C10: TV and PV Stenosis Flashcards
Is congenital TS usually associates with other congenital heart abnormalities
Yes
angle b/w the TV and PV
45 degrees
3 commissures of the TV
anteroseptal
anteroposterior
posteroseptal
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
most common cause of acquired TS
other causes
rheumatic fever
carcinoid heart disease
Tv vegetation
Rt heart tumors or thrombus
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
is stenosis of the TV usually severe
why or why not
no, because the valve itself is so big
does rheumatic TS usually cause TS and TR
yes
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
specimen appearance of carcinoid heart disease on the TV
milky-white plaque like deposits on the endocardial surfaces and myocardium
is the Lt heart often affected by hormones release from the carcinoid tumour
no, lungs will filter out the serotonin
what is cor triatriatum dexter
perforated membrane siting in the RA
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
symptoms of TS
fatigue
abdo discomfort
swelling
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
w/ what type of TV disease is the RV spared
if theres stenosis only…. not w/ regurg
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
how much can the TV inflow vary with respiration to be considered normal
up to 25% (is this right?)
which is more important w/ TS, mean PG or max PG
mean PG
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
how dose the size of the TV affect its CW wave profile
lower velocity profile w/ rapid deceleration time
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
anterior
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
