1. The tricuspid and pulmonic valves are often overlooked but are important in assessing right heart function and pressures. 2. Echocardiography is useful for evaluating the etiology and severity of tricuspid regurgitation (whether organic/structural or functional) as well as assessing right heart pressures and sizes. 3. Tricuspid regurgitation is most commonly "functional" due to right ventricular dilation rather than specific leaflet pathology, while pulmonic stenosis is usually congenital but tricuspid and pulmonic valve disease can also be caused by conditions like rheumatic fever or carcinoid heart disease.

1. Tricuspid and Pulmonic Valves:
The forgotten valves
Michael G. Katz, MD
Fellow in Cardiovascular Disease
August 10, 2012

2. Normal TV
1. TV annulus is non-planar
2. Unequal leaflet size
3. Direct chordae attachment into septum
4. Small or absent papillary muscle

3. TR: Role of Echo
• Assessment of TR etiology
• Assessment of hemodynamic burden
– IVC, RA, RV size
– RV function
• Visual assessment, dp/dt, RIMP
• Annular DTI, TAPSE
– LV size and function
• Measure RV and PA pressures

4. Functional TR
Tricuspid regurgitation that is at least moderate or greater in
severity is most frequently “functional” in nature
• not related to specific tricuspid leaflet pathology
• right ventricular dilatation, distortion of the subvalvular
apparatus, tricuspid annular dilatation, or all three

5. Causes of Functional (non-organic) TR

6. Functional TR
• Normal TV leaflets except
for mild thickening
• Progressive RV enlargement
• Annular dilatation
• Asymmetric geometrical
alterations
• Malaligned papillary muscles
• Tethering of the TV leaflets
• Tenting of the TV leaflets
• Incomplete coaptation
• Tricuspid regurgitation
• Significant impact on
survival in severe HF

7. Organic TR
• Degenerative • Radiation Rx
• Endocarditis • Carcinoid
• Traumatic • Hypereosinophilia
• Congenital • Drug induced
– (Ebstein anomaly) – (ergots, anorectics)
• Rheumatic • PPM or ICD lead

8. Qualitative Evaluation

9. Clinical and Echo features of
ORGANIC TR

10. PASP
PASP = tricuspid regurgitation gradient + RA-pressure (RAP)
PASP = 4(Vmax² ) + RAP

11. RA pressure
5 mmHg 10 mmHg
Normal Size/>50% Collapse Normal Size/<50% Collapse
15 mmHg 20 mmHg
Dilated IVC/Minimal Collapse Dilated IVC/No Collapse

12. Significant TR
Systolic PAP > Systolic PAP <
55 mm Hg 40 mm Hg
TV likely Primary TV
lesion likely
normal (exceptions: RV
(functional) infarct, ASD)
Circulation 2006;114;450-527

14. Color Doppler
TR jet area measurement
• Best done at Nyq~50-70 cm/s
• Underestimate eccentric TR
• Overestimate central jet

17. CW Doppler
Mild

18. Both examples of Severe
“dagger-shaped” early
peaking tricuspid regurgitant
jet
profile due to early
equilibration of pressures
between the right atrium
and right ventricle

21. Normal HV flow

25. Semi-Quantitative Analysis
• All valvular regurgitations have three
components:
1. PISA (proximal isovelocity surface area),
2. vena contracta, and
3. regurgitation jet

43. Tricuspid Stenosis
• Rheumatic fever
– Thick leaflets/ restricted motion
– Fusion, shortening of chordae
– Reduced separation of leaflet tips
• Isolated TV congenital malformations rare
• Carcinoid heart disease
• Impedance of flow by RA tumor, TV vegetation, or
• Other structures
• Prosthetic valve degeneration or thrombosis

44. Qualitative 2D
• valve thickening
and/or
calcification,
• Restricted
mobility with
diastolic doming,
• reduced leaflet
separation at
peak opening, and
• right atrial
enlargement

45. Quantitative CW Doppler
• Mean gradient
– < 2 mm Hg is
normal
– > 7 mm Hg is severe
– Measure in held
expiration or
average of >= 5
cycles
• PHT >= 190 msec is
severe
• TVA = 190/PHT

46. Caveats to CW analysis
• PHT is not reliable when there is significant RV
dysfunction or PR
• Significant TR will increase mean gradient

47. Pulmonic Stenosis
• 95% of cases are congenital
• may also occur as part of
more complex congenital
lesions such as tetralogy of
Fallot, complete
atrioventricular canal,
double outlet RV, and
univentricular heart
• Peripheral pulmonary
artery stenosis may co-exist
with valvular pulmonary
stenosis such as in
Noonan’s syndrome and
Williams syndrome.

50. Pulm HTN : Loss of
pulmonic A wave and mid-
systolic notching.

52. PS: thickened
valve with
accentuated A
wave > 6 mm

53. AT < 70 to 90 msec c/w PASP >70 mm Hg
Normal: > 140 msec

57. Pulmonary Regurgitation

58. PHT < 100 c/w significant PR
PADP = RVEDP + deltaPpv

59. Virtual RHC when there’s no PS
Mean PA
= VTITR + RAP
PAEDP = 4(PREDV)2 + RAP
RVSP = PASP = 4(Vmax² ) + RAP
J Am Soc Echocardiogr 2009;22:814-819

61. PCWP

63. J Am Soc Echocardiogr 2009;22:814-819