Skip to content

Echo Reference — Valve Stenosis

Tricuspid and Pulmonary Stenosis: Echocardiographic Assessment

Native tricuspid and pulmonary stenosis on echocardiography — the findings that support significant tricuspid stenosis, pulmonary stenosis severity thresholds, Doppler acquisition, measurement pitfalls, and RVSP versus estimated PASP when RVOT obstruction is present.

Clinically reviewed by Dr Reza Moazzeni, MD FRACP — Consultant Cardiologist Last reviewed: October 2026
Scope: native valves in adults. The thresholds on this page do not transfer to prosthetic valves, surgically repaired valves or right ventricle–to–pulmonary artery conduits — see Prosthetic Valve Assessment. Right-sided stenosis is assessed by integrating valve morphology, Doppler findings and the right-heart response; no single number establishes severity.

Tricuspid Stenosis

Tricuspid stenosis (TS) is the least common stenotic valve lesion. Rheumatic disease is the classic cause and rarely affects the tricuspid valve in isolation — it usually accompanies rheumatic mitral stenosis. Other causes are carcinoid heart disease, congenital malformations, and acquired or iatrogenic obstruction: device-lead adhesions or endocarditis, lupus valvulitis, and tumour or large vegetations obstructing inflow. TS almost always coexists with tricuspid regurgitation (TR), which increases transvalvular flow and therefore the gradient.

Because right-sided pressures are low, clinically important TS produces small gradients — typically 2–10 mmHg, averaging about 5 mmHg.

Findings Supporting Haemodynamically Significant Native Tricuspid Stenosis

The ASE/EAE recommendations do not define mild and moderate bands for TS. In a valve that looks stenotic on 2D imaging, the findings below support haemodynamically significant stenosis. They are read together — not every criterion needs to be present.

Swipe to see all columns →

ParameterSupportive findingInterpretation
Mean diastolic gradient≥ 5 mmHgDepends on heart rate, flow and respiration; raised further by TR
Pressure half-time≥ 190 msLonger PHT indicates greater obstruction; influenced by compliance, RV relaxation and TR
Tricuspid inflow VTI> 60 cmCW Doppler, traced diastolic envelope
Valve area (continuity)≤ 1.0 cm²Method-limited — underestimated when TR is more than mild
Associated findingsRA enlargement (at least moderate); dilated IVCSupportive, not specific

Source — ASE/EAE 2009, Table 10 (ref 1): mean gradient ≥ 5 mmHg indicates haemodynamically significant TS. ESC/EACTS 2025 (ref 2) describes a mean gradient > 5 mmHg at a normal heart rate as indicating severe TS. The two documents label a similar threshold differently; state which is being applied.

The gradient is not a fixed property of the valve. It rises with tachycardia, high output, inspiration and accompanying TR, and falls with bradycardia or low output. A gradient below 5 mmHg does not, on its own, exclude anatomically important stenosis.

Valve Morphology and Associated Findings

On 2D imaging, the features are leaflet thickening or calcification, commissural fusion, restricted mobility with diastolic doming, and reduced leaflet separation at peak opening. The valve is examined from the parasternal RV inflow, parasternal short-axis, apical four-chamber and subcostal views. Colour Doppler shows a narrowed, aliased diastolic inflow jet. 3D echocardiography shows the relationship of the three leaflets and the orifice, but 3D orifice area is not standardised.

Right atrial enlargement and a dilated IVC support significant obstruction, but they also occur with TR, RV dysfunction and pulmonary hypertension. Hepatic vein systolic flow reversal is a sign of significant TR rather than stenosis; the regurgitant lesion is graded separately — see Tricuspid & Pulmonary Regurgitation.

Acquisition Checklist — Tricuspid Inflow

Swipe to see all columns →

StepTechniqueReason
Heart rate and rhythmRecord both beside the mean gradient. Assess at a controlled rate where possible — under 100 bpm, ideally 70–80 bpm.Gradient and PHT are rate dependent; fast rates prevent PHT measurement
WindowLow parasternal RV inflow or apical four-chamber view.Best alignment with tricuspid inflow
CW alignmentAlign CW Doppler with inflow using colour guidance; sweep speed 100 mm/s.Malalignment underestimates velocity
Mean gradientTrace the full diastolic CW envelope.Primary Doppler measure of TS
RespirationAverage across the respiratory cycle, or record during quiet end-expiratory breath-holding.Inflow velocity rises with inspiration
Atrial fibrillationAverage at least five cycles.Beat-to-beat variation in filling

Source — ASE/EAE 2009 (ref 1).

Valve Area Estimates

Mean gradient

Mean of 4v² across diastole

Traced CW envelope

Pressure half-time

TVA ≈ 190 ÷ PHT

TVA in cm², PHT in ms

Continuity equation

TVA = SV ÷ VTITV inflow

SV from LVOT or RVOT; inflow VTI by CW

Valve area does not grade TS on its own. 190 ÷ PHT is an estimate. The constant is less well validated than the mitral equivalent, and the result is influenced by right atrial and ventricular compliance, RV relaxation, respiration and TR.

Continuity-derived area requires an accurate transtricuspid stroke volume. Substituting LVOT or RVOT stroke volume is valid only without significant TR; as TR increases, valve area is progressively underestimated. A value ≤ 1.0 cm² still reflects a significant haemodynamic burden from the combined lesion.

Pulmonary Stenosis

Pulmonary stenosis (PS) is almost always congenital — most often a thin, doming valve, less often a dysplastic one. Acquired PS is rare; carcinoid heart disease is the most common acquired cause, usually with predominant regurgitation. Obstruction can also sit below the valve (infundibular hypertrophy, double-chambered RV) or above it (main or branch pulmonary arteries), and more than one level may coexist.

Severity is graded by the transpulmonary gradient. Planimetry of the pulmonary valve is not feasible, and continuity-derived valve area is not validated.

Severity Grading — Native Pulmonary Stenosis

ParameterMildModerateSevere
Peak velocity (m/s)< 3.03.0 – 4.0> 4.0
Peak gradient (mmHg)< 3636 – 64> 64

Source — ASE/EAE 2009, Table 11 (ref 1). Gradients are peak instantaneous Doppler gradients (4v²). ACC/AHA ACHD 2025 (ref 3) also lists a mean gradient > 35–40 mmHg under severe obstruction, and cautions that ventricular dysfunction can lead to underestimation of severity.

Acquisition Checklist — RVOT and Pulmonary Valve

Swipe to see all columns →

StepTechniqueReason
WindowsParasternal short-axis, subcostal, and a modified apical five-chamber view angled to the RVOT. Report the highest well-aligned velocity.The best-aligned window varies; the subcostal view can give the highest gradient
CW alignmentColour-guided, parallel to the jet.Malalignment underestimates the gradient
PW mappingStep the sample volume from the RV body through the infundibulum and valve into the main pulmonary artery; note where velocity accelerates.Localises the level of obstruction
Signal shapeEarly-peaking, rounded signal: fixed valvular obstruction. Late-peaking, dagger-shaped signal: dynamic infundibular obstruction.Separates fixed from dynamic obstruction
Cross-checkEstimate RVSP from the TR jet and compare it with the measured outflow gradient.A gradient that does not account for the RVSP suggests a further level of obstruction

Source — ASE/EAE 2009 (ref 1).

Level of Obstruction

PW Doppler shows where flow accelerates, but it does not allow each lesion to be graded separately. When infundibular and valvular stenosis lie in series, CW Doppler records the highest velocity along the beam and the individual contribution of each level usually cannot be determined precisely. Pressure recovery between the two lesions can also make the Doppler gradient exceed the net pressure drop. The report describes the levels involved and the overall gradient, rather than two independent gradients. The distinction is clinically relevant because balloon valvuloplasty addresses only the valvular component.

Right Ventricular Hypertrophy

An RV free-wall thickness above 5 mm indicates RV pressure loading. It does not establish the severity of PS or identify its cause — pulmonary hypertension and other causes of pressure load produce the same finding. Long-standing severe obstruction can lead to RV dilatation and systolic dysfunction, which in turn lowers the gradient. See RV Size & Function.

Doppler Versus Catheter Gradients

Doppler measures the peak instantaneous gradient — the largest pressure difference at any moment in systole. Catheterisation usually reports the peak-to-peak gradient — peak RV pressure minus peak pulmonary artery pressure, which do not occur at the same instant. The Doppler peak gradient is therefore typically higher than the catheter peak-to-peak gradient; in one study the Doppler mean gradient tracked the catheter value more closely. The two measurements are not interchangeable, and the report states which one is quoted.

RVSP and PASP With RVOT Obstruction

The TR jet reflects the systolic pressure difference between the RV and RA. Adding estimated right atrial pressure gives RV systolic pressure (RVSP). RVSP equals pulmonary artery systolic pressure (PASP) only when there is no obstruction between the RV and the pulmonary artery. With PS or any RVOT obstruction, the TR velocity still measures RVSP — not PASP.

Step 1 — RVSP

RVSP = 4 × (TR Vmax)² + RAP

RAP stated explicitly

Step 2 — RV–PA gradient

ΔPRV–PA = 4 × (Vmax)²

Highest CW velocity across the RVOT and pulmonary valve

Step 3 — Estimated PASP

PASP ≈ RVSP − ΔPRV–PA

An approximation

ΔPRV–PA is the total gradient between the RV and the pulmonary artery, so the same formula applies whether the obstruction is subvalvular, valvular or supravalvular (ASE/EAE 2009, ref 1; RAP estimation per the ASE 2025 right-heart guideline, ref 4).

Worked Example

MeasurementValueDerivation
TR velocity4.5 m/sTR gradient 4 × 4.5² = 81 mmHg
Estimated RAP15 mmHgAssumed from the IVC
Estimated RVSP96 mmHg81 + 15
Pulmonary obstruction gradient64 mmHgOutflow Vmax 4.0 m/s; 4 × 4.0²
Estimated PASP32 mmHg96 − 64

A gradient of 64 mmHg (4.0 m/s) sits at the boundary between moderate and severe PS. The RAP of 15 mmHg is an assumption: with a RAP of 8 mmHg the same Doppler data give an RVSP of 89 mmHg and an estimated PASP of 25 mmHg.

An elevated RVSP does not establish pulmonary hypertension when RVOT obstruction is present. Obstruction between the RV and pulmonary artery is excluded before a high TR velocity is interpreted as pulmonary hypertension — see Pulmonary Haemodynamics.
Estimated PASP is an approximation. It subtracts a peak instantaneous gradient from a peak pressure, and the two peaks are not simultaneous. It is unreliable with an incomplete TR or outflow Doppler envelope, an uncertain RAP, severe TR, or obstruction at more than one level. Where the result is implausible or will change management, invasive haemodynamic assessment should be considered.

RVSP and Estimated PASP

RVSP and estimated PASP are displayed separately. RAP must be entered — no default is assumed.

Complete CW envelope, highest velocity from any window.
From IVC size and collapse. Required.
Highest CW velocity across the RVOT and pulmonary valve.

TR gradient (4v²)—
RVSP (TR gradient + RAP)—
RV–PA peak gradient (4v²)—
Estimated PASP (RVSP − RV–PA gradient)—

Carcinoid Heart Disease

Carcinoid heart disease produces a characteristic appearance: thickened, retracted leaflets fixed in a semi-open position, with reduced or absent excursion. The tricuspid valve is affected most often, followed by the pulmonary valve. The usual result is regurgitation — often severe — with a variable degree of stenosis, so both lesions are graded (see Tricuspid & Pulmonary Regurgitation).

Left-sided valves are usually spared because vasoactive substances are inactivated in the lungs. Left-sided involvement occurs with a right-to-left shunt such as a patent foramen ovale, with a functioning bronchial neuroendocrine tumour, or with very high circulating levels of vasoactive substances (ENETS; ref 5).

Measurement Pitfalls

Swipe to see all columns →

PitfallEffectApproach
Poor Doppler alignmentUnderestimates velocity and gradientColour-guided CW from multiple windows; report the highest well-aligned signal
Flow dependenceGradients rise with tachycardia and high output, and fall with low output or RV dysfunctionRecord heart rate and rhythm; read the gradient against RV function and stroke volume
Significant regurgitationTR with TS, or pulmonary regurgitation with PS, increases transvalvular flow and gradient; continuity valve area is underestimatedGrade both lesions; avoid relying on valve area
Respiratory variationTricuspid inflow velocity rises in inspirationAverage across the respiratory cycle or record at end-expiration
Irregular rhythmBeat-to-beat variation in gradientAverage at least five cycles
Serial obstructionCW records the highest velocity along the beam; individual gradients cannot be reliably separatedPW mapping to localise; describe the levels; cross-check against RVSP
Incomplete TR envelope or severe TRRVSP, and therefore estimated PASP, is unreliableReport TR velocity quality; avoid quoting a pressure from a poor signal
Uncertain RAPError passes directly into RVSP and estimated PASPState the RAP used and how it was estimated
Doppler versus catheter gradientPeak instantaneous Doppler gradient exceeds catheter peak-to-peak gradientState which gradient is quoted
Prosthetic or repaired valveNative-valve thresholds do not applyUse prosthesis-specific criteria

Reporting Checklist

ItemDocumentation
Valve morphologyThickening, calcification, doming, mobility, commissural fusion; likely aetiology
Level of obstructionSubvalvular, valvular, supravalvular or combined; whether fixed or dynamic
Velocities and gradientsPeak velocity, peak and mean gradient, and the window used; PHT and inflow VTI for TS
Rhythm and heart rateRhythm, heart rate at the time of measurement, number of beats averaged
Associated regurgitationSeverity of TR and pulmonary regurgitation
Right heartRA size, IVC size and collapse, RV size, wall thickness and systolic function
Pressure estimatesTR velocity, RAP used, RVSP, estimated PASP, and the limitations of each
ScopeNative valve, or prior repair, valvuloplasty or prosthesis

Frequently Asked Questions

What indicates haemodynamically significant tricuspid stenosis on echocardiography?

In a valve with stenotic morphology, a mean diastolic gradient of 5 mmHg or more, a pressure half-time of 190 ms or more, an inflow VTI above 60 cm and a continuity valve area of 1.0 cm² or less support haemodynamically significant stenosis, together with right atrial enlargement and a dilated IVC (ASE/EAE 2009). The findings are integrated; no single value is sufficient, and the gradient is read against heart rate, flow and accompanying tricuspid regurgitation.

Why does tricuspid inflow vary with respiration, and how is it measured?

Inspiration increases systemic venous return, so tricuspid inflow velocity and gradient rise in inspiration and fall in expiration. Measurements are averaged across the respiratory cycle or recorded during quiet end-expiratory breath-holding, and at least five cycles are averaged in atrial fibrillation.

Why are Doppler gradients higher than catheter gradients in pulmonary stenosis?

Doppler measures the peak instantaneous gradient, the largest pressure difference at any moment in systole. Catheterisation usually reports the peak-to-peak gradient, the difference between peak RV and peak pulmonary artery pressures, which do not occur at the same instant. The Doppler peak gradient is therefore typically higher, and the two values are not interchangeable.

Does a high RVSP mean pulmonary hypertension when pulmonary stenosis is present?

No. With obstruction between the right ventricle and the pulmonary artery, the TR velocity reflects RV systolic pressure, not pulmonary artery pressure. Estimated PASP is approximately RVSP minus the RV–PA gradient. This is an approximation that depends on complete Doppler envelopes and a sound estimate of right atrial pressure.

Related Echocardiography References

References

  1. ASE/EAE 2009. Baumgartner H, Hung J, Bermejo J, et al. Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for clinical practice. J Am Soc Echocardiogr. 2009;22(1):1–23. doi:10.1016/j.echo.2008.11.029
  2. ESC/EACTS 2025. Praz F, Borger MA, Lanz J, et al. 2025 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J. 2025;46(44):4635–4736. doi:10.1093/eurheartj/ehaf194
  3. ACC/AHA ACHD 2025. 2025 ACC/AHA/HRS/ISACHD/SCAI Guideline for the Management of Adults With Congenital Heart Disease: a report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. Published online December 2025. doi:10.1161/CIR.0000000000001402
  4. ASE 2025 right heart. Mukherjee M, Rudski LG, Addetia K, et al. Guidelines for the echocardiographic assessment of the right heart in adults and special considerations in pulmonary hypertension: recommendations from the American Society of Echocardiography. J Am Soc Echocardiogr. 2025;38(3):141–186. doi:10.1016/j.echo.2025.01.006
  5. ENETS 2022. Grozinsky-Glasberg S, Davar J, Hofland J, et al. European Neuroendocrine Tumor Society (ENETS) 2022 guidance paper for carcinoid syndrome and carcinoid heart disease. J Neuroendocrinol. 2022;34(7):e13146. doi:10.1111/jne.13146
  6. ACC/AHA 2020. Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA Guideline for the management of patients with valvular heart disease. Circulation. 2021;143(5):e72–e227. doi:10.1161/CIR.0000000000000923

← Back to Echo Reference Tools