You pay attention to these tables. You are
in fantastic shape.
Take a look at coronary steal syndrome now.
In order for you to understand this, once
again comes back to functional anatomy of
the heart. Let me set this up for you. First
and foremost, I want to you to come down and
take a look where is this coronary vasculature. You
see that. Now that is the lumen and I want
you to guide and call this the left ventricular
wall. Are you with me so far? Okay. So that
is the left ventricular wall and where is
this coronary vasculature. I need you to think of
that as being a lumen of your left ventricle.
That is a chamber. So that would be the endocardium
right. Now as we move superficial, we are moving
towards the surface. So we are moving through
the myocardium, you see where is the myocardium and then
we are getting to pericardium right now. Is
this picture perfectly clear to you? It should
be. Next, you see where's the pericardial cavity, what is
it called again? When you had sudden rupture
of that ventricular wall especially when you
had a macrophage degradation? It is called
a left ventricle pseudoaneurysm. And what are
you worried about? You are worried about rupture.
And what is that called when you have rapid
accumulation of fluid in your pericardial
cavity? It is called pericardial tamponade.
I said that fast because we already covered that.
Okay now. In order for you to understand further, there're
a couple of things that are ridiculously important.
Take a look at that coronary artery. You see that
coronary artery and that is then supplying
your surface of the heart. In other words,
closer to the pericardium. As we move deeper
down through the myocardium and then eventually
to the subendocardium, understand that you
are now branching into your arterioles. Okay.
And the reason that this is all important
to you clinically, is the fact that say that
you had a coronary artery massive occlusion
in which you had a MI. Okay. There is a myocardial
infarction taking place at the coronary artery.
I am purposely emphasizing artery. You tell
me, is that entire wall underneath the coronary
artery being draped and undergoing infarction
or is it only the subendocardial portion?
Now, the coronary arteries supplying blood
down through the branches and tributaries.
So it only makes sense that if there is coronary
artery occlusion completely and a patient
had myocardial infarction, then entire wall
trans, what does wall mean? Mural. Transmural
type of myocardium infarction would be a myocardium
infarction or occlusion taking place in your
coronary artery. Why is that so important to
you? Because you are expected to know, on your
EKG the type of ST change that you would find
with the transmural type of myocardial infarction
and you will tell me what kind. ST elevation
or non-ST elevation. ST elevation with transmural
type of infarction. Good. Take a look at arterials.
You see that. Say that you had a myocardial
infarction of an arteriole and it is way
down by the where is this coronary vasculature and see
if you had an arteriole type of occlusion,
are you going to suffer from myocardial infarction?
Of course you are. But then why would you
call this? Not transmural but subendocardial
myocardial infarction. Are we clear? How
can you tell the difference. Well first and
foremost, in both MIs are you going to find cardiac
enzymes? Do not let that question fool you.
Of course you are. It is a myocardial infarction.
What is the gold standard? One more time.
I am the most amazing medical student because
you know it is troponin I. Right. So in both
instances you will find a gold standard cardiac
enzyme being elevated, granted. But then how can you tell
the difference between transmural coronary
artery occlusion versus your arteriole type
of subendocardial myocardial infarction? Non-STEMI,
which is an ST depression type of issue would
be with your subendocardium. Coronary artery,
transmural would be STEMI. We will talk about
this again, but I need you to visualize the
anatomy here so that you're clearly seeing as to when
you are having a drape type of infarction
Next when we get into coronary steal syndrome,
there are times when you might want to use
certain drugs in which you might then cause
coronary arteries to dilate. Okay. Now, what
is that going to do? I will quickly walk you through this
and then we are good to go. And then in the next couple of
slides, then the information is all here.
I need you to listen to me right now. Listen
first, then see. Now you give a drug that
is going to cause immediate vasodilation and
why would you want to do this in a patient?
Well your patient has something like stable
angina, and what is stable angina? What do
you know about the atherosclerotic plaque?
Rather minimal and the pain occurred when?
During exertion. Now you tell me,
when you exercise from physiology, what kind
of factors then have on your blood vessels
when you have exercise? Obviously when you
exercise, all of your muscles require greater
amounts of oxygen. So just by sheer common
sense, what then happens to your blood vessels?
They are going to dilate. They have to. Why in the world
would you want your blood vessels to constrict
when your exercising? That wouldn't mean that
you are supplying more oxygen. Is that clear?
"But Dr. Raj, I thought exercise meant sympathetic?"
Of course it does. I'm not saying that it doesn't. But
when you exercise, you … that it cannot
be strictly sympathetic activity on your blood
vessels because that would cause vasoconstriction
and it would defeat the purpose of supplying
oxygen to a skeletal muscle or your heart muscle.
So then you have certain metabolites. What
are those metabolites called? ATP stand for
adenosine triphosphate. What kind of effect does adenosine
have on your blood vessels? Vasodilate. What
about lactic acid? Vasodilate. What about
carbon dioxide? Where is carbon dioxide coming
from? What happens to amount of carbon dioxide
production with exercise? Increase, doesn't
it? Of course it does. You have more glycolysis,
more TCA cycle from biochemistry, releasing
more carbon dioxide. All those are vasodilatory
metabolites on your blood vessels. Is that
clear? So my point is this when you induce
stress, let us say that it is going to be
physical stress with the patient with stable
angina, you are trying to then create an area
where you have increased coronary artery dilation,
so that that area where it's undergoing your
occlusion feels the pain. Are you feeling
the pain right now? I hope not. If not, go
to the doctor right now, but point is this.
If the patient is feeling pain doing exercise,
then you know you can find ST depression and such. You
know your patient has stable angina. Can
you mimic this medically? Of course again
exactly what we just did. Instead of exercise,
why not replace it with a vasodilator such
as adenosine or its analog that exactly what
you want to do. And when you do so, you cause your
coronary artery to then dilate, it will then
steal the blood from the area where it is
stenosed, to your coronary artery, which is
now open and what is your patient is going
to feel? Pain. Clear? Now other drugs that you might
want to use including dobutamine as well in
which it's a chemical stress test. But understand
the concept of coronary steal syndrome please.
Here you will find your two different types
of myocardial infarction. You will find your subendocardium,
which will be arteriolar type of MI versus
transmural. What kind of coronary artery or
arteriole? It will be a coronary artery, transmural.