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Tricuspid Valve Lesions II: Tricuspid Regurgitation (TR)

Updated on January 14, 2014

The Human Heart Valves

The usual symptoms are easy fatigability and effort intolerance resulting from reduction of cardiac output. In severe cases, there is usually peripheral edema and in some cases, there may be ascites
The usual symptoms are easy fatigability and effort intolerance resulting from reduction of cardiac output. In severe cases, there is usually peripheral edema and in some cases, there may be ascites | Source

Introduction

Tricuspid regurgitation (TR) results from inadequate closure of the tricuspid orifice by the valve leaflets. Right ventricular blood regurgitations into the right atrium during systole. The most frequent cause of TR is functional incompetence secondary to pulmonary hypertension which may be primary or secondary. As the right ventricle dilates secondary to the effect of pulmonary hypertension, the valve becomes incompetent. In primary tricuspid regurgitation, which is relatively rare, the valve is abnormal.

Causes of primary TR

  1. Rheumatic valvulitis
  2. Congenital anomalies (Ebstein’s malformation, atrioventricular cushion defects)
  3. Carcinoid syndrome
  4. Infective endocarditis, and
  5. Trauma

With the onset of TR, the pressure in the right atrium increases during systole. The elevated mean right atrial pressure is reflected back as elevation of the systemic venous pressure. Ultimately, the right atrium and right ventricle dilate with clinical features of systemic venous hypertension.

Heart Model, Showing All The Valves

Heart valve diseases
Heart valve diseases | Source

Clinical Presentations

Clinical features

The usual symptoms are easy fatigability and effort intolerance resulting from reduction of cardiac output. In severe cases, there is usually peripheral edema and in some cases, there may be ascites. The liver is enlarfed and tender and shows systolic pulsation. The most conspicuous finding is elevation of jugular venous pressure with prominent ‘v’-wave and exaggerated ‘y’ collapse. When the jugular veins are overdistended, pulsations may not be prominent. In such cases, the ear lobes and the eyeballs may reveal pulsation. Atrial fibrillation is present in 80-90% of patients with TR. When atrial fibrillation is present, the pulsation in the jugular vein is monophasic with only prominent ‘v’-wave. The characteristic murmur of TR is a high pitched pansystolic murmur best heard in the lower left sterna border. This murmur increases in intensity with inspiration. Inspiratory augmentation of the murmur may not be very conspicuous in cases with severe congestive cardiac failure.

In primary TR, the murmur is medium-pitched and short. The inspiratory augmentation is less conspicuous. When TR is severe, there is usually a third heart sound as well as a mid-diastolic flow murmur heard along the lower left sterna border. The ECG and X-ray chest may show evidence of right atrial enlargement. Echocardiography is helpful in the assessment of TR. Cardiac catheterization and angiography serve in assessing the lesion fully.

Course and prognosis

With treatment of congestive heart failure, the features of seconday TR comes down, and the duration of the murmur comes down. If the damage to the right ventricle is irreversible, such cases follow a downhill course.

Treatment

Medical treatment is given for these cases with functional tricuspid regurgitation. Valvuloplasty or valve replacement may be necessary in cases with primary TR.

© 2014 Funom Theophilus Makama

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