By Adem Lewis / in , , , , , , , , , , , , , , , , , , , , , , , , , , , /

I am welcome to another MedCram lecture
we’re going to talk about aortic stenosis and specifically the pathology
the pathophysiology and the clinical aspects of this condition first I want
to just remind you the anatomy of the heart for those of you who are starting
with us knew here so we know we’ve got the right atrium
which then blood from the right atrium goes into the tricuspid valve through
the tricuspid valve into the right ventricle and then that goes out through
the pulmonic valve to the lungs then the lungs oxygenate it and it goes to left
atrium through the mitral valve then 8 through the aortic valve and then out to
the body and then from there back to the right atrium the part that we want to
talk about specifically today is the aortic valve okay so the aortic valve is
the area that we’re talking about we’re talking specifically about a aortic
stenosis stenosis simply means closure or the inability for this valve to open
so what are the possible causes of aortic stenosis now we can kind of break
this down into those who are thirty years old or younger greater than 30
years between 30 and 70 and greater than 70 so for those who are less than 30
years of age and they get a or text enosis that’s pretty rare and the cause
of that is calcification of a uni comas ural valve now what does that mean the
valve it usually has three parts so if you were to look look at it directly on
it would look like a Mercedes Benz sign well a unique Amish oral valve is one
that only has one part going through it okay not bicuspid but unique or masu
rural and these could become calcified and that’s what we give you
calcification and stenosis before the age of 30 what’s the most common cause
between 30 and 70 years of age that’s bicuspid bicuspid that would be a valve
that looks like that so these become calcified very early and they are the
most common cause of Aric stenosis overall and specifically
between the ages of 30 and 70 what about after the age of 70 here you’ve got a
normal valve you simply get calcification of normal valve okay but
overall if they were to ask you what’s the most common cause of aortic stenosis
it would be bicuspid before the age of 70 okay so what are we going to see in
this type of a situation well because there is stenosis at this area right
here we’re going to start to see that the pressure builds up inside this in
this left ventricle and as a result the muscle here is going to get thicker than
it already is and that’s going to cause what we see in terms of hypertrophy the
compliance of this area is going to go down and we know that compliance by
definition is the change in volume over the change in pressure what does that
mean if the compliance goes down then that means it’s going to take a very
large change in pressure to make a very small change in the volume of this left
ventricle so what we’re seeing here in other words if the compliance is going
down is that this is going to become very stiff now why is that important
remember is going to be coming in trying to go
into the left ventricle now as a result it’s going to need to fill this up and
if this is very stiff the pressure in this chamber is going to go up as a
result you’re going to see the pressure in the left atrium also go up that
pressure is going to be transmitted back to the lungs if you’re not careful
and as a result that pressure will be transmitted back to the right ventricle
to the right atrium and systemically back to the body and you’ll get systemic
venous hypertension also very briefly as a result of this stenosis here at the
aortic valve there’s going to be less cardiac output and as a result of that
the peripheral vasculature is going to dilate this low compliance in the left
ventricle is going to make it difficult for these EPI pericardial blood vessels
to supply blood to that area and as a result you’re going to actually get a
reduction in oxygen perfusion to this muscle over a period of time and that’s
even worse than you think because it’s going to take more oxygen for this
muscle to contract because it has to pump against a higher what we call after
load we’ll talk about after load a little bit in some of the other lectures
but after load basically is the amount of force or it’s the amount of pressure
or tension that this left ventricle needs to overcome and it’s directly
related to oxygen consumption so here you have a situation where oxygen
consumption is increasing because of the because of the pressure that needs to be
overcome and yet the myocardium isn’t in no position to accept the more ox
because it’s compliance has essentially decreased now as a result of this you
get symptoms such as angina or angina this is pain angina pectoris is
essentially the same as chest pain you also get syncope syncope is where you
basically pass out you could also get dis Nia that’s simply shortness of
breath that’s another symptom of this a sign is something called pulsus tardes
and also parvis this simply means slow and late-breaking
so tardes is late and parvis is smaller so the thing is is that if this valve
here the aortic valve is not opening as well when the pulse finally gets through
into the peripheral vasculature when you put your finger on that pulse it’s going
to have a slower upstroke and a later upstroke that’s the pulses parvis a
tardis and so some of the complications that you’ll see is something called
sudden death where finally become so bad that this valve opens so little that the
heart goes in into arrhythmia and you could die so this is pretty serious
let’s go over the pathophysiology so as we said it’s all about the specifics of
this valve because this valve doesn’t open we see a enlargement of the left
ventricle and specifically we see hypertrophy and so what we get is after
load increasing so after load goes up and you see thickening of the left
ventricular wall this is called left ventricular hypertrophy and this is one
of the compensation mechanisms that is used as we mentioned the
all becomes very stiff and as a result of that something called left
ventricular and diastolic pressure and left ventricular end-diastolic volume
increases but specifically the pressure goes up
left ventricular end diastolic pressure simply means what is the pressure in the
left ventricle right before it contracts if that pressure is very high which is
what happens in a stiff ventricle then the pressure is also going to be high in
the left atrium if that occurs the left atrial size is going to increase and the
reason is is because the left atrial wall does not have a very thick wall in
fact it’s very thin it’s not designed to undergo a lot of pressure that can be a
problem because if this left atrial wall becomes enlarged something can happen
called atrial fibrillation now why is that important if this left ventricle is
very stiff then it’s very difficult for blood to get in to this ventricle for to
be pumped out and you depend very specifically on something called
atrial kick it is the contraction of the atria right before the ventricle
contracts that gets just a little bit more blood back into the left ventricle
before it gets pumped out through it the aortic valve in atrial fibrillation
however you lose all of that contraction you see P waves disappear on the EKG now
there is no more what we call atrial Kick
so no atrial kick and as a result of that cardiac output
drops precipitously so if you have a patient with aortic stenosis their left
ventricular starts to increase then their left atrial size starts to
increase and that causes atrial fibrillation they will they could
decompensate very quickly now as we said because of the increased
demand for oxygen and the fact that the compliance of the left ventricular wall
is so low you’re going to get increased oxygen demand and decreased oxygen
supply that’s going to cause angina we already talked about that weight and you
can also get shortness of breath and you can also get syncope we talked about
that but the other thing that you’ll see is a low pulse pressure that means
instead of seeing something like 120 over 80 where this is the systolic
pressure generated by the force of blood leaving the left ventricle and going
into the aorta and 80 being a sign of the diastolic pressure you’ll see that
these numbers instead of being 40 apart are going to be much closer to each
other because of the stenosis at this a Orting valve and so you might see
pressures more along the lines of 110 over 90 for instance this is not
uncommon to see the other thing that you will see on your physical examination is
that when you examine the patient it is normal to listen at the apex of the
heart in this area which corresponds to this area’s here to find the maximal
beat if you will when you listen you can also feel this now normally when the
heart gets enlarged for instance in congestive heart failure when the heart
becomes enlarged you’ll see a direction to the left however an aortic stenosis
because the size of the heart the size of the left ventricle itself is not
increasing but only the wall thickness you’ll see that the the apex will stay
around the same area the apical impulse however will be sustained what does that
mean that means that it’s taking a longer period of time to get that blood
out through the aortic valve and therefore it will be an hole
old more time during the time cycle and so what you see there is you will have a
sustained apical impulse which is unmoved you might also see something
called an S for now if you’ll remember your heart sounds you remember there is
an s 1 and s 1 is simply the sound that is first made in the cardiac cycle s 1
as you recall is the closure of the atrial ventricular valves of it or the
tricuspid valve and the mitral valve closing this indicates systole and goes
through until s2 occurs and if you recall s 2 is the closure of the
semilunar semilunar valves which are the pulmonic and aortic valves so that’s the
closure of those then you have s 3 which apparently is blood coming in and
hitting the left ventricle usually it’s a distended left ventricle that’s why it
makes an S 3 and so that’s usually indicative of a big distended left
ventricle and then finally S 4 which can be heard specifically when the left
atria contract forcing blood into a very stiffened left ventricle and so what you
can see an aortic stenosis is something known as an S 4 and that indicates the
contraction of this left atrium assuming that you’re not an H or fibrillation if
you are you will never hear an S 4 but if you do get contraction of the left
atria and s 4 the blood that goes through hitting a very stiffened left
ventricle will cause an S 4 and that is a low frequency sound best heard on the
left side because the systole begins here between s 1 and s 2 the type of
murmur that you would see is called a crescendo decrescendo and it simply is
proportional to the velocity of blood going out of the aortic valve this is
called a crescendo decrescendo murmur and it is heard best at the second right
intercostal space now as a result of the pathophysiology anything that increases
the gradient around this valve or the amount of blood in the left ventricle is
going to increase the murmur anything that decreases the gradient or decreases
the left ventricular size is going to decrease the murmur and so what we see
here is that if we decrease the blood pressure here in the aorta with using
things like amyl nitrate a will nitro will actually decrease the blood
pressure in the aorta which will increase the gradient and that will
increase the murmur of aortic stenosis if you do something called a valsalva
maneuver which is where you bear down that it usually has the effect of
shrinking both ventricles both the right and the left as a result of that since
there is less blood in the left ventricle to pump through the aortic
stenosis doing a valsalva will decrease the murmur of aortic stenosis a few more
things in regard to symptoms specifically the three symptoms that we
talked about known as angina syncope and congestive heart failure these three
symptoms are very important as a study was done on these and it shows that
angina is one of the milder symptoms of aortic stenosis syncope is a more severe
symptom of aortic stenosis and congestive heart failure is the worst
symptom of aortic stenosis and the recent study found that if someone has
angina in air duct stenosis they have less than 5
years of life expectancy if someone has syncope they have less than three years
of life expectancy however if someone has congestive heart failure they have
less than two years of life expectancy and knowing that order may be testable
information so finally what’s the treatment well they do things called balloon
valvuloplasty where they actually put a balloon in here and try to open it up
but this is only temporary and it really doesn’t work the best treatment is
actually surgery and there’s two options for surgery either you can do something
called a bio prosthetic valve and bio prosthetic is either made out of pig or
cow or bovine etc the nice thing about this is that it is not thrombogenic and
that you don’t need to be on chronic anticoagulation so no anti coagulation
the bad thing is however is that it doesn’t last long doesn’t last ten plus
years so if you have less than ten years of life expectancy then it’s best to use
a bio prosthetic valve if however you have more than ten years of life
expectancy then a mechanical valve is the way to go for that however you do
need anticoagulation and the standard of care is warfarin with an INR of 2.0 23.0
generally speaking now the flow past this valve is quite high and so the
thrombogenic risk relatively is not as bad as it would be in an area with a
slow flow now this valve opens much more and so the flow through here is much
slower as a result if you have to put a mitral valve replacement in you would be
dealing with an INR of 2.5 to 3.5 but we’re talking
or tech it’s usually pretty fast and the recommendation is 2.0 to 3.0 generally
speaking okay so that pretty much sums it up but before I go I wanted to say
one more thing and that’s something that you might see called reverse splitting
of the second heart sound so what does this mean well real quick we’re talking
about the second heart sound as you know that’s the closure of the aortic valve
and the pulmonic valve well in actuality the aortic valve closes first that’s a –
and then you get P – okay but it happened so quickly that it’s we’ve
group it into the second heart sound well anything that makes the aortic
valve or the left side this is the left side here this is the right side
anything that makes the left side delayed enclosure of this a or take
valve is going to make a to go in this direction to the point where a – is now
after P – so how would you know that and how wise is called paradoxical well
when you take a deep breath in real quickly P 2 goes this way and then when
you breathe out it comes back this way this way for breathing in this way for
breathing out and so as a result of that you should see that the difference
between a 2 and P 2 in other words the splitting of that second heart sound
should get bigger on inspiration and smaller on exhalation however if you run
into a situation where a 2 is no longer here and it’s all the way over here this
is still going to move relative to breathing and so when it moves over here
you’re still going to hear this split but instead of it being larger on
inhalation it’s going to be smaller on him elation and it’s going to be larger
on exhalation this is exactly the opposite of what you
would expect and that’s why it’s called paradoxical or reverse splitting of the
second heart sound and it happens because a two gets transposed on the
other side of p2 so what would do that what would cause a two to be so late in
relation to p2 well it’s anything that causes the left side to slow down
relative to the right side or anything that causes the right side to speed up
relative to the left side so there’s two things that will cause the left side to
slow down one of them is the thing that we’ve been talking about today which is
a or text enosis so a Artic stenosis is one of the causes of paradoxical
splitting or reverse splitting of the second heart sound the other thing is a
left bundle branch block that’s obvious why that would slow down the left side
contraction is because there’s a block in the conduction but the other thing
that could cause it is tricuspid regurgitation because tricuspid
regurgitation means the right ventricle is going to pump blood out of its
ventricle faster because now it’s got two places to pump it out and so as a
result of that the pulmonic valve closes much earlier and p2 goes over here on
the other side of a – and so when it moves it’s going to cause paradoxical
splitting of the second heart sound I’ll give a lecture on heart sounds and
splitting and that sort of thing but I just want to make sure you knew that
a or text enosis can cause paradoxical splitting of the second heart sound
thanks very much you

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