13 Tricuspid valve disease Flashcards
What are the causes of TS?
RHD, IE, carcinoid, prolapse, congenital and functional.
In rheumatic TS, bacterial infection causes inflammation. This causes fibrosis and scarring, and, therefore, thickening, calcification and commissural fusion, of the TV. This restricts TV mobility.
In IE, the bacterial infection causes vegetations on the TV which damage the leaflets.
In carcinoid TS, metastatic carcinoid tumours secrete serotonin causing fibrosis, calcification and thickening of the TV, and PV.
In prolapse, one or more TV leaflets bulge into the RA during systole. TV myxomatous degeneration causes leaflet thickening and elongation.
Congenital TS can be isolated (e.g. dysplastic TV leaflets) or part of a CHD (e.g. Ebstein’s anomaly).
In functional TS, TV anatomy is normal but the TV blood flow is abnormal because a RA mass is blocking the TV.
What are the TTE characteristics of TS?
Thickened and calcified TV leaflets, restricted TV leaflets, decreased TVA, increased TV Vmax, and/or increased TV PG.
Systolic leaflet doming, annular calcification, TV masses and/or Ebstein’s anomaly.
In rheumatic TS, there is commissural fusion.
In IE, there are vegetations.
In TV prolapse, there is leaflet prolapse and increased leaflet motion during systole.
What are the symptoms and signs of TS?
Fatigue, peripheral oedema and/or symptoms of the underlying cause.
Prominent A wave in the JVP, tricuspid opening snap and/or diastolic murmur at the left sternal edge.
What are the quantitative methods used to assess TS?
Vmax, mean PG, PHT and TVA.
How is TV area estimated from the PHT?
TVA = 190 / (TV PHT)
The PHT is the time taken for the transtricuspid PG to decrease to half of its original value.
What are the effects of TS on chamber size and function?
RA pressure overload, RA dilatation, normal or decreased RV size with normal RV systolic function, dilated IVC and hepatic veins, systemic venous congestion and decreased CO.
TS obstructs blood flow from the RA to the RV so increases RA volume and pressure. This causes RA dilatation. TS obstructs blood flow from the RA to the RV so decreases RV volume and pressure. This decreases RV volume (RVEDV). However, RV systolic function is preserved in the absence of pulmonary hypertension. This decreases the RV preload which decreases the RV CO. This causes decreased exercise tolerance. The LA and LV are normal in size and function. In TS, the increased RA pressure causes IVC dilatation and decreased inspiratory collapse and hepatic vein dilatation. In TS, the increased RA pressure causes increased CVP which causes peripheral oedema and ascites.
What are the BSE values for the assessment of TS?
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What are the causes of TR?
RHD, IE, carcinoid, prolapse, congenital, functional, traumatic and device leads.
In rheumatic TR, bacterial infection causes inflammation. This causes fibrosis and scarring, and, therefore, thickening, calcification and commissural fusion, of the TV. This impairs TV coaptation.
In IE, the bacterial infection causes vegetations on the TV which damage the leaflets.
In carcinoid TR, metastatic carcinoid tumours secrete serotonin causing fibrosis, calcification and thickening of the TV, and PV which impairs coaptation.
In prolapse, one or more TV leaflets bulge into the RA during systole. TV myxomatous degeneration causes leaflet thickening and elongation which impairs coaptation.
Congenital TR can be isolated (e.g. dysplastic TV leaflets) or part of a CHD (e.g. Ebstein’s anomaly).
In functional TR, RA and/or RV dilatation (e.g. secondary to pulmonary hypertension and chronic lung disease) cause tricuspid annular dilatation which impairs TV leaflet coaptation.
In traumatic TR, blunt or penetrating chest trauma causes TV leaflet injury and/or chordae tendineae and papillary muscle rupture.
Pacemaker, ICD and/or CRT leads, implanted in the RV, pass via the TV ad impair coaptation.
What are the TTE characteristics of TR?
Thickened TV leaflets, impaired TV coaptation , systolic regurgitant flow.
Systolic leaflet prolapse, annular dilatation (annular dilatation if >35mm or >21mm/m2), chordae tendineae and/or papillary muscle rupture, TV masses and/or Ebstein’s anomaly.
In rheumatic TR, there is commissural fusion and mild central TR.
In IE, there are vegetations and severe eccentric TR.
In carcinoid TR, there is plaque and severe eccentric TR.
In TV prolapse, there is leaflet prolapse and increased leaflet motion during systole and mild to moderate eccentric TR.
In traumatic TR, there is leaflet injury and/or leaflet flail, chordae tendineae and/or papillary muscle rupture, acute severe TR, right sided HF and/or other injuries.
In patients with implantable devices, there are RV leads, entanglement, restricted leaflets with impaired leaflet coaptation and/or mild to severe TR directed on the path of the lead.
What are the symptoms and signs of TR?
Fatigue, dyspnoea, peripheral oedema, ascites and/or palpitations.
JVD, hepatomegaly, peripheral oedema, ascites, right sided S3 or S4 gallop, holosystolic murmur at the left sternal edge, cyanosis and/or cold hands/feet.
What are the qualitative methods used to assess TR?
TR size (TR jet size to LV size), TR origin, and TR direction (central or eccentric).
Abnormal TV leaflets, RV size, RA size, IVC diameter, hepatic vein flow, colour flow convergence and TR jet density with CWD.
What are the quantitative methods used to assess TR?
Colour flow area, colour flow area to RA area, regurgitant volume by PISA, regurgitant fraction, regurgitant orifice area by PISA or 3D, vena contracta by 2D or 3D, PISA, TV E wave velocity and TV E/A ratio.
How is TR PISA calculated?
PISA = 2πr²
In TR, the blood flows towards a circular orifice and converges to form a set of hemispheric shells with every shell becoming smaller and faster as it moves towards the orifice. If the aliasing velocity (Niquist limit) is adjusted to match the blood flow velocity of the shells, there is a blue red interface at the point of the shells where there is aliasing (blood flow velocity = aliasing velocity).
In the modified A4C view, decrease the sector width and the depth and zoom in on the TR jet at the level of the TV. Use CFD and adjust the aliasing velocity by adjusting the zero on the colour flow scale until a hemisphere of converging blood flow on the ventricular side of the TV is observed and there is a red blue interface (Niquist limit 28cm/s). Measure the radius of the hemisphere from the edge of the hemisphere (red blue interface) to the centre of the TV orifice.
How are the regurgitant flow rate, regurgitant area and regurgitant volume calculated for TR using the PISA?
PISA = 2πr²
RFR = PISA x aliasing velocity
ROA = (regurgitant flow rate) / (maxiumum TR velocity)
RV = EROA x VTI TR
Why is there hepatic vein systolic flow reversal in TR?
In subcostal use PWD to assess hepatic vein flow.
In no TR or mild TR, the systolic hepatic vein flow is dominant. In moderate TR, the systolic hepatic vein flow is blunted. In severe TR, the systolic hepatic vein flow is reversed.
In TR, the incompetent TV causes the blood to flow from the RV to the RA during systole. This increases the RA pressure causing retrograde blood flow into the IVC and HV.
