Secondary Logo

Journal Logo

Functional Tricuspid Regurgitation in a Patient with Endocarditis

Richardson, John S., MD; Little, Michael B., MD

doi: 10.1213/ANE.0b013e3181b544af
Cardiovascular Anesthesiology: Echo Rounds

From the Department of Anesthesiology, University of Texas Health Science Center, San Antonio, Texas.

Accepted for publication May 15, 2009.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (

Address correspondence and reprint requests to John S. Richardson, MD, 7703 Floyd Curl Drive, San Antonio, TX 78229. Address e-mail to

A 39-yr-old man presented with chest pain, cough, fever, chills, and weight loss. A transthoracic echocardiogram revealed vegetations on the mitral valve (MV) and the aortic valve (AV) with severe mitral regurgitation (MR) and severe aortic regurgitation (AR). No vegetations were seen on the tricuspid valve (TV), but severe tricuspid regurgitation (TR) was noted. The estimated pulmonary artery systolic pressure (PASP) was 71 mm Hg. The left ventricular ejection fraction was normal. The size of the right atrium (RA) and right ventricle (RV) was not mentioned in the report. With a diagnosis of infective endocarditis, the patient was started on antibiotics, furosemide, and hydralazine.

After 5 days, a transesophageal echocardiogram (TEE) revealed a mildly dilated left atrium, normal size left ventricle (LV), normal left ventricular ejection fraction, vegetations on the MV and AV, severe MR, severe AR, moderate TR, and a normal PASP. The size of the RA and RV was not mentioned in the report. The patient was now in renal failure requiring dialysis and had some degree of coagulopathy. He was scheduled the following day for MV replacement and AV replacement. The short duration of the disease process, the decrease in PASP, and less TR in response to medical management led to the preoperative assessment that repair of the left-sided lesions would result in resolution of the TR.

After induction of general anesthesia, a pulmonary artery catheter was inserted, and a TEE was performed. The right atrial pressure was 30 mm Hg, and the pulmonary artery pressure was 49/33 mm Hg. The TEE confirmed the presence of AV and MV vegetations with severe MR and AR. At this time, the TEE demonstrated a structurally normal TV, a dilated RA, dilated RV, dilated tricuspid annulus (TA), and severe TR. The patient underwent MV replacement, AV replacement, as well as a tricuspid annuloplasty based on severe TR demonstrated by the intraoperative TEE. After weaning from cardiopulmonary bypass, there was no TR, and the aortic and mitral bioprosthetic valves were functioning normally.

The echocardiographic evaluation of TR has been problematic, because there is no quantitative definition of severity. It is also challenging because it is dependent upon variable preload, afterload, and right ventricular function. The echocardiographic examination is used mainly to determine the etiology and provide a semiquantitative estimate of severity.1 Criteria for severe TR are listed in Table 1. Our patient was shown to have a vena contracta width of 1.09 cm (Fig. 1) (Video 1, see Supplemental Digital Content 1,, midesophageal right ventricular inflow/outflow view with color flow Doppler showing regurgitant jet; RA = right atrium; LA = left atrium, RV = right ventricle), reversal of systolic hepatic vein flow (Fig. 2B), a dilated RA (Fig. 3A) with the interatrial septum bulging into the left atrium, and a dilated TA (Fig. 3B). The RV appeared dilated and was almost as large as the LV in the midesophageal four-chamber view (ME4C) and even larger in the transgastric view (Video 2, see Supplemental Digital Content 2,, transgastric and midesophageal four-chamber views showing right atrial and right ventricular dilation; RA = right atrium, RV = right ventricle, LA = left atrium, LV = left ventricle).

Table 1

Table 1

Figure 1.

Figure 1.

Figure 2.

Figure 2.

Figure 3.

Figure 3.

The vena contracta width correlates more closely with the severity of TR than does the color jet area2 and is often measured in the midesophageal right ventricular inflow-outflow view. The TR velocity to calculate the PASP can be measured in that same window. Measurement of the RA dimensions is usually done in the ME4C at end systole. RV size is frequently evaluated semiquantitatively. Increased chamber size is expected in significant TR but is a nonspecific sign. Reversal of systolic hepatic vein flow, although nonspecific, is consistent with severe TR and is indicative of increased RA pressure in a patient in sinus rhythm.

The presence of TR in a structurally normal valve is usually caused by annular dilation resulting from pulmonary hypertension.3 Referred to as functional TR, it is often secondary to left-sided lesions such as MR.4 The TA is frequently measured in the ME4C during mid-diastole (Fig. 3C), because there are reference values for that dimension. Note that the TA dimension during diastole will be larger than the systolic TA dimension.

As shown in Figure 4A, the TA maximally dilates from the anterior-septal commissure to the anterior-posterior commissure,4 thus the ME4C will not cap-ture the maximum dimension. Measurement of the TA in a transgastric right ventricular inflow view correlates best with the maximal dimension measured by the surgeon in a flaccid heart;5 however, there are no reference values for that dimension.

Figure 4.

Figure 4.

Surgical intervention for TR alone is uncommon and is usually done as an adjunctive procedure, especially during MV surgery.1,3 Current guidelines recommend repair of severe TR when undergoing MV surgery; usually tricuspid annuloplasty is sufficient (Video 3, see Supplemental Digital Content 3,, midesophageal four-chamber view after suture annuloplasty of the tricuspid valve with no evidence of regurgitation; RA = right atrium, LA = left atrium, RV = right ventricle, LV = left ventricle). Repair is also recommended for even mild TR in the presence of a dilated TA or pulmonary hypertension, because annular dilation appears to be a continuing process that worsens over time.3 Improvement or resolution of TR after MV surgery is unpredictable. Decreasing the pulmonary hypertension with MV surgery may decrease the TR provided that reverse remodeling of the dilated TA and RV occurs.4

In summary, presented with a dilated TA and TR at the time of MV surgery, current literature supports TV repair regardless of the degree of TR.4,6 For surgical decision-making purposes, some echocardiographers and surgeons consider a TA diameter >21 mm/M2 in the ME4C to be dilated enough to warrant consideration of annuloplasty.5,6

Back to Top | Article Outline


1. Zoghbi WA, Sarano ME, Foster E, Grayburn PA, Kraft CD, Levine RA, Nihoyannopoulos P, Otto CM, Quinones M, Rakowski H, Stewart WJ, Waggoner A, Weissman NJ. Recommendations for evaluation of the severity of native valve regurgitation with 2D and Doppler echocardiography. J Am Soc Echocardiogr 2003;16:777–802
2. Tribouilloy CM, Sarano ME, Bailey KR, Tajik AJ, Seward JB. Quantification of tricuspid regurgitation by measuring the width of the vena contracta with doppler color flow imaging: a clinical study. J Am Coll Cardiol 2000;36:472–8
3. Bonow RO, Carabello BA, Chatterjee K, de Leon AC, Faxon DP, Freed MD, Goosch WH, Lytle BW, Nishimura RA, O'Gara PT, O'Rourke RA, Otto CM, Shah PM, Shanewise JS. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease. J Am Coll Cardiol 2006;48:e1–148
4. Dreyfus GD, Corbi PJ, Chan J, Bahrami T. Secondary tricuspid regurgitation or dilatation: which should be the criteria for surgical repair? Ann Thorac Surg 2005;79:127–32
5. Maslow AD, Schwartz C, Singh AK. Assessment of the tricuspid valve: a comparison of four transesophageal windows. J Cardiothorac Vasc Anesth 2004;18:719–24
6. Colombo T, Russo C, Ciliberto GR, Lanfranconi M, Bruschi G, Agati S, Vitali E. Tricuspid regurgitation secondary to mitral valve disease, tricuspid annulus function as a guide to tricuspid valve repair. Cardiovasc Surg 2001;9:369–77
Back to Top | Article Outline

Clinician's Key Teaching Points

By Nikolaos J. Skubas, MD, Roman M. Sniecinski, MD, and Martin J. London, MD

Functional tricuspid regurgitation exists with structurally normal leaflets and is usually caused by annular dilatation. This is often secondary to left-sided lesions such as mitral regurgitation.

The tricuspid annulus should be measured in mid-diastole using the midesophageal 4-chamber view.

The severity of tricuspid regurgitation can be evaluated using the width of the vena contracta, which is the narrowest “neck” of the jet as it crosses the tricuspid annulus plane. In severe tricuspid regurgitation the vena contracta is >7 mm when the Nyquist limit is 50–60 cm/s.

Other echocardiographic parameters suggestive of severe tricuspid regurgitation include reversal of hepatic venous flow (imaged with Doppler in a modified midesophageal 4-chamber view with a rightward turn of the probe), an enlarged right atrium (minor axis >4.5 cm), and leftward shift of the interatrial septum.

A tricuspid annulus >21 mm/m2 (measured in mid-diastole in the midesophageal 4-chamber view) usually warrants tricuspid annuloplasty, irrespective of tricuspid regurgitation severity.

Supplemental Digital Content

Back to Top | Article Outline
© 2009 International Anesthesia Research Society