TRICUSPID REGURGITATION Anatomy Pathophysiology Clinical Evaluation Management

TRICUSPID REGURGITATION TV -- anatomy Complex apparatus Largest valve orifice area

TRICUSPID REGURGITATION Pathophysiology Primary TR Secondary TR (functional) Hypertensive (RVSP > 55 mm Hg) Normotensive (RVSP < 40 mm Hg)

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

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

Normotensive functional TR RV dilatation due to any cause RV infarction Myocarditis RV cardiomyopathy Uhls anomaly ASD Fluid overload Hyperdynamic circulation

TRICUSPID REGURGITATION 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

TRICUSPID REGURGITATION Clinical cardiomegaly ; RV apex; RA+ S 1.. Loud in RHD, ASD, Ebstein S2 primary 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

TRICUSPID REGURGITATION Clinical murmurs Hypertensive TR loud, high pitched, PSM.. best over LLSB / epigastrium Normotensive TR low intensity, soft, early systolic heard well over apex also dynamic variation is more impressive increases with inspiration - Carvallo sign Muller’s maneuver

TRICUSPID REGURGITATION 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

TRICUSPID REGURGITATION Echocardiogram presence of TR anatomy of TV apparatus etiology of TR severity of TR hemodynamics.. esp. RVSP RV function underlying / associated lesions

RVEMF

TR JET Normotensive TRHypertensive TR

HEPATIC VEIN FLOW Normalsevere TR

TRICUSPID REGURGITATION 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

TRICUSPID REGURGITATION MildModerateSevere Jet area(cm 2 ) 10 Vena contr.Not definednot defined> 0.70 cm (but < 0.70 cm) PISA dia (cm) 0.9 CW jetsoft / parabolicdense / dense variable shapetriangular early peak Hepatic normalsystolic bluntingsystolic reversal Vein flow IVC size 20 mm respirophasicnormalnormalabsent mild blunting

TRICUSPID REGURGITATIOM RV function RV fractional area change RV area (d) – RV area (s) Normal.. 35 – 65 % RV area (d) TAPSE … 15 – 30 mm TDI … annular velocity … cm / s MPI (PWD) – 0.40 RVEF.. 45 – 70 %

TRICUSPID REGURGITATION CMR Limited role To assess anatomy, RV function

TRICUSPID REGURGITATION Staging of TR Stage Aat risk of TR clinically normal / normal hemodynamics ECG / CXR – normal Echo.. early / mild anatomical changes no / trace TR Stage Bprogressive TR mild / moderate TR progressive anatomic changes ( not severe) asymptomatic Stage Casymptomatic severe TR gross anatomical deformity severe annular dilatation ( > 21 mm / m 2 or > 40 mm) Stage Dsymptomatic severe TR ( stage C + symptoms)

TRICUSPID REGURGITATION 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