TRICUSPID REGURGITATION Anatomy Pathophysiology Clinical Evaluation Management.

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Transcript of TRICUSPID REGURGITATION Anatomy Pathophysiology Clinical Evaluation Management.

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TRICUSPID REGURGITATION

• Anatomy

• Pathophysiology

• Clinical

• Evaluation

• Management

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Pathophysiology

Primary TR

Secondary TR(functional)

Hypertensive(RVSP > 55 mm Hg)

Normotensive(RVSP < 40 mm Hg)

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TR - Pathophysiology

• Primary TR …. Due to structural defects in TV apparatus

• Secondary normotensive TR

• Secondary hypertensive TR

Due to RV and tricuspid annular dilatation

Secondary to elevated RVSP

PAH / RVOT obstruction

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Primary TR

Congenital

• isolated TR• Ebstein• AV canal defects• VSD + TR• Hypoplastic RV

Acquired

• rheumatic• prolapse• carcinoid• EMF• endocarditis• tumors• SLE• drugs – methysergide• postop• pacemaker lead

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Normotensive functional TR

RV dilatation due to any cause

RV infarctionMyocarditisRV cardiomyopathyUhls anomalyASDFluid overloadHyperdynamic circulation

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Clinical features

Secondary TR > symptoms and findings of basic disease

Primary TR

well tolerated till they develop RV failure

• low volume pulse / AF

• JVP - prominent V ;CV (S) wave in severe TR sharp Y descend

• systolic pulsation over liver

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Clinical

• cardiomegaly ; RV apex; RA+

• S 1 .. Loud in RHD , ASD , Ebstein

• S2primary TR .. Normal / soft P2

hypertensive TR .. Loud P2 + features of PAH

split of S2 .. Variable

severe TR / no PAH or RVF …early P2

RVF … delayed P2

• RV S3 / S4 / OS / NEC

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Clinical

murmurs

Hypertensive TR

loud , high pitched , PSM .. best over LLSB / epigastrium

Normotensive TR

low intensity , soft , early systolicheard well over apex alsodynamic variation is more impressive

increases withinspiration - Carvallo signMuller’s maneuver

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ECG . CXR

• findings of underlying disease

• usually in AF

• RV volume / pressure overload pattern

• cardiomegaly with RV / RA / SVC / azygos prominance

• pleural effusion

Depends on the type of TR and its severity

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Echocardiogram

• presence of TR

• anatomy of TV apparatus

• etiology of TR

• severity of TR

• hemodynamics .. esp. RVSP

• RV function

• underlying / associated lesions

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RVEMF

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TR JET

Normotensive TR Hypertensive TR

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HEPATIC VEIN FLOW

Normal severe TR

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Echo.. Assessment of severity

2 D … RV / RA size ; IVS motion ; dilated vena cava / cor. sinus tricuspid annular diameter

Doppler• jet area

• venacontracta

• PISA

• CW jet configuration

• hepatic vein flow pattern

• IVC pattern

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Mild Moderate Severe

Jet area (cm2) < 5 5 -10 > 10

Vena contr. Not defined not defined > 0.70 cm(but < 0.70 cm)

PISA dia (cm) < 0.5 0.5 – 0.9 > 0.9

CW jet soft / parabolic dense / densevariable shape triangular

early peak

Hepatic normal systolic blunting systolic reversalVein flow

IVC size < 15 mm 15 -20 mm > 20 mm respirophasic normal normal absent

mild blunting

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RV function

• RV fractional area changeRV area (d) – RV area (s)

Normal .. 35 – 65 %RV area (d)

• TAPSE … 15 – 30 mm

• TDI … annular velocity … 6 -14 cm / s

• MPI (PWD) .. 0.15 – 0.40

• RVEF .. 45 – 70 %

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CMR

Limited role

To assess anatomy , RV function

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Staging of TR

Stage A at risk of TRclinically normal / normal hemodynamicsECG / CXR – normalEcho .. early / mild anatomical changes no / trace TR

Stage B progressive TRmild / moderate TRprogressive anatomic changes ( not severe)asymptomatic

Stage C asymptomatic severe TRgross anatomical deformitysevere annular dilatation ( > 21 mm / m2 or > 40 mm)

Stage D symptomatic severe TR( stage C + symptoms)

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Management

• treatment of underlying disease

• control of CHF / heart rate in AF / anticoagulation SOS

Stage C / D consider surgery

Secondary TR …. Tricuspid annuloplasty

Suture(unsupported)

Ring

Primary TR …. TVR (bioprosthesis)

TR in IE .. If infection is not controlled .. consider surgery

total excision of TV … bioprosthesis after 6 – 9 months

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