Critical Care Medicine

Tricuspid incompetence, tricuspid Regurgitation

Tricuspid Incompetence (TI)

Also known as: Tricuspid Regurgitation (TR)

Related conditions

Functional Tricuspid Regurgitation

Right Heart Failure

Pulmonary Hypertension

1. Description of the problem

Physiological TI is commonly observed in patients with structurally normal hearts, with the prevalence increasing with age. Approximately 90% of cases of pathological TI are functional, due to either pulmonary hypertension or intrinsic right ventricle pathology. The other 10% are due to a primary tricuspid valve problem.

Clinical features

Symptoms

Severe TI may be asymptomatic and well tolerated for a long period of time. Chronic severe TR may culminate in fatigue and poor exercise tolerance due to reduced cardiac output. Symptoms of associated diseases may also be present.

Signs

The severity and chronicity of the disease determine the clinical findings present. These may include:

  • Large jugular venous cv waves

  • A high-pitched pansystolic murmur in the lower left sternal edge louder on inspiration (Carvallos sign) - this finding may be lost in right ventricular failure when the ventricle can no longer increase filling during inspiration

  • If TI is of primary etiology, murmur may be shorter (limited to the first half of systole) and low-pitched.

  • A mid-diastolic murmur may be present in severe regurgitation.

  • Hepatic pulsation in systole

  • Signs related to the cause of TR (eg, mitral fascies and mid-diastolic murmur at apex in mitral stenosis; right ventricular heave and palpable and/or loud P2 in pulmonary hypertension; clubbing and splinter hemorrhages in infective endocarditis)

  • General signs of right heart failure such as ascites and peripheral edema are also frequently present in a patient with significant TR.

Key management points

Mild TR does not warrant intervention. In all cases of moderate or severe TR, treatment of any underlying cause, including medical treatment of pulmonary hypertension as per guidelines, is indicated. Initial treatment for severe TR associated with right heart failure includes diuretics and sodium restriction. The decision to proceed to surgical treatment depends largely on the etiology of the regurgitation, the clinical status of the patient and the echocardiographic evaluation of the right ventricle. The type of surgery required depends on the mechanism of regurgitation; annular dilatation is treated with annuloplasty, whereas valve/leaflet lesions require either valve repair (usually with annuloplasty) or replacement.

2. Emergency Management

Acute TI is rare. It may arise as a complication of blunt chest trauma causing injury to the valve leaflets themselves or rupture of the subvalvular structures. Clinical suspicion and an appropriate imaging modality are required, such as 3D-TOE. Urgent surgical repair is recommended. Acute TI may also occur in the setting of infective endocarditis complicated by leaflet destruction or perforation. Urgent surgical consultation is recommended. In chronic severe TI patients may present acutely with decompensated heart failure or complications related to pulmonary hypertension; immediate management is as per appropriate guidelines followed by identifying and treating any precipitants.

3. Diagnosis

Diagnostic criteria and tests

Echocardiography

2-dimensional echocardiography and Doppler echocardiography are the main tools for both diagnosis and evaluation of severity of TR as well as its potential causes and resultant cardiac sequelae. Assessments of leaflet morphology, annular dimensions, and pulmonary artery pressure are particularly important for determining subsequent management. Key elements of the echocardiographic assessment include:

1. Structural evaluation of the valve

The key question here is whether or not the TI is functional or primary. The degree of annulus dilatation as well as the presence of leaflet abnormalities (flail in myomatous disease, thickened or retracted in carcinoid or rheumatic disease, apical displacement of the septal leaflet in Ebstein's anomaly) will help to determine this. In addition the presence or absence of vegetations (attached to leaflets/annulus/catheters or pacing leads traversing the valve) should be noted.

2. Semi-quantitative evaluation of TR severity

This is usually done using a combination of the following methods:

  • Color jet characteristics – degree of right atrium occupied/eccentricity (wall-hugging jets should be upgraded by a grade)

  • Proximal convergence zone – large if severe

  • Vena contracta width – >0.7 cm if severe

  • Continuous wave Doppler signal – dense with early peak if severe

  • Pulse wave Doppler signal – prominent E wave >1 m/s if severe

  • Dilatation of the inferior vena cava – respiratory diameter variation <50% indicates severe

  • Reduction or reversal of systolic blood flow in the hepatic veins – systolic reversal indicates severe

3. Evaluation of right-sided chambers

Dilatation of the right ventricle with normal valve leaflets suggests functional TR; dilated right atrium may be an indicator of severity of TR or atrial septal defect. Right ventricular volume overload may be suggested by ventricular septal flattening in diastole or paradoxical septal motion. Global and regional right ventricular function assessment is also important – regional dysfunction may suggest previous right ventricular infarction; global dysfunction may indicate progression of a left-sided process to biventricular cardiomyopathy.

4. Measurement of peak right ventricular systolic pressure

By measuring peak tricuspid regurgitant velocity, systolic pulmonary artery pressure can be estimated. An accurate estimation of right ventricular systolic pressure is important in distinguishing between secondary and primary causes. Systolic pulmonary artery pressures of >55 mmHg are likely to cause TR with anatomically normal valves, whereas significant TR with systolic pulmonary artery pressures <40 mmHg is likely to be related to an underlying structural abnormality of the valve.

5. Left-sided assessment

Abnormal LV size and function may indicate functional TR secondary to pulmonary hypertension in the setting of dilated cardiomyopathy. LV function assessment is also important prior to considering surgery for tricuspid valve disease. As noted above, left-sided valve lesions, especially mitral valve lesions, are commonly seen causes of functional TI and must be excluded as part of the TI echo evaluation.

6. Other

Congenital lesions should be excluded, particularly atrial septal defects, which cause TR due to volume overload, or Ebstein's anomaly, which is associated with apical displacement of the tricuspid leaflets leading to atrialization of the right ventricle. Complex congenital lesions such as transposition of great vessels with systemic right ventricle causing TR due to progressive right ventricular failure may need to be considered, depending on clinical data.

Other Investigations

ECG is not diagnostic in TI but may provide clues into related electrical or mechanical abnormalities such as bifid p waves/p-mitrale in mitral stenosis, right atrial and/or right ventricular enlargement/hypertrophy in right-sided strain and q waves and other ischemic changes in prior myocardial infarction affecting the right or left ventricle. Incomplete right bundle branch block may indicate an atrial septal defect.

Chest radiographs may show right atrial enlargement or filling in of the retrosternal air space on a lateral chest film indicating right ventricular enlargement. Left atrial enlargement in mitral stenosis may present with straightening of the left hand border or a 'double density.' Prominent pulmonary arteries at the hilum with rapid tapering may be seen in pulmonary hypertension.

Cardiac catheterization in the presence of moderate to severe TR may show a dominant V wave in the right atrial pressure curve and increased right ventricular end-diastolic pressure. It also allows measurement of the pulmonary vascular resistance and cardiac output. It is indicated whenever clinical and echocardiographic assessments of right-sided pressures are discordant or if pulmonary vascular resistance and its responsiveness to therapy need to be measured.

More recently advances in three-dimensional echocardiography and cardiac MRI have contributed to a greater understanding of tricuspid valve pathology and are invaluable not only in determining the etiology and severity of TR, but also in assessing right ventricular function and pulmonary artery pressure. Cardiac MRI is the gold standard for evaluation of right ventricular function and morphology.

How do I know this is what the patient has?

As with other forms of valvular heart disease, echocardiography is the key to confirming its diagnosis as well as assessing the severity of the regurgitation and providing key information regarding etiology and prognosis. Any patient with a murmur suggestive of TI or other clinical features suggestive of right heart failure or pulmonary hypertension should undergo an echocardiogram. If transthoracic echo windows are of suboptimal quality, transesophageal echo imaging or cardiac MRI should be considered. Of note, clinically significant TI may be seen on color Doppler in many normal individuals; hence it is important to combine the echo findings with clinical correlation and judgment.

Differential diagnosis

Differential diagnosis of the pansystolic murmur heard in TI includes mitral regurgitation and ventricular septal defect. Mitral regurgitation produces a pansystolic murmur that is loudest in the apex on expiration and classically radiates to the axilla. Ventricular septal defect is a harsh holosystolic murmur also heard loudest in the lower left sternal border but will not be associated with loudening on inspiration or a mid-diastolic murmur.

Confirmatory tests

Color flow and continuous wave Doppler on trans-thoracic echocardiography confirm the presence of tricuspid valve regurgitation as well as guiding the assessment of its severity.

4. Specific Treatment

In the case of moderate to severe TI, the clinical status of the patient and the etiology of the valvular regurgitation determine the optimal management strategy.

Medical therapy

Diuretics are indicated to improve signs of congestion in TI associated with clinical right-sided heart failure. Sodium restriction is also important. Specific medical treatments depend on the underlying cause (eg, antibiotics in TI associated with infective endocarditis).

Surgical therapy

In summary, in those undergoing left-sided valve surgery, tricuspid valve repair is universally recommended in the presence of severe coexistent TR; the simplicity of tricuspid valve repair and potential high risk for secondary surgical correction are additional incentives for TV surgery in this situation. in those with isolated severe TR, surgery is recommended in the presence of symptoms or progressive right ventricular dilatation or dysfunction or pulmonary hypertension.

Limited data are available regarding the timing of surgery, but as a general principle, surgery should be carried out before irreversible right ventricular dysfunction occurs. If technically feasible, valve repair with annuloplasty is preferred to valve replacement. Intraoperative transesophageal Doppler echocardiography allows refinement of annuloplasty techniques to optimize outcome. Use of prosthetic rings leads to better long-term results than the stitch technique, with the 5-year incidence of TR being 10% and 20-35% respectively.

In certain cases of TR associated with trauma or endocarditis, valve and/or chordal reconstruction can be attempted. If tricuspid valve leaflets are diseased or destroyed, such as in infective endocarditis, valve replacement may be required. Regarding prosthetic valve replacement, 10-year survival ranges from 30-50%, the main predictors including preoperative biventricular function and functional class as well as prosthetic valve complications. Large bioprostheses are currently favored over mechanical valves due to the high risk of thromboembolic complications with mechanical prostheses in the tricuspid position.

ESC Guidelines for intervention in tricuspid regurgitation

Severe TR in a patient undergoing left-sided valve

surgery (IC)

Severe primary TR and symptoms despite medical therapy without severe right ventricular dysfunction (IC)

Moderate organic TR in a patient undergoing left-sided valve surgery (IIaC)

Moderate secondary TR with dilated annulus (>40 mm) in a patient undergoing left-sided valve surgery (IIaC)

Severe TR and symptoms, after left-sided valve surgery, in the absence of left-sided myocardial, valve, or right ventricular dysfunction and without severe pulmonary hypertension (systolic pulmonary artery pressure >60 mmHg) (IIaC)

Severe isolated TR with mild or no symptoms and progressive dilation or deterioration of right ventricular function (IIbC).

5. Disease monitoring, follow-up and disposition

Expected response to treatment

Limited data available on the natural history of severe primary TI suggest a poor prognosis even if it has been well tolerated for years. When significant TI accompanies left-sided heart disease or pulmonary hypertension of other etiology, the natural history is determined by the primary disease.

Incorrect diagnosis

Moderate or severe TI may be present without the classic clinical features. A detailed echocardiographic examination with adequate acoustic windows including 2D, color flow and continuous wave Doppler imaging, that does not find evidence of TI of more than mild severity should lead to suspicion of an incorrect diagnosis.

Follow-up

No specific guidelines exist for follow-up of TI. Patients with severe primary TI should be monitored at regular intervals by both clinical assessment to monitor for the development of symptoms and by echocardiography to monitor for the development of right ventricular dilatation or dysfunction.

Patients with severe isolated TI should be monitored for the development of symptoms or progression of right ventricular dilatation or dysfunction. Patients with moderate functional TI should be monitored for progressive tricuspid annular dilatation (>40 mm) as annular dilatation is an ongoing process that may progress to severe TI if left untreated.

Pathophysiology

Tricuspid regurgitation decreases the amount of blood returning into the right atrium and, if severe enough, will limit cardiac output. Increased venous pressure leads to fluid extravasation.

Functional TR occurs as a result of elevation of right ventricular systolic and/or diastolic pressure, increased RV cavity size and annular dilatation due to right ventricular pressure and/or volume overload conditions. Most commonly, functional TR is due to pressure overload from pulmonary hypertension due to left-sided valve lesions (particularly mitral stenosis), other left-sided heart disease, cor pulmonale, idiopathic pulmonary arterial hypertension and the other various causes of pulmonary hypertension.

Pulmonic valve stenosis is a rare cause of functional TR due to increased RV systolic pressure. Right ventricular volume overload from atrial septal defects or other intrinsic disease of the right ventricle, including RV cardiomyopathy and right ventricular infarction, can also lead to functional TR.

Causes of organic TR include endocarditis, rheumatic heart disease, carcinoid heart disease, myxomatous disease causing tricuspid valve prolapse/floppy valves, radiation therapy, trauma (including repeated endomyocardial biopsies), connective tissue disease, Marfan syndrome, endomyocardial fibrosis, anorectic drugs, tumor on leaflet(s) and congenital abnormalities such as Ebstein's anomaly or cleft tricuspid valve due to an atrioventricular canal malformation. Rheumatic tricuspid valve involvement usually results in both stenosis and regurgitation.

Tricuspid valve annular circumference and leaflet area are useful measurements in establishing etiology as dilated annuli >12 cm are associated with Ebstein's anomaly, myoxomatous/floppy valves, and multiple causes of pulmonary hypertension. Increased leaflet areas are associated with floppy valves and Ebstein's anomaly. Annular insertion site separates floppy tricuspid valves from Ebstein's anomaly.

Epidemiology

Pathological TR is more prevalent in women and in those with a past history of myocardial infarction and heart failure. In a study of 45 post-mortem patients with clinically documented isolated tricuspid regurgitation, conditions producing pulmonary hypertension (cor pulmonale, mitral stenosis) were the most frequent etiology at 47%. Next most common was floppy/myoxomatous valves at 16%, rheumatic at 11%, idiopathic dilated cardiomyopathy at 9%, Ebstein's anomaly at 7% and miscellaneous conditions at 10%.

Prognosis

Severe TR of any cause generally has a poor prognosis long term due to RV dysfunction and/or systemic venous congestion. Functional TR may improve or disappear as right ventricle failure improves following treatment of its cause (eg, correction of left-sided valvular lesions) but may also persist. Risk factors for persistence or late worsening of TR after surgical correction of mitral valve disease include pulmonary hypertension, reduced right ventricular function and degree of dilatation of tricuspid annulus.

Special considerations for nursing and allied health professionals.

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What's the evidence?

"ESC Guidelines on the management of valvular heart disease. The Taskforce on the Management of Valvular Heart Disease of the European Society of Cardiology". European Heart Journal. vol. 28. 2007. pp. 230-268.

Bonow, RO. "A Report of the ACC/AHA Taskforce on Practice Guidelines". JACC. vol. 52. 2008. pp. e1-e142..

Irwin, RB, Luckie, M, Khattar, RS. "Tricuspid regurgitation: contemporary management of a neglected valvular lesion". Postgrad Med J. vol. 86. 2010 Nov. pp. 648-55.

Joseph, G. Murphy. "Valvular Regurgitation". Mayo Clinic Cardiology Review. 1999.

Waller, BF. "Etiology of pure tricuspid regurgitation". Cardiovasc Clin. vol. 17. 1987. pp. 53-95.

Conaglen, PJ, Ellims, A, Royse, C, Royse, A. "Acute repair of traumatic tricuspid valve regurgitation aided by three-dimensional echocardiography". Heart Lung Circ. vol. 20. 2011 Apr. pp. 237-40.

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