C11: TV And PV Regurg Flashcards
3 subgroups of TR
- Functional or secondary
- Organic or primary causes
- Mechanical causes
How do functional causes of TR cause regurg
what can cause this
by causing annular dilation, usually the TV leaflets have normal structure
dilated cardiomyopathy
ASDs
pulmonary hypertension
How do organic causes of TR cause regurgitation
By causing disorders of the TV complex
Possible causes of mechanical TR
Pacemaker leads
Implantable cardioverter debrillator leads
If rheumatic is affecting the TV, are other valves often affected
Which other valves are usually affected
Yes, it rarely occurs it isolation w/ only the TV
MV and/or the AV
US appearance of TV w/ rheumatic
Where does the thickened go start
Thickened and retraction of TV leaflets
TV diastolic doming (stenosis)
Dilation of the TV annulus (causes regurgitation)
Leaflet tips
Describe TR due to carcinoid HD
Causes
Rare malignant neuroendocrine tumor that secretes excessive amount of serotonin w/ damages right heart valves
US of TV w/ carcinoid
TV becomes thickened, retracted and rigid
You’ll see both stenosis and regurg…. value remains in a fixed, semi-open position, throughout the cardiac cycle
Key difference b/w carcinoid and rheumatic
Involvement of the MV/AV w/ rheumatic…. with carcinoid the PV will be involved and left heart if not effected
Why is the TV more susceptible to injury than the MV
RV is easier to compress making the Tv more susceptible
What type of TR does trauma cause
Acute TR
Describe TV prolapse
Systolic bowing of the belly of the leaflets into the RA during systole
TVP usually occurs with what other pathology of the L heart
MVP
Describe Ebsteins anomaly
4 main characteristics
A congenital malformation of the TV leaflets
- Adhesion of the septal and post leaflets to the myocardium
- Exaggerated apical displacement of the septal leaflet
- Atrialization and dilation of a portion of the RV inflow tract
- Small functional RV
What does exaggerated apical displacement of the TV septal leaflet cause
Leaflets cant coapt which leads to TR
Ebsteins anomaly is associated w/ which other abnormalities
- PFO or ASD
- Congenitally corrected transposition of great vessels
- VSDs
- hypoplastic pulmonary artery
How can Ebsteins affect the development of conduction pathways
What can this lead to
May lead to maldevelopment of the conduction pathway from the atria to the ventricles…..
… Wolfe-Parkinson White syndrome
What is Wolfe-Parkinson White syndrome
Early scoop of the QRS complex
Criteria for diagnosing Ebsteins anomally
To which insertion point should you compare it
TV septal leaflet displaced apical >2 cm
MV in the A4CH view
How can Ebsteins affect the movement and appearance of the anterior and septal TV leaflets
Anterior may have restricted motion
Septal may have whip-like motion and be longer w/ redundant tissue?
what should you always assess for w/ spectral doppler if the patient has ebsteins
ASD or PFO w/ colour and PW
if theres an IAS w/ ebsteins, how might the direction be different
what is this called
shunt direction may be from right to left instead of left to right due to increased right heart press from TR
Eisenemnger’s
w/ ebsteins how will the bowing of the IVS change
will be to the LV…. the L heart will look squished
common causes of annular dilation of the TV leading to functional TR
dilated cardiomyopathy
ASDs
pulmonary hypertension
ASD can cause pulmonary hypertension
how do large ASDs affect the right heart
larger ASDs can have significant shunts of > 50% to the R heart which causes the R heart chambers to dilate
chronic, severe pulmonary hypertension (PHT) is associated w/ dilation of which structures
RV and TV annulus
what happens to the TV leaflets as the pap muscles in the RV migrate away from the TV annulus
tenting and lack of coaptation
does TR peak velocity reflect the severity of the TR?
no
what does TR peak velocity reflect
press difference b/w the RV and RA during systole
does severe TR usually have a high or low velocity jet
usually low, because of the larger opening of the TV which will lower the PG b/w the RV and RA
w/ RV volume overload, when will you see the “D” sign of the LV is short axis
only during systole
w/ RV pressure overload, when will you see the “D” sign of the LV is short axis
common cause of press overload
throughout the entire cardiac cycle
lung damage
does volume overload often lead to press overload
yes
severe/progressive TR will show what signs
signs of RHF: increased JVP hepatomegaly peripheral edema ascites
3 ways we indirectly estimate the severity of TR w/ colour doppler
- colour jet are
- vena contracta width
- flow convergence radio (PISA)
4 ways we indirectly estimate the severity of TR w/ spectral doppler
- TV inflow (PW)
- hepatic vein profile (reversal during systole)
- Intensity of TR signal
- TR jet contour
2 quantitative parameters to assess severity of TR
- regurgitant volume
- effective regurg orifice area
BOTH USING PISA TR
limitations of colour doppler for TR severity
- overestimation of TR jet:
- jet displaces blood already sitting in the chamber…. trace only the aliased area
- over gained
- underestimation of TR jet:
- occurs w/ eccentric jets which hug the atrial wall
- severe lack of coaptation leads to huge hole in the TV and leads to only dark blue colour jet due to lower velocity (wont be aliased)
what is it called when an eccentric jet hugs the atrial wall
coanda effect
how do we determine the TR jet area
trace around the aliased part of the jet in systole, dont not trace any dark blue (represents the displaced blood)
value for mild TR jet area
severe
Mild: < 5 cm^2
severe: >10 cm^2
value for mild TR vena contracta
severe
mild: < 3mm (use MR value)
severe: > 7 mm
can you use the vena contracta and PISA method when there are multiple jets
no
in which views can you measure vena contracta for TR
RVIT or 4CH
should zoom
in which views can you measure PISA for TR
how do you do it
A4CH
zoom and lower colour scale to 28 cm/s
value for PISA for mild TR
severe
mild: = 0.5 mm
severe: >/= 9 mm
how will the TV inflow change w/ TR
velocity over what value could indicate severe TR
velocity of the inflow will increase, as well as volume since the volume from the TR is also going through the valve
> 1 m/s for the E wave: called E wave dominant
how will the HV flow profile change with TR
you will see reversal in later systole… w/ at least moderate TR, and the flow becomes diastolic dominant
is reversal in the HV sensitive or specific to severe TR
sensitive…. b/c there are other causes of HV systolic flow reversal
why does the liver get enlarged w/ TR
theres less forward flow in the the IVC, blood backs up into the liver
technical factors that limit the accuracy of TR CW brightness to determine severity
- gain -over-gaining or under-gaining… use inflow as control
- doppler angle, get as aligned as possible
shape of mild TR w/ CW
why
parabolic
b/c the press gradient b/w the RV and RA is maintained throughout all of systole
shape of severe TR w/ CW
why
triangular with an early peak
the press gradient drops off rapidly throughout systole due to a quick rise in pressure in the RA from the regurg volume.
name for the triangular appearance of severe TR
V cut off
TR peak velocity w/ massive TR
< 2 m/s
formula for EROA
EROA = (2 x pie x r^2 x Vn) / V of TR
what does the 2 x pie x r^2 represent in the EROA
surface areA of the hemispheric shell derived from flow convergence radius prox to the TV
what does the Vn represent in the EROA
colour nyquist limit (what the colour scale is set to below the baseline)
formula for the regurg volume using the EROA
RV = EROA x VTI of TR
value for Regurg volume for mild TR
severe
mild: < 30 ml
severe: >/= 45
value for EROA for mild TR
severe
mild: = 0.20 cm^2
severe: >/= 0.40 cm^2
2 general causes of PR
functional/secondary: causes that lead to annular dilation, and then poor coaptation of the cusps…. PR valve anatomy is normal
organic/primary: PR due to abnormalities of the cusps
clinical manifestation of PR
symptoms are due to RV volume overload:
dyspnea peripheral edema fatigue increased JVP liver engorgement
etiology of functional PR
RV cardiomyopathy RV infarction PHT Pulmonary artery dilation congenital heart disease
etiology of organic PR
carcinoid congenital lesions iatrogenic rheumatic valve disease trauma
in which view do you want to measure jet width for PR
PSAX RVOT due to lateral resolution
when do you start to see flow reversal in the main PA w/ PR
what would be a strong indicator of severe PR
moderate PR
seeing PR in the R or L pulmonary artery branches… the more distal, the more severe
what is the jet width ratio for PR
formula
ratio of the width of the PR jet to the RVOT diameter
PR jet width/RVOTd
what does a jet width of 0.7 mean
the width of the jet is >/= 70% of the RVOT diameter
jet width for severe PR
> 0.7
how does steepness of the PR slow correlate w/ severity
steeper the slope = more severe… short decel time that ends before the end of diastole may be severe
value for moderate press 1/2 time
severe
mod: > 100 ms
severe: < 100 ms
why does the PR velocity slow?
PA press falls due to regurg back into the RV and inflow into the RV, which equalizes the press b/w the chambers
what is the pulmonary regurg index (PRI)
a measure of the ratio of the duration of the PR signal to the total duration of diastole.. the earlier the PR signal ends, the more severe the PR, b/c press is equalizing fast
values for mild PRI
severe
mild: 1
severe: < 0.77
when would pre-systolic flow occur w/ PR and why does it happen
w/ severe PR or other conditions like RV diastolic dysfunction (RV very stiff)
when the RVEDP exceeds the PA press, forward flow occurs
when there is severe PR and we see forward diastolic floe, what do we assume is the cause
severe PR
when there is PR present, which pressure should we be calculating instead of RVSP
PAEDP and mPAP
formula for PAEDP and mPAP
PAEDP: 4 (v^2) + RAP
mPAP: 4 (v^2) + RAP
where are PAEDP and mPAP located
mPAP is at the peak diastolic velocity of the PR
PAEDP is at the lowest diastolic velocity of PR
