Let us continue our discussion of ischemic
heart disease and now we'll take a look at acute
coronary syndrome. What does that mean to
you? It means that we are one step closer
to having a myocardial infarction, but not
completely. So acute coronary syndrome, we
understand that our patient has pain and may
require rest and before we get into all of
those, just make sure that we understand some
simple basic anatomy because as we get to
the tail end of our lecture series I will
have you take a look at EKGs. This is that
you know clearly the difference between what
is known as STEMI an ST elevation myocardial
infarction versus a non-STEMI. Before we get
to any of that, there we are going to build
a pathology and our understanding
so that we would be able to clearly see this.
First, we have the aorta, but then we have
the left coronary artery. After left coronary
artery that which is moving down between the
ventricle. It would be your left anterior descending
as you should know from anatomy. That left
anterior descending if it underwent major
mass of atherosclerosis and had an area in
which there was myocardial infarction. You
have any ideas to what leads of your EKG that you
might be paying attention to? What is important
for you to understand? And we will when the time
is right. But just to give you an idea, if
it is anterior 2/3rds of the interventricular
septum that the left anterior descending is
supplying and it is also supplying the lateral
aspect of the heart a little bit. Then what
might you be thinking about? The interventricular
septum you still thinking about things like
V1 and V2 leads. Does that make sense to you?
And then as we move towards the apex of the
heart, then you start thinking about V3 and
V4, aren’t you? I am hoping that you have
a pretty good idea as to what the leads of
an EKG is going to be representing on the
heart. And if you don't, that is quite alright
because we will be paying attention to this
as move further. Acute coronary syndrome is
which you are seeing
here as a bracket. Before we get into acute
coronary syndrome, which will be a combination
of unstable angina, acute MI and I cannot
have you memorize this. It is a buildup of
atherosclerosis. Let us go back to the concept
of supply and demand. Do you remember that? Well,
supply, what then happen? The coronary arteries
underwent occlusion and there was a progressive
occlusion that was taking place that eventually
resulted in pain in the chest even, at rest
and what about before that? Well before that
it was stable angina and you keep this out
of the discussion of acute coronary syndrome.
Take a look at stable angina, who is your
patient? Coronary arterial disease, atherosclerosis
head to toe. Remember we talked about this
with cardiovascular disease including peripheral
vascular disease, cerebrovascular accident
and our topic at hand, which is coronary
arterial disease. Under stable angina, the
precordial chest pain is exacerbated by either
stress or exercise. Now, by stress, there
are a couple of ways that we can get induced
,can’t we? What does that mean? Well
your patient let us say it is 67-year-old
female and she tells you "Hey doc, I am having chest
pain when I am walking a few blocks here,
when I am walking up the stairs. When I stop,
the chest pain goes away." You do an EKG at
rest. What happens? Everything comes back
to normal. You say bye bye. Have a nice day.
No. My goodness. You want to stay in practice
right and so therefore you have to then induce
a stress test. Now if your patient has arthritis
and is debilitating, please don’t be a masochist
and put your patient on a treadmill. That
sounds very nice. Be nice to your patient.
So we will get into what is known as your
chemical stress test because that is incredibly
important. And what kind of changes which
you expect to see an EKG when you induce a
stress. We will talk about that coming up.
Now once this patient is giving you such a
history, what would you want to give that patient
automatically? You give this patient something
in which there is going to be relief from
the chest pain. Correct? What does that mean to you?
It means underneath the tongue anytime that
there's chest pain, you place nitroglycerin correct? Sublingual.
So when you place sublingual and it then dissolves
and enters your circulation, what is it going
to do your veins? Good. Vasodilate. When you
vasodilate your veins, what is that effect?
Preload or afterload please. Good. Preload.
You are going to decrease preload and so therefore
you are going to decrease demand, aren’t
you? Of the heart for oxygen exactly what
you are going for and then what about afterload?
Well, it also causes arteriolar vasodilation.
When you have arteriolar vasodilation, you are
going to decrease TPR. Let us move on. So
now with stable angina, what does this mean
to you? What kind of changes? In the very beginning,
we looked at the pathogenesis of an atherosclerotic
plaque. Do you remember that? We talked about how
there might be endothelial injury? We talked
about how there was a thrombotic event. We
also referred to your monocytes coming in
and smooth muscle cells that are being recovered
from the intima coming into the media and
all this is then forming a fibrous cap and
what happen in the middle? A necrotic core
of LDL, foam cells and such. If that atherosclerotic
plaque continues to build,
what may then happen? 90 percent occlusion.
We are moving towards to what kind of angina?
Unstable angina. What does that mean to you?
"Hey doc, I am having chest pain." When? Even
at rest. Not good. Now this comes under what?
This comes under the category of acute coronary
syndrome. Is that clear? Is this is a myocardial
infarction? Not at all. Is that clear? Are
you going to find elevated cardiac enzymes?
What's your gold standard please for cardiac
enzyme? You all should know troponin I, not C. Is
that clear. Troponin I. We are going to find
troponin I with unstable angina, yes or no?
Good. No. Is that clear? It is that crystal
clear for you to differentiate between unstable
angina a.k.a. crescendo. What are you crescendoing
towards? Crescendoing towards leaving this
planet. What does that mean? It means you
are moving towards myocardial infarction. You won't want that.
Is that clear? So another name for unstable
angina. We will never forget that. You have
a crescendo. You are moving towards the myocardial
infarction. How can you tell the difference?
In myocardial infarction obviously that gold
standard cardiac enzyme is troponin I. In
unstable angina, yes you are going to have chest
pain at rest. But this is not a myocardial
infarction and you can come from that, how?
Without finding any cardiac enzymes. Or you
are going to find changes on EKG, you could.
And it is called the non-STEMI. We will talk
about this and now,
I want to take a look at acute coronary syndrome.
Are we clear about definitions? Are we clear
about concepts? We now understand what is
going on from the beginning of the lecture
series up to where we are right now. It is all about
building up this information so that you integrate
across the board from biochemistry or physiopath
because that is what medicine is and there
was a type of question. There was type of
patients walking through the door all the
time. So symptoms at rest. Number 1 minimal exercise
perhaps. May not be relieved by nitrates because
it is really beyond the point of that type
of therapy. Classified based on ECG changes.
Now it could be STEMI or non-STEMI. If it
is non-STEMI, we will talk about that being
perhaps an ST-depression. A STEMI is ST elevation
myocardial infarction and we will get into
further detail. Not to worry at this point.
Next, the distinction is essential for management
is reperfusion therapy or not is dependent
on whether or not your patient has STEMI. Now
reperfusion is another topic that we will
have to go into further detail when the time
is right. This is all under acute coronary
syndrome. We are going to keep repeating that
so that you clearly know where we are. What is your mainstay
treatment? So you have a clot. A clot is rather
large, 90 percent perhaps. Let's do antiplatelet
therapy. Let's do anticoagulants. Let's do,
maybe the drugs are not working properly
and you have to get in their percutaneous and
you have to get in there with what is known
as angioplasty. What does angioplasty mean?
That type of intervention, percutaenous type
of intervention, angioplasty is ballooning,
isn't it? Maybe place a stent. Maybe in that cath lab,
is not able to get in there putting a stent,
which is your only step of management
at this point. Next step of management CABG,
coronary artery bypass surgery.
Let us continue. Now if it is STEMI, ST elevation
myocardial infarction, what you do? .
What does that mean to you? You have your
reperfusion type of issues that we will talk
about. That is something we have to discuss
in greater detail.
Next acute coronary syndrome, myocardial infarction.
What are the complications that you are worried
about post-MI? Number 1 complication you worry about
arrhythmias, don't you? And so therefore, you want to try to
give you patient antiarrhythmics. Now post-MI,
let it be your boards, clinically it might
be a little bit different, but remember antiarrhythmics
are quite a complicated topic, isn't it? Now
we will deal with a little bit and right now
your first introduction post-MI arrhythmia,
your best drug to give is something like your
class IB drug. B for best. In general, when you say
class I antiarrhythmic, then what channel
are you blocking, please? Sodium channel, good.
What kind of sodium channel? Voltage-gated
or ligand-gated? How important is that? Really
important from physio. It's your oltage-gated sodium
channel. Is that clear? This is something
that you will be talking about and have discussed
in pharmacology. All I am doing is reiterating
it and clearly see where to bring all this
information into play. Next beta-blockers,
perhaps. Post-MI, think about metoprolol. Anti-platelet
therapy drugs such as statins and so forth.
Also, what else am I worried about with my cardiac infarction
and as being a complication? How about congestive
heart failure? And if it is congestive heart
failure, then you do everything in your power to decrease
the mortality increase survival and those are type of drugs
which you are looking for, aren't you? So,
therefore, those include spironolactone, metoprolol.
We are also looking at drugs such as ACE inhibitors.
Now mainstay of treatment eventually is the
fact that you are trying to decrease the demand
for oxygen by the heart. You are trying to
increase the supply of oxygen continously.
Nitrates perhaps and eventually once it get
past the hurdle and the emergency has been
properly managed, then you get into lifestyle
modification. Is your patient obese? Is your
patient a smoker? Those things that you cannot
control, but you must educate your patient
with including the fact that you have familial
issues. The beautiful slide, the beautiful
little explanation, a table in which it gives
you really a storyline between stable angina
moving into myocardial infarction and we will
get into all the detail as we move through
here. Quickly walk through stable angina