Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Recognise right-sided valve disease, define RV consequences and refer before irreversible right-heart failure.
Right-sided lesions are often secondary or congenital and may remain clinically subtle until venous congestion, exercise limitation or arrhythmia appears. Decision-making therefore depends more on serial RV structure and function than on murmur intensity alone.
Management combines treatment of the driver, careful decongestion and timely anatomical correction. Advanced liver or kidney dysfunction, severe pulmonary vascular disease and established RV failure can make a late intervention futile or hazardous.
Left-heart disease, pulmonary hypertension, atrial fibrillation or right-ventricular remodelling can dilate the tricuspid annulus and/or tether the leaflets, creating regurgitation despite initially normal valve tissue.
Endocarditis, an intracardiac device lead or congenital leaflet abnormality can directly prevent coaptation. Mechanism-focused imaging is needed because a nearby lead is not necessarily causal.
A doming pulmonary valve is the usual congenital valvar substrate. Dysplastic leaflets or obstruction below or above the valve alter the physiology and procedural options.
Tetralogy repair, pulmonary valvotomy or right-ventricular-to-pulmonary-artery conduit surgery may impair valve competence, leaving chronic regurgitation and progressive right-ventricular volume loading.
Tricuspid annular dilatation or leaflet injury permits systolic backflow into the right atrium. Pulmonary stenosis obstructs systolic right-ventricular outflow, whereas pulmonary regurgitation permits diastolic backflow into the right ventricle.
Pulmonary stenosis creates a right-ventricular pressure load; pulmonary regurgitation creates a right-ventricular volume load. Tricuspid regurgitation volume-loads the right atrium and ventricle while reducing effective forward stroke volume.
Pulmonary stenosis tends to produce right-ventricular hypertrophy, while pulmonary regurgitation tends to produce right-ventricular dilatation. In tricuspid regurgitation, right-atrial and annular enlargement can further impair coaptation; advanced pulmonary lesions may also cause secondary tricuspid regurgitation.
Severe pulmonary stenosis directly limits pulmonary flow. Severe regurgitation can reduce effective forward flow, particularly once right-ventricular dysfunction develops, leading to exertional intolerance and, in advanced disease, hypotension, syncope or low-output decompensation.
Tricuspid regurgitation directly transmits systolic pressure into the systemic veins; pulmonary stenosis or regurgitation does so mainly after right-ventricular failure raises right-atrial pressure. The result may be prominent venous waves, pulsatile hepatomegaly, ascites, oedema and end-organ congestion.
Raised JVP with prominent v waves, oedema, ascites, hepatomegaly or pulsatile liver suggests important TR and right-heart failure.
A left-lower-sternal pansystolic murmur that becomes louder on inspiration supports TR; severe low-flow TR can be soft.
Ejection click, harsh upper-left-sternal systolic murmur, RV heave and exertional dyspnoea/syncope suggest significant RV outflow obstruction.
Previous tetralogy-of-Fallot repair, pulmonary valvotomy or RV-PA conduit plus falling exercise capacity, palpitations or RV dilatation is a key pattern.
Fever, injection-drug exposure or an intracardiac lead with new right-heart failure raises endocarditis or lead-related injury; obtain cultures and urgent imaging.
Hypotension, cool peripheries, oliguria, lactate rise, syncope or cyanosis indicates low output or critical obstruction and needs emergency escalation.
Pulmonary crackles, left-sided valve disease or primary left-ventricular dysfunction may drive secondary right-heart signs. Echocardiography clarifies whether tricuspid disease is cause or consequence.
Raised JVP, oedema and ascites can resemble severe tricuspid disease. Respiratory ventricular interaction, pericardial thickening or calcification and a non-regurgitant valve support constriction.
Pulmonary hypertension or acute embolism can cause right-ventricular dilatation and functional regurgitation without primary leaflet disease. Pulmonary pressure, vascular imaging and clinical onset discriminate.
Cirrhosis and kidney disease cause oedema or ascites, but usually lack prominent tricuspid v waves, a pulsatile liver and valve-specific abnormalities on echocardiography.
A pulmonary flow murmur with right-heart enlargement may reflect an atrial shunt rather than pulmonary stenosis. Fixed splitting of the second sound and imaging identify the communication.
Persistent pressure or volume overload can eventually exceed right-ventricular compensation, causing low forward output together with worsening venous congestion and reduced exercise capacity.
Chronically raised hepatic venous pressure can produce painful hepatomegaly, abnormal liver function and fibrosis. Advanced hepatic injury can increase procedural risk and limit benefit from late intervention.
Renal venous congestion and reduced perfusion lower filtration, promote sodium retention and make decongestion more difficult, reinforcing oedema and worsening prognosis.
Right-atrial enlargement and surgical scar promote atrial flutter or fibrillation. Loss of coordinated filling and rapid conduction can precipitate right-heart decompensation.
Abnormal right-sided valves, prosthetic conduits and intracardiac leads can become infected. Septic pulmonary emboli, valve destruction or acute regurgitation may follow.
Inspiratory augmentation supports TR, but marked regurgitation with equalised pressures can produce little audible change.
Persistent severe secondary TR can progress despite successful treatment of the left-sided lesion; timing should be decided before RV failure is fixed.
A lead may impinge a leaflet, but association alone is not causation; 3D imaging distinguishes direct injury from annular functional TR.
The crescent-shaped RV is difficult to quantify by 2D echo, so serial CMR trends often determine pulmonary-valve timing.
A transcatheter pulmonary valve treats the conduit/valve lesion but does not remove arrhythmia, RV or endocarditis risk.
Calling severe TR harmless because it is secondary or the murmur is quiet.
Using diuretics as definitive treatment while RV size, function and hepatic congestion worsen.
Accepting an echo-derived pulmonary pressure at face value when severe TR makes the estimate unreliable.
Sending repaired congenital pulmonary disease to a general valve pathway without adult congenital expertise.
Waiting for severe symptoms before referral despite progressive RV dilatation or arrhythmia.
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A 68-year-old is accepted for mitral valve surgery. TTE shows moderate secondary TR with annular dilatation and preserved but enlarged RV function. What is the best valve strategy?
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes
Check blood pressure, weight, sodium, potassium and creatinine; excessive diuresis can reduce preload and cardiac output in RV failure or severe obstruction.