shorter with more severe PR, but this is not as well investigated as in the case of aortic regurgitation. Measurements derived from the CW Doppler recording also provide estimates of end-diastolic pulmonary artery pressure using the Bernoulli equation as follows348: [4(PR end-diastolic velocity)2 + central venous pressure (CVP).

Tricuspid Valve

Tricuspid stenosis (TS) is usually rheumatic in origin, and coexistent mitral and aortic valvular disease is the rule. Congenital or acquired (nonrheumatic) causes of TS are quite uncommon. On rare occasions, tricuspid stenosis may be caused by carcinoid heart disease or by leaflet adhesions to permanent pacemaker leads. Because of the large size of the tricuspid annulus, obstruction by masses, even multiple vegetations, is unlikely to cause stenosis (Chap. 59).

Regardless of the etiology, diastolic doming of the valve leaflets suggests stenosis.349,350 CW Doppler interrogation is also helpful and mimics the findings of MS (high diastolic velocity with prolonged pressure half-time).349 The pressure half-time equation of mitral valve area calculation cannot be applied directly to the tricuspid valve, and large studies comparing Doppler echocardiography with right heart catheterization in TS are not available.

Tricuspid regurgitation (TR) is much more common than TS, and like PR is present to a mild degree in many normal individuals (Chap. 59). Hemodynamically significant TR may be caused by endocarditis, rheumatic valvular disease, pulmonary hypertension, congenital heart disease (for example, Ebstein's anomaly), carcinoid heart disease, flail TR leaflet (which can occur as a complication of cardiac trauma or endomyocardial biopsy), and tricuspid valve prolapse. Echocardiographic findings in patients with TR generally mirror those found in MR.354 Although 2D imaging can detect abnormalities associated with TR, such as incomplete leaflet coaptation, flail leaflet, and right-sided chamber enlargement, the technique cannot accurately quantify TR grade. Doppler echocardiography, especially color-flow mapping, has become the procedure of choice to detect TR, and has reasonable accuracy for semiquantitation of severity.352,353 As with MR, severity of TR can be estimated by regurgitant jet area, ratio of jet area to right atrial area, and size of proximal flow convergence zones354 Fig. 13-31). Doppler interrogation of the hepatic vein is also useful, as systolic flow reversal within the vein suggests severe TR355 (Q-hB; Fig. 13-87). Peak right ventricular (and pulmonary artery) pressure can be estimated using measurements of peak TR velocity by CW Doppler (see section on Bernoulli equation, above). If necessary, intravenous echocardiographic contrast agents can be injected to accentuate the TR Doppler jet and facilitate more accurate measurements of pulmonary artery pressure.352-354

Right Ventricular Function and Pulmonary Hypertension

Right ventricular (RV) enlargement and pulmonary hypertension can be diagnosed and assessed by echocardiography355'356 (B*;B; Fig. 13-88/1 and B). Because of the asymmetrical and crescentic shape of the RV, accurate volume calculations are difficult.357,358 Nonetheless, 2D imaging provides useful general information regarding RV size and function. In the apical four-chamber view, the RV should appear somewhat smaller than the LV; therefore RV enlargement can be diagnosed qualitatively when the RV cross-sectional area exceeds that of the LV. RV chamber area measurements in the apical four-chamber imaging plane can also be compared to standardized normal values.359 Although not well standardized, measurements of RV wall thickness can be performed from the parasternal view; a value of 5 mm is generally accepted as the upper limit of normal.360,361 Systolic motion of the RV free wall and LV lateral wall toward the interventricular septum should be similar and roughly symmetrical in normal situations. Asymmetrical hypokinesis of the RV free wall indicates RV dysfunction.362

RV volume overload can lead to RV hypertrophy, chamber enlargement, and, in advanced stages, depressed RV systolic function. TR can result from or cause RV overload, and the TR Doppler velocity allows estimation of the peak RV systolic pressure. The interventricular septum also becomes abnormal in RV overload and tends to flatten or even bulge toward the LV Fig.

13-89).363 The pattern of septal movement can help distinguish between volume and pressure overload: in pure volume overload, the RV diastolic pressure may equal or exceed that of the LV, while the systolic pressure of the LV greatly exceeds that of the RV. Therefore, the interventricular septum flattens during diastole and returns to its normal curvature during systole.363,364 With RV pressure overload, however, the abnormally high RV pressures persist through the entire cardiac cycle and the interventricular septum remains deformed during both systole and diastole.364

The hallmark of pulmonary hypertension by Doppler echocardiography is a high-velocity TR jet in the absence of PS. Peak TR jet velocity can be converted to peak systolic PA pressure as follows365:

In the setting of severe pulmonary hypertension, the main PA and the inferior vena cava are often dilated. If RA pressure is elevated, the inferior vena cava (IVC) does not decrease in diameter with inspiration as normally expected.366 M-mode examination of the pulmonic valve in pulmonary hypertension may show a characteristic W-shaped motion of the valve leaflet during systole367-369 (0-»-B; Fig. 13-90) and loss of the normal a dip caused by partial opening of the valve during atrial contraction. The loss of the a wave is probably due to the large pressure difference between the RV and pulmonary artery during late diastole and the resulting inability of the atrial contraction to partially open the pulmonic valve. The midsystolic closure of the valve and partial reopening in late systole (sometimes called the flying W) may be caused by elevated pulmonary vascular resistance and oscillation of a pressure wavefront within the pulmonary artery.370

Characteristic pulsed-wave Doppler abnormalities in pulmonary hypertension include a decrease in the velocity-time integral of flow through the pulmonic valve (secondary to depressed RV stroke volume) and a shortening of the acceleration time (measured from beginning of flow through the pulmonic valve to peak velocity). The acceleration time (in milliseconds) can be used to estimate the mean pulmonary artery (PA) pressure374 as:

Mean PA pressure - 80 - (accderation time/2)

Pulmonic regurgitation is also common in the setting of pulmonary hypertension and is usually well recorded by pulsed Doppler. As discussed above, the end-diastolic PR velocity can be used to estimate PA end-diastolic pressure by the Bernoulli equation.


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