Tricuspid regurgitation peak gradient
TRG (from TR Vmax) · Continuous-wave Doppler through the TR jet from multiple windows (RV-focused apical 4-chamber, parasternal RV inflow, subcostal)
Normal range & thresholds
TR peak gradient = 4 × (TR Vmax)2. Normal TR velocity <2.8 m/s (gradient <31 mmHg).
2025 ASE graded TR velocity: normal <2.8 · mild 2.8–3.1 · moderate 3.2–3.5 · severe >3.6 m/s.[3]
Note — TR severity is a separate question from TR velocity: the 2025 ESC/EACTS guidelines adopt a five-grade scheme — mild, moderate, severe, massive, torrential — because outcomes and transcatheter eligibility differ markedly across what was previously lumped together as ‘severe’.[6,81,104]
2022 ESC/ERS echocardiographic probability of pulmonary hypertension (using peak TR velocity alone, then modified by other signs): ≤2.8 m/s = low · 2.9–3.4 m/s = intermediate · >3.4 m/s = high probability.[8] The 2022 guideline deliberately moved away from an estimated systolic pressure toward the measured velocity, because the added right atrial pressure estimate introduces most of the error.
2025 ASE graded TR velocity: normal <2.8 · mild 2.8–3.1 · moderate 3.2–3.5 · severe >3.6 m/s.[3]
Note — TR severity is a separate question from TR velocity: the 2025 ESC/EACTS guidelines adopt a five-grade scheme — mild, moderate, severe, massive, torrential — because outcomes and transcatheter eligibility differ markedly across what was previously lumped together as ‘severe’.[6,81,104]
2022 ESC/ERS echocardiographic probability of pulmonary hypertension (using peak TR velocity alone, then modified by other signs): ≤2.8 m/s = low · 2.9–3.4 m/s = intermediate · >3.4 m/s = high probability.[8] The 2022 guideline deliberately moved away from an estimated systolic pressure toward the measured velocity, because the added right atrial pressure estimate introduces most of the error.
Pathophysiology
With no obstruction between the right ventricle and the right atrium in systole other than the incompetent valve, the peak TR velocity encodes the peak systolic pressure difference between the two chambers by the simplified Bernoulli relation. Adding the estimated right atrial pressure converts it to RV systolic pressure, which equals pulmonary artery systolic pressure in the absence of pulmonary stenosis or RVOT obstruction. The relation is a pressure difference, so it is blind to how high the absolute pressures are, and it fails completely when the two chambers are in near-equilibrium — which is what happens in torrential tricuspid regurgitation.[3,46]
Raised by
- Pulmonary hypertension of any group — group 2 (left heart disease) is by far the commonest
- Left heart failure, mitral valve disease, HFpEF
- Chronic lung disease, obstructive sleep apnoea, high altitude
- Acute and chronic pulmonary embolism
- Left-to-right shunt with high pulmonary flow
- Pulmonary arterial hypertension (group 1), connective tissue disease, portopulmonary, HIV, drug-induced
Lowered by
- Normal pulmonary pressures
- Severe RV systolic failure — a failing RV cannot generate a high pressure, so the velocity falls as the patient deteriorates: the most dangerous false reassurance in right heart echocardiography
- Torrential tricuspid regurgitation with a wide-open orifice — early RV–RA pressure equalisation, a dagger-shaped, low-velocity, early-peaking jet
- Hypovolaemia; inadequate Doppler alignment; no measurable jet at all (about 20–25% of studies)
Technique & pitfalls
- Interrogate from every window and take the highest complete envelope; the jet is often eccentric.
- Use agitated saline contrast to enhance a faint or incomplete jet — underused, and it converts a non-diagnostic study into a diagnostic one.[3]
- Trace only a complete, well-defined envelope; never over-read a fuzzy edge, which inflates the velocity and manufactures pulmonary hypertension.
- Report the velocity and the derived gradient and the estimated right atrial pressure separately, so the reader can see where the number came from.
- Average 3 beats in sinus rhythm, 5–10 in atrial fibrillation.
- Recognise the low-velocity, early-equalising envelope of torrential TR and report it as such, not as a low pulmonary pressure.
Pseudo-change & artefact
- Over-reading a faint spectral edge — the commonest cause of over-diagnosed pulmonary hypertension.
- Angle error — underestimates, and TR jets are frequently eccentric.
- Severe RV failure and torrential TR — falsely low.
- Pulmonary stenosis or RVOT obstruction: TR gradient then reflects RV pressure, not pulmonary artery pressure — subtract the transpulmonary gradient.
- An error in the estimated right atrial pressure propagates one-for-one into the reported systolic pulmonary pressure.
- Exercise, anxiety, pain and hypoxaemia at the time of the study raise it transiently.
Treatment thresholds
- Diastolic function: peak TR velocity >2.8 m/s is one of the three primary variables of the 2025 ASE algorithm for elevated left atrial pressure.[2]
- Pulmonary hypertension: the velocity assigns the echocardiographic probability that determines who is referred for right heart catheterisation — the gateway to the entire treatment pathway.[8]
- Diastolic stress echocardiography: exercise TR velocity >2.8–3.4 m/s with E/e′ ≥15 confirms HFpEF.[105,106]
- Mitral valve disease: systolic pulmonary artery pressure >50 mmHg at rest is an accepted trigger to intervene in asymptomatic severe primary mitral regurgitation (class IIa), and pulmonary hypertension influences the timing of mitral stenosis intervention.[6,7]
- Tricuspid intervention: the presence of precapillary pulmonary hypertension excludes patients from transcatheter tricuspid therapy in the 2025 ESC/EACTS guidelines — here the number decides who is not treated.[6]
Next step
- Next: add the estimated RA pressure for systolic pulmonary artery pressure; assess RV size and function, septal shape, PAAT and the pulmonary artery diameter.
- Then: assign the ESC/ERS echocardiographic probability of pulmonary hypertension.[8]
- Then: determine the group — echo for left heart disease, pulmonary function tests and CT for lung disease, and V/Q scanning for every unexplained case.[8]
- Then: right heart catheterisation to confirm the diagnosis and define precapillary versus postcapillary physiology before any pulmonary vasodilator is prescribed.[8]
Drugs
- Falls with: treatment of left heart disease (diuretics, GDMT, valve intervention) in group 2; pulmonary vasodilators in group 1 and in CTEPH; oxygen in hypoxic pulmonary vasoconstriction; anticoagulation and reperfusion in thromboembolic disease.[8]
- Rises with: volume loading, hypoxaemia, hypercapnia, acidosis, and drugs known to cause pulmonary arterial hypertension (dasatinib, interferon, some anorexigens, methamphetamine).
- Do not give pulmonary vasodilators for group 2 pulmonary hypertension — they cause harm by increasing pulmonary blood flow into a congested left atrium.[8]
Reversibility
Highly reversible when the cause is postcapillary or acute. In group 2 disease, effective decongestion and treatment of left-sided valve disease can drop the TR gradient by 20–40 mmHg within days to weeks. After successful mitral valve intervention, pulmonary pressures fall substantially within 3–6 months in most patients. Acute pulmonary embolism: near-complete normalisation with reperfusion in most survivors. Established precapillary remodelling is only partly reversible; and remember that a falling velocity in a deteriorating patient may mean a failing right ventricle rather than an improving circulation.[3,8]