C10: TV and PV Stenosis Flashcards by M B

Is congenital TS usually associates with other congenital heart abnormalities

Yes

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angle b/w the TV and PV

45 degrees

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3 commissures of the TV

anteroseptal
anteroposterior
posteroseptal

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possible congenital causes of TS

various malformations of the TV complex:

mal-developed leaflets
shortened chordae
annular hypoplasia
abnormalities of the pap muscles
cor triatriatum dexter

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most common cause of acquired TS

other causes

rheumatic fever

carcinoid heart disease
Tv vegetation
Rt heart tumors or thrombus

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describe rheumatic TS

anatomic changes seen w/ rheumatic TS

starts at the leaflet tips, infection occurs several years after the initial beta-hemolytic streptococcus infection as an autoimmune response

thickening, fibrosis, fused leaflets and chordae which causes diastolic dooming… you will see the equivalent of the hockey stick w/ the MV

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is stenosis of the TV usually severe

why or why not

no, because the valve itself is so big

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does rheumatic TS usually cause TS and TR

yes

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describe carcinoid heart disease

how does it cause TS

rare, malignant neuroendocrine tumor that secretes serotonin which damages both the TV and the PV due to the formation of plaque… plaque causes the valve and chordae to thicken, retracted and rigid

second most common cause of TS

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specimen appearance of carcinoid heart disease on the TV

milky-white plaque like deposits on the endocardial surfaces and myocardium

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is the Lt heart often affected by hormones release from the carcinoid tumour

no, lungs will filter out the serotonin

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what is cor triatriatum dexter

perforated membrane siting in the RA

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describe the pathophysiology of TS

TS reduces tha area of the conduit b/w the RA and the RV… RA press must rise in order to maintain cardiac output which increases the driving press across the valve…
….eventually the increase in press works its way backwards towards the systemic veins

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symptoms of TS

fatigue
abdo discomfort
swelling

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how to tell the difference b/w carcinoid HD and rheumatic HD

carcinoid will involve the TV AND PV, and never the MV

rheumatic almost always involves the MV, where as PV is the last to be affected by rheumatic

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w/ what type of TV disease is the RV spared

if theres stenosis only…. not w/ regurg

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how do you performing a measurement for the Mean TV press gradient and VTI

measure from the view which is most parallel to TV inflow jet
trace the TV inflow envelope which will give you the mean PG and the VTI
measurement should be done w/ a normal HR

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how much can the TV inflow vary with respiration to be considered normal

up to 25% (is this right?)

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which is more important w/ TS, mean PG or max PG

mean PG

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what does the Tv press half time measure

what does the diastolic slope represent

the time it takes for the early diastolic PG to fall to half it’s original value…

the PG b/w the RV and RA during diastole

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how dose the size of the TV affect its CW wave profile

lower velocity profile w/ rapid deceleration time

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what PHT value measured @ end-expiration indicates severe TS

> 190 ms

ideally, when should you measure the PHT for TS

end expiration, or avg over several beats

formula to calculate TV area

TVA = (pie x r^2)LVOT x VTI of LVOT) / VTI of TV

limitation of TVA

- suboptimal alignment to the jet direction - improper LVOT diameter or VTI measurement - significant TR (cant use continuity equation for TVA)

when cant we use TVA to assess TS severity what do we do instead

if there is significant TR which alters the SV.... use PHT or mean gradient instead

mean gradient value for significant TS

>/= 5 mmHg

inflow VTI value for significant TS

> 60 cm

PHT value for significant TS

>190 ms

TVA value for significant TS

= 1 cm^2

supportive findings for severe TS

enlarged RA > or = moderate | dilated IVC

treatment for TS

- surgical de-bulking of tumor or vegetation - diuretics, or nitrates to relieve venous congestion - transvenous balloon valvuloplasty

cusps of the TV and PV

TV: anterior, posterior, septal PV: right, left, anterior

is the PV supported by the IVS? where does it get its support

no muscular ridge called the infundibulum, located b/w the RVOT and LVOT

relationship of PA to AO

RVOT possible levels of obstruction

subvalvular/infundibular valvular supravalvular pulmonary artery branches

common cause of PS

almost always congenital... acquired is uncommon

3 types of congenital PS

typical domed shaped PV dysplastic PV unicuspid or bicuspid PV

cause of acquired PS

``` rheumatic HD carcinoid HD hypertrophic cardiomyopathy tumors, thrombus vegetation extraneous TV tissue PV sinus of valsalva aneurysm ```

why would we measure the PV annulus w/ PS why is this important in which view do we measure

for possible PV valvuloplasty crucial to select the correct size balloon PSAX RVOT

what changes in the RV can we look for to support the finding of PS

RVH due to high afterload to the RV

is RVH symmetrical

no, asymmetrical, unlike the LV

2 criteria used to assess the severity of PS

peak PV velocity | maximum gradient

peak PV velocity value for mild PS severe

< 3 > 4

peak PV maximum gradient value for mild PS severe

< 36 > 64 (4 times the peak velocity squared will give you this) e.g. 4 (3^2) = 36 (mild PS) 4 (4^2) = 64 (severe PS)

do we calculate the PV area using the continuity equation

no, this method is not used for the PV

procedure of choice for sever congenital PS

PV valvuloplasty

when is RVSP equal to PASP what about if the RVOT is obstructed

when theres no obstruction of the RVOT RVSP will be higher than the PASP

w/ mild or moderate RVOT obstruction, what formula do we use to calculate PASP

PASP = RVSP - mPG of the PV mPG = mean pressure gradient (do a CW through the PV and trace it to get this)

w/ severe or critical RVOT obstruction, what formula do we use to calculate PASP

PASP = RVSP - MIPG of the PV MIPG = maximum instantaneous PG

spectral waveform shape of mild PS critical

mild: V shape w/ early peaking waveform (press equalizes faster) critical: parabolic w/ mid peaking waveform

Why is mean gradient more useful than peak velocity for TS

There’s more than 1 peak during the diastolic cycle and the diastolic cycle is longer than the systolic

Why do you average several beats when tracing the TV inflow for mean gradient and VTI

To account for changes in venous return with respiration

Limitation of P1/2 T

Tachycardia