and welcome to another MedCram lecture we're gonna 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 new 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 and the lungs oxygenate it and it goes
to left atrium through the mitral valve then 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 30 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 aortic stenosis 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 Homer cyril and these could become calcified and
that's what would 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 gonna 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 gonna 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 so 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
pressure that needs to be overcome and yet the myocardium isn't in no position
to accept the more oxygen 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
this a sign is something called pulsus TARDIS and also parvis this simply means
slow and late-breaking so TARDIS 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 and to the peripheral vasculature when
you put your finger on that pulse it's gonna 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 becomes so
bad that this valve opens so little that the heart goes 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 wall 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 it 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 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 but 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 course
bonds to this areas here to find a 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 beat and hold 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 s4 now if you'll remember your
heart sounds you remember there is an s-1 an s-1 is simply the sound that is
first made in the cardiac cycle s1 as you recall is the closure of the
atrioventricular valves or the tricuspid valve and the mitral valve closing this
indicates systole and goes through until s2 occurs and if you recall s2 is the
closure of the semilunar valves which are the pulmonic and aortic valves so
that's the closure of those then you have s3 which apparently is blood coming
in and hitting the left ventricle usually it's a distended left ventricle
that's why it makes an s3 and so that's usually indicative of a big distended
left ventricle and then finally s4 which can be heard
specifically when the left atria contract forcing blood into a very
stiffened left ventricle and so what you can see in a aortic stenosis is
something known as an s4 and that indicates the contraction of this left
atrium assuming that you're not in a chor fibrillation if you are you will
never hear an s4 but if you do get contraction of the left atria in s4 the
blood that goes through hitting a very stiffened left ventricle
will cause an s4 and that is a low frequency sound best heard on the left
side because the systole begins here between s1 and s2 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 has 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 amyl nitrate 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 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 text enosis they have less than five 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 at a pig or
cow 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 than 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 had to
put a mitral valve replacement in you would be dealing with an INR of 2.5 to
3.5 but we're talking aortic 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 an actuality
the aortic valve closes first that's a two and then you get p2 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 attic valve is going to make a to go in this
direction to the point where a two is now after p2 so how would you know that
and why is this called paradoxical well when you take a deep breath in real
quickly p2 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 p2 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 latian and it could 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 artic
stenosis 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 a 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 Artic stenosis can cause paradoxical
subletting of the second heart sound thanks very much
you