Valvular heart disease Flashcards
with a normal mitral valve, how much overlap/touching is there in the centre of the valve area?
usually there is 8mm of touching surface. when a heart dilates, this then is stretched apart, and less and less is touching. this means that the mitral valve can accommodate less and less pressure.
describe what happens to the mitral valve when there is prolapse
due to a lengthening in the supporting structures of the leaflets, there is decreased opposition of the two leaflets. this then means that there is less ability to deal with inc. pressure
describe what happens to the mitral valve when there is ischaemic changes?
as opposed to prolapse, in ischaemic changes, the supporting structures get fibrosed and shorten. in this setting, the abnormal supporting structure leads to “under-riding” of the valve leaflet. this also leads to decreased oppostion of the leaflets, and less ability to deal with inc pressure
which mitral leaflet is more commonly associated with prolapse?
the posterior is much more common, about 4:1 for post: ant
why does bileaflet MVP cause a late systolic murmur?
this is because there is opposition until right at the end of systole, once the leaflets finally prolapse. it takes a little longer for the pressure to push the leaflets back.
This is more prominent in bileaflet MVP (as opposed to single leaflet pathology, where there is weakness of leaflet opposition)
is there an echo finding looking at flow direction across the mitral valve that is an indication for surgical intervention?
systolic pulmonary vein flow reversal. (see echo picture)
how does the echo work out regurgitant fraction?
Doppler can measure the forward volume over the mitral valve. It can also measure the forward volume over the aortic valve.
If we subtract the forward volume from the aortic from the total that went foward over the mitral, then we have an idea how much went backwards
the fraction is the “regurg volume”/total forward flow over mitral
which vessels supply the pap muscles of the mitral valve?
see image, but basically
RCA supplies the posteromedial pap muscle
the LCx supplies the anterolat pap muscle
BE AWARE THAT THE PAP MUSCLES SUPPLY BOTH ANT AND POST LEAFLETS. THEY SUPPLY EITHER THE LATERAL OR THE MEDIAL ASPECTS OF THE VALVE
what happens if you rupture a pap muscle?
this is an emergency because it leads to acute pulm oedema
what happens in mitral stenosis
it is almost exclusively a disease associated with prior rheumatic disease.
the strep antibodies antigenically overlap with the valve leaflets. they cause
how do we calculate the mitral valve area?
this is a silly old school thing that I think we shouldn’t be expected to know.
anyway
MVA = 220/ pressure half-time
(pressure half time is the time for gradient to fall to half of its peak diastolic gradient)
describe the three cusps of the aortic valve (location)
there is left coronary
right coronary
non-coronary (next to sinus of valsalva)
how do we work out the aortic valve gradient?
quantification is based on Doppler studies.
PEAK VALVULAR GRADIENT IS WHAT WE’RE AFTER
The formula is “change in pressure = 4 v^2” (4 times V(peak) squared)
in disease, the speeds increase because smaller space for flow
what is the severity scoring for aortic stenosis
see image
what are the severity scores for mitral stenosis?
mean gradient is >10mmHg in severe disease
normal is
valve area:
severe
mod 1.0-1.5
what happens to stenotic lesions during inc. output?
the stenosis becomes greater
this holds true for mitral and aortic lesions
what is the strongest finding on cath lab print out that suggests a patient will do badly on a mitral valve replacement?
the strongest is if there is HIGH pulmonary vascular resistance.
once the pulm vasculature is cooked, it is game over.
what is the standard of care for a patient with a thrombosed artificial mitral valve?
the standard of care is now thrombolysis, but previously it was urgent valve replacement.
what causes widened splitting of the P2 and A2 during expiration?
what’s normal?
normally A2 closes before P2.
during inspiration, the increased venous return leads to greater blood in the RV, which leads to delayed P2.
during expiration, there is normal volume in the RV, and so the splitting is even closer, and A2/P2 overlap.
“WIDE SPLITTING” is from conditions that delay RV emptying (PS, RBBB)
REVERSE SPLITTING - this is another name for splitting during expiration - from AS, LBBB, HCM
FIXED SPLITTING - ASD
