Tricuspid Valve

The tricuspid valve consists of anterior, posterior, and septal leaflets. Leaflet identification by 2D echocardiography is imperfect because all three leaflets are rarely visualized simultaneously.

Evaluate leaflet morphology, annular size, coaptation, device-lead interaction, stenosis, regurgitation, and the response of the RA and RV.

Routine Assessment¶

Assess:

Leaflet thickness, mobility, and coaptation
Prolapse, flail leaflet, restriction, or vegetation
Pacemaker or ICD lead interaction
Tricuspid annular dilation
TR mechanism and severity
RA and RV size
RV systolic function
IVC size and estimated RAP
Hepatic vein flow
Estimated RVSP or PASP

A normal tricuspid annular diameter is:

≤4.0 cm
≤2.1 cm/m² when indexed to body surface area

Measure the annulus at end-diastole from the apical four-chamber view. The 2D measurement underestimates the true size of the nonplanar annulus.

Tricuspid Regurgitation¶

Mechanism¶

TR may be primary or secondary.

Primary TR results from intrinsic valve pathology:

Endocarditis
Prolapse or flail leaflet
Carcinoid heart disease
Rheumatic disease
Ebstein anomaly
Trauma or iatrogenic leaflet injury
Device-lead impingement, entanglement, or perforation

Secondary TR accounts for most cases and results from annular dilation or leaflet tethering.

Ventricular functional TR: RV dilation, pressure overload, or leaflet tethering
Atrial functional TR: RA and annular dilation, commonly associated with atrial fibrillation

Document whether a device lead directly interferes with leaflet motion. The presence of a lead alone does not establish lead-mediated TR.

TR Severity¶

Use an integrated assessment. TR severity varies with respiration, volume status, pulmonary pressure, and RV function.

Parameter	Mild	Moderate	Severe
Vena contracta width	<0.3 cm	0.3–0.69 cm	≥0.7 cm
PISA radius at Nyquist 30–40 cm/s	≤0.5 cm	0.6–0.9 cm	>0.9 cm
EROA	<0.20 cm²	0.20–0.39 cm²	≥0.40 cm²
Regurgitant volume	<30 mL	30–44 mL	≥45 mL
Tricuspid inflow	A-wave dominant	Variable	E velocity ≥1.0 m/s
Hepatic vein flow	Systolic dominant	Systolic blunting	Systolic flow reversal

Findings supporting severe TR include:

Flail leaflet or large coaptation defect
Large central or eccentric color jet
Vena contracta ≥0.7 cm
Dense, triangular CW Doppler envelope
Early-peaking or sine-wave CW profile
Hepatic vein systolic flow reversal
RA, RV, and IVC dilation
RV volume-overload septal flattening

Color jet area alone is unreliable. Severe TR may produce a low-velocity jet because RA and RV pressures rapidly equalize.

PISA may underestimate TR because the regurgitant orifice is frequently noncircular, irregular, and dynamic.

RVSP and PASP¶

In the absence of pulmonic stenosis or RV outflow obstruction:

\[ RVSP = 4(TRV)^2 + RAP \]

\[ PASP \approx RVSP \]

Use the highest complete TR envelope obtained from multiple windows.

A faint or incomplete envelope should not be traced. Agitated saline may improve the Doppler signal when clinically necessary.

Severe TR may make RVSP estimation unreliable because:

The Doppler envelope may be truncated
RA and RV pressures equalize early
Estimated RAP may be inaccurate
The highest velocity may be difficult to obtain

An absent TR jet does not exclude pulmonary hypertension.

Tricuspid Stenosis¶

Tricuspid stenosis is uncommon and is usually associated with rheumatic mitral valve disease.

Other causes include:

Carcinoid heart disease
Congenital valve disease
Endocarditis
Device-lead adhesions
Large vegetations or right atrial masses

Findings supporting significant tricuspid stenosis include:

Thickened, restricted leaflets
Diastolic doming
Mean gradient ≥5 mm Hg
Peak inflow velocity ≥1.0 m/s
Pressure half-time ≥190 ms
Valve area ≤1.0 cm²
RA and IVC dilation

Record the gradient from multiple respiratory cycles and report the heart rate. The gradient increases with tachycardia and high cardiac output.

Carcinoid Heart Disease¶

Typical findings include:

Thickened, retracted leaflets
Severe restriction with failure of coaptation
Mixed tricuspid regurgitation and stenosis
Associated pulmonic valve involvement

The leaflets may appear fixed in a partially open position.

Suggested Reporting¶

The tricuspid valve leaflets are structurally normal with normal excursion. There is trace tricuspid regurgitation.

Severe functional tricuspid regurgitation is present secondary to annular dilation and leaflet malcoaptation. There is systolic flow reversal in the hepatic veins.

Severe tricuspid regurgitation is present due to RV dilation and leaflet tethering. The RV is ___ dilated with ___ systolic function.

A transvenous device lead impinges on the septal tricuspid leaflet, resulting in severe eccentric tricuspid regurgitation.

The tricuspid valve is thickened with restricted diastolic excursion. The mean gradient is ___ mm Hg at ___ bpm, consistent with tricuspid stenosis.

Estimated RVSP is ___ mm Hg based on an estimated RAP of ___ mm Hg.

Pulmonary pressure cannot be estimated because an adequate TR Doppler envelope is not present.

Key Points¶

Most TR is secondary rather than primary.
Distinguish ventricular from atrial functional TR.
Hepatic vein systolic flow reversal strongly supports severe TR.
Severe TR may cause underestimation of RVSP.
An absent TR jet does not exclude pulmonary hypertension.
Document the mechanism and hemodynamic consequences, not severity alone.
A device lead is causal only when it interferes with leaflet motion.