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.
- TTE grades lesion severity and assesses RV size/function and pulmonary pressure; CMR is especially valuable when RV volumes or pulmonary regurgitant fraction will determine intervention.
- Diuretics relieve congestion but do not correct the valve or halt progressive RV dysfunction.
- Moderate or severe TR should be considered for repair when mitral surgery is already planned; isolated severe disease needs early valve-centre review before major RV or end-organ damage.
- Balloon pulmonary valvuloplasty suits significant doming valvar stenosis; dysplastic valves, sub/supravalvar obstruction or associated lesions may require surgery.
- A dysfunctional RV-to-pulmonary-artery conduit may be treated by transcatheter pulmonary valve implantation in an adult congenital heart disease centre when anatomy is suitable.
Key red flags
Ejection click, harsh upper-left-sternal systolic murmur, RV heave and exertional dyspnoea/syncope suggest significant RV outflow obstruction.
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.