Synopsis
Recognise right-sided valve disease, define RV consequences and refer before irreversible right-heart failure.
- Most tricuspid regurgitation (TR) is secondary to annular dilatation from left-heart disease, pulmonary hypertension, atrial fibrillation or RV remodelling; exclude device-lead injury and endocarditis.
- Severe TR causes giant v waves, a pulsatile liver, ascites, oedema and a pansystolic murmur that increases on inspiration; a quiet murmur does not exclude advanced disease.
- Pulmonary stenosis is usually congenital; pulmonary regurgitation commonly follows repaired tetralogy of Fallot or prior valvotomy/conduit surgery.
Key red flags
Ejection click, harsh upper-left-sternal systolic murmur, RV heave and exertional dyspnoea/syncope suggest significant RV outflow obstruction.
Investigation priorities
Detect AF, atrial enlargement, RV hypertrophy and ventricular arrhythmia.
Management branches
Severe TR with symptoms, RV enlargement/dysfunction, end-organ congestion or planned left-sided surgery.
- Confirm primary versus secondary mechanism and optimise AF, left-sided valve disease, pulmonary pressure and congestion.
- If mitral surgery is planned and TR is moderate or severe, discuss concomitant tricuspid repair with the Heart Team.
Key medicines
FurosemideUsually 20-40 mg by mouth once daily initially; titrate to congestion and renal response, with IV treatment for acute decompensation.