Functional tricuspid regurgitation may occur whenever the right ventricle dilates, e.g. in cor pulmonale, myocardial infarction or pulmonary hypertension.
Organic tricuspid regurgitation may occur with rheumatic heart disease, infective endocarditis, carcinoid syndrome, Ebstein’s anomaly (a congenitally malpositioned tricuspid valve) and other congenital abnormalities of the atrioventricular valves.


The valvular regurgitation gives rise to high right atrial and systemic venous pressure. Patients may complain of the symptoms of right heart failure. Physical signs include a large jugular venous cv wave and a palpable liver that pulsates in systole. Usually a right ventricular impulse may be felt at the left sternal edge, and there is a blowing pan-systolic murmur, best heard on inspiration at the lower left sternal edge. Atrial fibrillation is common.


Functional tricuspid regurgitation usually disappears with medical management. Severe organic tricuspid regurgitation may require operative repair of the tricuspid valve (annuloplasty or plication). Very occasionally, tricuspid valve replacement may be necessary. In drug addicts with infective endocarditis of the tricuspid valve, surgical removal of the valve is recommended to eradicate the infection. This is usually well tolerated in the short term. The insertion of a prosthetic valve for this condition is considered.


This is usually a congenital lesion, but it may rarely result from rheumatic fever or from the carcinoid syndrome. Congenital pulmonary stenosis may be associated with an intact ventricular septum or with a ventricular septal defect (Fallot’s tetralogy).
Pulmonary stenosis may be valvular, subvalvular or supravalvular. Multiple congenital pulmonary arterial stenoses are usually due to infection with rubella during pregnancy.


The obstruction to right ventricular emptying results in right ventricular hypertrophy which in turn leads to right atrial hypertrophy. Severe pulmonary obstruction may be incompatible with life, but lesser degrees of obstruction give rise to fatigue, syncope and the symptoms of right heart failure. Mild pulmonary stenosis may be asymptomatic. The physical signs are characterized by a harsh midsystolic ejection murmur, best heard on inspiration, to the left of the sternum in the second intercostal space. This murmur is often associated with a thrill. The pulmonary closure sound is usually delayed and soft. There may be a pulmonary ejection sound if the obstruction is valvular. A right ventricular fourth sound and a prominent jugular venous a wave are present when the stenosis is moderately severe. A right ventricular heave may be felt.


Chest X-ray

The chest X-ray usually shows a prominent pulmonary artery due to poststenotic dilatation.


The ECG demonstrates both right atrial and right ventricular hypertrophy, although it may sometimes be normal even in severe pulmonary stenosis.

Cardiac catheterization

The passage of a catheter through the right heart allows the level and degree of the stenosis to be established by measuring the systolic pressure gradient.


Treatment of severe pulmonary stenosis requires pulmonary valvotomy (balloon valvotomy or direct surgery).


• This is the most common acquired lesion of the pulmonary valve. It results from dilatation of the pulmonary valve ring, which occurs with pulmonary hypertension. It is characterized by a decrescendo diastolic murmur beginning with the pulmonary component of the second sound (Graham Steell murmur) that is difficult to distinguish from the murmur of aortic regurgitation. Pulmonary regurgitation usually causes no symptoms and treatment is rarely necessary.


There are two groups of prosthetic heart valve: tissue and mechanical. Tissue valves are usually fashioned from a pigartic valve (xenograft); occasionally a human aortic valve is used (homograft). Mechanical valves are of various types, the most common being a ball-and-cage design (Starr-Edwards valve), a tilting disc (Bjork-Shiley valve) or a double tilting disc (St Jude valve). The disadvantage of the mechanical valve over the tissue valve is that formal anticoagulation is required. However, mechanical valves are much harder wearing; a tissue valve tends to degenerate after about 10 years. Unlike a tilting disc valve, the ball of a ball-and-cage valve presents some obstruction to flow through the valve. Although ball-and-cage valves have always been mechanically satisfactory some tilting disc valves have been mechanically insecure. Prosthetic valves may become detached from the valve ring, thrombose, stick, degenerate or become infected. Echocardiography is often helpful, but echoes are scattered from the mechanical valve making assessment of the structure of the valve rather difficult. This is particularly troublesome with the mitral valve, but the advent of transoesophageal echocardiography has largely overcome this problem. Transoesophageal echo cardiography is the investigation of choice when prosthetic valve endocarditis is suspected.

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