Tricuspid Regurgitation: Echocardiographic Assessment

Tricuspid regurgitation (TR) is backward flow of blood from the right ventricle into the right atrium during systole. It may be acute or chronic, and — as with mitral regurgitation — the distinction between primary (anatomic) and secondary (functional) TR matters enormously for both severity assessment and management. This tutorial covers etiology and echocardiographic evaluation, with criteria drawn from the 2020 ACC/AHA and 2025 ESC/EACTS valvular heart disease guidelines — the latter reflecting a substantial recent expansion in how TR is understood and graded, driven largely by the growth of transcatheter tricuspid interventions.

Etiology

TR is broadly classified as secondary (functional) — a structurally normal valve rendered incompetent — or primary (anatomic) — a structural abnormality of the valve itself. Only around 8–10% of patients with TR have primary TR; the large majority is secondary.

Secondary (functional) causes:

• Pulmonary hypertension (e.g., secondary to mitral stenosis or left-sided heart disease)
• Right ventricular infarction
• Annular dilation

Primary (anatomic) causes:

• Rheumatic heart disease
• Infective endocarditis
• Tricuspid valve prolapse (myxomatous disease)
• Ruptured chordae tendineae — rarely a consequence of congenital absence of the pericardium, from the exaggerated cardiac motion that condition produces
• Papillary muscle dysfunction
• Carcinoid syndrome
• Ebstein’s anomaly
• Chest radiation
• Trauma, including iatrogenic valve damage (e.g., after endomyocardial biopsy)
• Cardiac implantable electronic device (CIED) lead-related damage

On the last point: CIED-related TR is now recognized as warranting its own diagnostic approach, since it matters clinically whether the lead is truly the cause of TR (CIED-related TR — the lead interferes with leaflet coaptation) or simply present alongside unrelated TR (CIED-associated TR). This distinction can affect whether lead extraction is part of the management plan.

Secondary TR Phenotypes

Secondary TR is now further divided into two recognized phenotypes, each with a different primary driver:

• Atrial secondary TR — driven mainly by atrial fibrillation, characterized by marked right atrial and annular dilation without significant leaflet tethering, and with preserved RV size/function, normal pulmonary pressure, and normal LV function.
• Ventricular secondary TR — annular dilation combined with leaflet tethering, arising as a consequence of left-sided heart disease (post-capillary pulmonary hypertension), pre-capillary pulmonary hypertension, or primary RV cardiomyopathy/ischemia.

At an advanced disease stage, these two phenotypes can become difficult to distinguish, which is why early characterization — before the picture becomes mixed — is valuable for understanding the underlying driver and informing management.

Signs and Symptoms

• Often asymptomatic or well tolerated when mild
• Weakness and fatigue
• Jugular venous distension
• Hepatomegaly, peripheral edema, and ascites — signs of right-sided heart failure

Complications

• Severe right-sided heart failure
• Renal failure, from chronic venous congestion affecting renal perfusion

Cardiac Auscultation

• A holosystolic, high-pitched, blowing murmur, best heard at the left sternal border (the tricuspid area), accentuated by inspiration (Rivero-Carvallo’s sign), reflecting increased venous return to the right heart during inspiration
• A right-sided S3, which may also be accentuated with inspiration

Diagnostic Testing Beyond Echocardiography

• ECG — right atrial enlargement, incomplete right bundle branch block, and atrial fibrillation are common
• Chest X-ray — right atrial and right ventricular enlargement

Echocardiographic Findings

M-Mode

• An RV volume overload pattern: RV enlargement with paradoxical septal motion
• A “B bump” or notch, thought to indicate elevated RV end-diastolic pressure

2D Echocardiography

• Right atrial and right ventricular enlargement
• Tricuspid annular dilation — an annular diastolic diameter >40 mm (or >21 mm/m² indexed) is the specific threshold the current ACC/AHA guideline uses to decide whether to add tricuspid repair in a patient already undergoing left-sided valve surgery. This is a related but distinct criterion from the parameters that directly grade TR severity (below) — annular size is a risk factor and a trigger for concomitant repair, not itself the definition of a severity grade.
• A dilated inferior vena cava and dilated hepatic veins, reflecting elevated right atrial pressure
• Systolic reflux — contrast or color flow reversal into the IVC and hepatic veins — supporting significant TR

Doppler Assessment

Pulsed-wave Doppler:

• Distinguish physiologic (trace/trivial) TR from hemodynamically significant TR by the regurgitant jet’s duration and length — physiologic TR is common in structurally normal hearts and is typically a brief, low-velocity, spatially limited jet
• Systolic flow reversal in the hepatic veins supports severe TR
• An unusually laminar (rather than turbulent) regurgitant flow pattern can also suggest significant TR

Continuous-wave Doppler:

• Compare the regurgitant spectral display against the tricuspid inflow Doppler tracing
• The TR jet velocity is used to estimate systolic pulmonary artery pressure (SPAP) — though echocardiography tends to underestimate pulmonary pressures specifically in cases of severe TR, since severe regurgitation can lower the measured gradient independent of the true pulmonary pressure

Color flow Doppler:

• Regurgitant jet area-to-right atrial area ratio — used to support grading severity, analogous to the same approach in mitral regurgitation, though subject to the same technical and flow-dependence limitations
• Flow convergence (proximal acceleration) indicates at least moderate-to-severe TR and underlies PISA-based quantitative EROA calculation
• Systolic flow reversal in the hepatic veins is a specific, supportive sign confirming severe TR

Guideline-Based Severity Grading

The core quantitative thresholds for severe TR (ACC/AHA 2020 Table 20) parallel those used for mitral regurgitation:

Stage	Vena contracta	Effective regurgitant orifice (EROA)	Regurgitant volume
Progressive	< 0.7 cm	< 0.40 cm²	< 45 mL/beat
Severe	≥ 0.7 cm	≥ 0.40 cm²	≥ 45 mL/beat

These native-valve thresholds are close to, but not identical to, the criteria used for a prosthetic tricuspid valve, which instead uses a vena contracta of 0.7 cm and an EROA of 0.4 cm² as its own severe-TR cutoffs alongside a large central jet area (>10 cm²).

A central jet occupying ≥50% of the right atrial area is a further supportive (not standalone) criterion for severe TR in the same table.

Beyond Severe: Massive and Torrential Grades

The 2025 ESC/EACTS guideline recognizes an extended five-grade scale — mild, moderate, severe, massive, and torrential — developed primarily to describe TR reduction after transcatheter tricuspid interventions (which can reduce a baseline “torrential” TR down to “moderate” without necessarily reaching “mild,” a meaningful clinical improvement the traditional three-tier scale doesn’t capture well). A few important points about how to use this scale:

• This finer grading is mainly a tool for describing baseline severity in candidates for transcatheter repair, and for tracking the degree of improvement after intervention.
• It does not change when to intervene. The guideline is explicit that intervention should be considered “without delay, as soon as TR is severe” — waiting to see whether TR is “merely” severe versus massive or torrential is not the point of this scale, and shouldn’t be used to justify delaying referral.
• Because this scale is newer and used somewhat differently across studies, expect it to be more common in structural/transcatheter-focused practices than in general echo reporting, at least for now.

RV Assessment in Severe TR

Assessing the right ventricle in the setting of significant TR is genuinely difficult, given the RV’s complex geometry and its high sensitivity to loading conditions — RV function is often overestimated by standard parameters in the setting of severe TR, so conservative interpretation of RV function is advised when TR is significant. Where precise RV volumes and function are needed for decision-making, cardiac MRI is preferred over echocardiography for its accuracy and reproducibility.

RV–pulmonary artery coupling, approximated non-invasively using the ratio of tricuspid annular plane systolic excursion to systolic pulmonary artery pressure (TAPSE/PASP), assesses whether the RV’s systolic performance can still match its afterload — a genuinely different question from RV function or pulmonary pressure viewed alone. A TAPSE/PASP ratio in the range of roughly 0.3–0.4 mm/mmHg is associated with RV-PA uncoupling and a meaningfully increased mortality risk, validated against invasive pressure-volume measurement across several right heart conditions, severe TR included. See the Right Ventricle Evaluation tutorial for the fuller picture of RV systolic function assessment, RV-PA coupling, and pulmonary pressure estimation that this all fits into.

Important Considerations

• Mild TR is extremely common in structurally normal hearts and is not itself a disease — the diagnostic task is distinguishing physiologic TR from something hemodynamically meaningful, using jet characteristics and the broader clinical picture rather than the mere presence of a jet.
• TR frequently coexists with mitral valve disease or pulmonary hypertension — evaluate the whole heart, not the tricuspid valve in isolation.
• Chronic, untreated severe TR progresses toward right-sided heart failure and systemic venous congestion, which can in turn cause renal impairment.
• Medical therapy (diuretics, in a stepwise approach) can control congestive symptoms but has very limited effect on the underlying progression of TR itself — it is a bridge to intervention, not a substitute for it, and shouldn’t be allowed to delay referral to an experienced center when TR is severe and symptomatic.
• Severe TR and right ventricular dysfunction are both recognized confounders when working up suspected constrictive pericarditis — each can independently produce elevated right heart filling pressure and systemic venous congestion, so screening for significant TR is part of a complete constriction workup, not an unrelated afterthought.