Tricuspid Valve - STS E Book Flashcards

1
Q

Describe the tricuspid valve

A

R sided b/w R atrium and R ventricle. Leaflets anterior (largest), posterior (multiple scallops), septal (smallest). Chordae tendinae, 2 papillary muscles (anterior and posterior), fibrous tricuspid annulus, R atrial and ventricular myocardium.

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2
Q

Why is the tricuspid septal leaflet spared from annular dilation?

A

The septal leaflet is the smallest and fixed.

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3
Q

The base of which tricuspid leaflet is used as a reference for sizing of tricuspid annuloplasty rings?

A

septal leaflet

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4
Q

Where do the chordae tendinae come from and go to in the tricuspid valve?

A

anterior papillary muscle supplies chordae to the anterior and posterior
posterior papillary muscle supplies chordae to the septal and posterior

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5
Q

Where are tricuspid accessory chordal attachments found and why are they important?

A

R ventricular free wall or the moderator band. May play a role in tricuspid regurgitation.

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6
Q

Why is the TV complex intimately associated with the conduction system?

A

Because the AV node lies within the triangle of Koch - tendon of Todaro, the septal leaflet of the TV, and the origin of the coronary sinus.

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7
Q

Pathology related to the TV is dependent on what three things?

A

Leaflet morphology, loading conditions of the heart, and degree of RV dysfunction.

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8
Q

How does RV dysfunction lead to tricuspid regurgitation?

A

RV dysfunction leads to chordal tethering, then loss of leaflet apposition, and thus TR. When the RV dilates, the tricuspid annulus enlarges (anterior/posterior dimension d/t septal leaflet fixed nature) causing failure of leaflet coaptation and TR.

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9
Q

Compare the TV to the mitral and aortic valves. What is the result of this difference?

A

The TV consists of a complex 3-dimensional structure, which is not symmetrical (unlike the other valves). As a result, loading conditions may change the orientation of the annular dimension significantly - eg during systole, there is a near 20% reduction in the size of the TA.

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10
Q

What is the most common L side pathology associated with TR?

A

mitral valve pathology - pulmonary HTN will develop as a result of L side overload from MR, the TA will dilate, and the leaflets will fail to coapt causing TR.
Less common etiologies - Eisenmenger syndrome and primary pulmonary HTN.

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11
Q

Is rheumatic heart disease more common in the developed or undeveloped portions of the world?

A

Undeveloped. Still an important cause of tricuspid regurgitation and stenosis.

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12
Q

How does connective tissue disorder cause tricuspid valvular incompetence?

A

Connective tissue disorders (eg Marfan) lead to myxomatous degeneration of TV leaflets, chordal elongation, prolapse, and therefore incompetence of the valve.

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13
Q

Infective endocarditis of the TV causing severe TR is most commonly associated with what?

A

IVDU. TV endocarditis in a non IVDU pt is rare. The exception is permanent pacemaker leads.

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14
Q

Why should surgical intervention for TV IE be performed with caution?

A

Pts tolerate TR well hemodynamically given the low pressure of the R heart. TV IE emboli to lungs are not as catastrophic as systemic emboli from L sided IE. IVDU pts have ongoing risks of reinfection, OD, and noncompliance.

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15
Q

How can carcinoid syndrome cause TR and TS?

A

R side heart involvement is common. White endocardial plaques may form on the TV leaflet surface, which can cause TR and TS, resulting from the inability of the leaflets to coapt.

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16
Q

TR presentation?

A

fatigue, decreased exercise tolerance 2/2 decreased cardiac output; right sided heart failure signs - ascites, congestive hepatopathy, peripheral edema; atrial stretch can cause a-fib

17
Q

TR diagnosis?

A

TTE.
Doppler flow map, vena contracta width assessed, direction and size of regurgitant jet is noted.
Need serial TTEs d/t volume status and afterload creating a dynamic process of TR.

Patients demonstrate a shift in the atrial septum to the left and paradoxical septal motion, consistent with R ventricular diastolic overload.