TextbookCardiologyTricuspid Regurgitation

Tricuspid Regurgitation

Backward flow of blood from the right ventricle into the right atrium during systole. Most commonly secondary (functional) due to RV dilatation from pulmonary hypertension or left-sided heart disease.

Key Facts

Most commonly functional/secondary (~85%): RV dilatation from pulmonary hypertension, left-sided heart disease, or RV infarction Primary causes: infective endocarditis (IV drug use), rheumatic disease, carcinoid syndrome, Ebstein anomaly, radiation Murmur: pansystolic at left lower sternal edge, increases with inspiration (Carvallo sign) Signs of right heart failure: elevated JVP with prominent CV waves, hepatomegaly (pulsatile), peripheral oedema, ascites Treatment: primarily directed at the underlying cause; diuretics for congestion Surgery: tricuspid annuloplasty at time of left-sided valve surgery if significant TR; isolated TV surgery less common

Overview

Key Facts

Tricuspid regurgitation (TR) is the backward flow of blood from the right ventricle to the right atrium during systole. Mild TR is extremely common and often physiological. Significant TR is most often secondary to right ventricular dilatation.

Epidemiology

  • Mild/trace TR: detected in up to 70-80% of normal echocardiograms
  • Clinically significant TR: prevalence ~0.5-1%
  • Functional TR accounts for ~85% of significant cases
  • Increasing prevalence with age and in patients with left-sided heart disease

Aetiology

Secondary (functional) — most common:

  • Pulmonary hypertension (any cause)
  • Left-sided heart disease (mitral valve disease, LV failure)
  • RV infarction
  • Atrial fibrillation (annular dilatation from RA enlargement)
  • Pulmonary embolism, cor pulmonale

Primary:

  • Infective endocarditis (especially IV drug users — right-sided)
  • Rheumatic heart disease (usually with mitral involvement)
  • Carcinoid syndrome (plaque deposits on valve)
  • Ebstein anomaly (apical displacement of tricuspid valve)
  • Radiation, drugs (ergotamine, fenfluramine)
  • Pacemaker/ICD lead impingement
  • Myxomatous degeneration, trauma

Pathophysiology

  • RV dilatation stretches the tricuspid annulus → leaflet coaptation failure → regurgitation
  • Volume overload of RA and RV → further dilatation → worsening TR (vicious cycle)
  • Elevated RA pressure transmitted to systemic veins → hepatic congestion, peripheral oedema, ascites
  • In severe TR, reversal of flow in hepatic veins during systole

Clinical Presentation

Typical Presentation

  • Often overshadowed by symptoms of the underlying left-sided heart disease
  • Right heart failure symptoms: peripheral oedema, abdominal distension (ascites), hepatomegaly
  • Fatigue, exercise intolerance (low cardiac output)
  • Dyspnoea (from associated pulmonary hypertension or left-sided disease)

Examination Findings

  • Pansystolic murmur at left lower sternal edge, increases with inspiration (Carvallo sign)
  • Elevated JVP with prominent CV waves (systolic waves from regurgitant flow)
  • Pulsatile hepatomegaly
  • Peripheral oedema, ascites
  • RV heave (parasternal lift)
  • In severe TR with low cardiac output: murmur may be soft or absent

Red Flags

  • Progressive right heart failure despite treatment of left-sided disease
  • Severe TR with RV dysfunction
  • TR with IV drug use (suspect endocarditis)
  • Carcinoid features: flushing, diarrhoea, wheezing

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
Mitral regurgitationPansystolic at apex, radiates to axilla, does not increase with inspirationEchocardiography
VSDPansystolic at LLSE, thrill, does not increase with inspirationEchocardiography
Pulmonary regurgitationEarly diastolic murmur at LUSEEchocardiography
Constrictive pericarditisElevated JVP (Kussmaul sign), pericardial knockEcho, CT, MRI
Hepatic cirrhosisAscites, jaundice, spider naevi — may coexistLFTs, USS liver
Budd-Chiari syndromeHepatomegaly, ascites, abdominal painHepatic vein Doppler

Diagnosis / Investigation

Bedside

  • ECG: AF, RA enlargement (tall P waves in II — P pulmonale), RVH, RBBB
  • JVP assessment: CV waves

Bloods

  • BNP/NT-proBNP: heart failure severity
  • LFTs: congestive hepatopathy (elevated bilirubin, transaminases)
  • FBC: polycythaemia in chronic hypoxia
  • Blood cultures: if endocarditis suspected
  • 5-HIAA (24h urine): if carcinoid suspected

Imaging

  • Echocardiography: TR severity (vena contracta, EROA, jet area), RV size and function (TAPSE, FAC), RA size, PA pressure estimation, valve morphology
  • Cardiac MRI: RV volumes and function (gold standard for RV assessment)
  • CT chest: pulmonary hypertension assessment

Special Tests

  • Right heart catheterisation: definitive haemodynamic assessment, PA pressures
  • Exercise echo: assess functional significance of TR

Management

Non-pharmacological

  • Sodium and fluid restriction for right heart failure
  • Treat underlying cause (left-sided heart disease, pulmonary hypertension)

Pharmacological

  • Diuretics: loop diuretics (furosemide 40-120mg OD) ± spironolactone 25-50mg OD for right heart congestion
  • Treat underlying cause: optimise LV function, control AF, manage pulmonary hypertension
  • Anticoagulation for AF if indicated

Surgical/Interventional

  • Tricuspid annuloplasty: performed at time of left-sided valve surgery if moderate or severe TR (NICE NG208)
  • Tricuspid valve replacement: if severe primary TR with valve destruction (e.g., endocarditis)
  • Transcatheter tricuspid valve repair (e.g., TriClip): emerging therapy for inoperable patients
  • Isolated TV surgery: higher operative mortality (~5-10%); reserved for severe symptomatic TR

Referral Criteria

  • Severe TR with right heart failure: cardiology assessment
  • TR associated with left-sided valve surgery: consider concurrent annuloplasty
  • Suspected endocarditis: urgent referral

Prognosis

  • Severe TR is associated with increased mortality regardless of LV function or PA pressures
  • Functional TR may improve with treatment of underlying cause (e.g., after mitral valve surgery, AF treatment)
  • Isolated severe TR: 5-year mortality ~25-40%
  • Post-tricuspid annuloplasty: good outcomes if performed at time of left-sided surgery
  • Isolated tricuspid surgery: operative mortality ~5-10%
  • Progressive RV dysfunction with severe TR carries poor prognosis

Other Relevant Information

Causes of Tricuspid Regurgitation by Category

CategoryExamples
FunctionalLV failure, pulmonary HTN, AF, RV infarct
InfectiveEndocarditis (IVDU)
CongenitalEbstein anomaly
RheumaticUsually with mitral disease
CarcinoidSerotonin-mediated plaque deposition
IatrogenicPacemaker/ICD leads, radiation

JVP Waveform in TR

WaveNormalIn TR
a waveAtrial contractionMay be absent in AF
c waveTricuspid closureMerged into v wave
v wavePassive atrial fillingGiant CV wave (regurgitant systolic wave)