Let us take a look at the management of your
patient who has stable angina, acute coronary
syndrome. Let us go back to quickly
our discussion. If it is stable, exertion,
angina, pain. If it is acute coronary
syndrome, then the plaque has gotten so big
that the pain is going to be at rest. Myocardial
infarction, acute, we've walked through in great detail
in our previous lectures. What is the two
immediate goals? Let us go back to the physiology
that we talked about where we are addressing
the demand and we are addressing the supply.
What do you want to do? If you know that your
heart is compromised due to whatever reason,
in this case the atherosclerosis, then would
that make sense to try to decrease the demand
of the heart. So, therefore, what kind of
receptor does the heart have in which its
activity is pretty much controlled or influenced?
Beta-1 receptor. When I try to control the
beta receptors, why not administer some calcium
channel blockers? Those are the thing that you
pay attention, now be careful though because
if you administer too much or if you have
your patient going into massive MI, then the
heart has no chance of recovering, you’re
going to kill your patient so be careful when
you are giving such drugs. Or what about the
supply? We know that the supply has already
been compromised when I try to get in there
and try to remove that clot and by doing so,
aren’t you addressing both goals?
By decreasing myocardial oxygen demand, we
have beta-blockers, slows down the heart
rate. Remember the two major factors or components
or constituents of your work of the heart
demand depended on heart rate and the ability
to pump. The heart rate when I try to give
a beta-blocker decrease heart rate. Nitrates
what they do? Well, we talked about how you could
have vascular resistance, which has increased,
which it does because of sympathetic activity
and so, therefore, nitrates might cause vasodilation.
Now you tell me, be careful,
how do you decrease your afterload? It is about
working on the arteries, arterial side or
is about working on the venous side? And you
will tell me correctly working on the arterial
side. Good. By doing that, you are then relieving
some of the resistance, aren’t you? And what
about morphine? It decreases the pain and
produce the adrenergic drive with morphine.
What about the supply? Let us give oxygen.
I have to give oxygen. What about that clot?
It is already too big, so when I try to get in there,
get rid of it. You've bust that clot. You call
this as a blood thinner and how important is that concept, vary
in hemodynamics, all the different ways in
which you can bust that clot. Aspirin or aspirin
alternatives including clopidogrel or "Plavix".
A clopidogrel enables your ADP and if your
ADP is not released from your platelet, then
you can't express what? Remember this from pharmacology,
pay attention, you can't express your glycoprotein IIb, IIIa.
You do not have that, you do not have
proper aggregation, do you? Or else might you
want to use something like cilostazol and
a couple of others as well. IV heparin, anticoagulant,
prevents thrombus formation. At some point,
let us say that you want to use a blood thinner
in which you try to bust that clotting and you have coags
or coagulation factors, important options
here including heparin. Heparin works to antithrombin
III as you should know and antithrombin III
is going to do exactly that, knock out thrombin.
Or you have direct thrombin inhibitors, don't
you? And this then brings you to important
topics in drugs such as dabigatran, direct
thrombin inhibitor or apixaban. We have got
a couple of these that you want to pay attention
to. Why? Because you want to try to increase
the supply of oxygen to your dying heart so
that you can then shift over into aerobic
glycolysis and proper ATP production.
Continuing our discussion, nitrates. Now rapid
reperfusion could be an issue. You want to
be careful here. Pay attention. So you had
this clot. How could this clot develop? A
clot was developing and over years and years
and years, and at some point in time, the tissue
distally, so if this is my clot and my tissue distally
became accustomed to that decreased perfusion,
didn't it? And then all of a sudden that clot
became so big and you are going to go in
there and use something like a plasminogen
analog, some type of plasminogen activator
and you gave a tissue plasminogen activator
such as alteplase or what have you, and you bust that clot. My
goodness, gracious. Water is good for you.
But you are doing kind of a fire hydrant, it will
kill you. Now that tissue distal to the stenosis,
drinking all this oxygen all of a sudden, oh!
My goodness, this excess oxygen that has been
introduced into the tissue, you think there
may be perhaps some of their oxygen might
lose electron and become a free radical? Exactly.
What's that called? Reactive oxygen species.
Welcome to rapid reperfusion, but we're specific
referring to reperfusion injury. And
calcium play a huge role. We will talk about
that. All this is to come while you are trying
to do that. You are trying to induce rapid
reperfusion. Here are some of your drugs such
as your thrombolytics, your tPAs and also you try to
go in there and say that the drugs aren’t
working well enough or you want to go in there
and really make sure that you prevent further
thrombi formation and so, therefore, you will
think about using percutaneous intervention
and you either have angioplasty in which you will
try to balloon in and while you're in there, you'll try to place
a stent as well. Worst case scenario, you can't go in
and place a stent, then you have to do bypass surgery.
Using thrombolytics, there is some absolute
relative type of contraindications, but keep
in mind, before we move on here, if your patient
is already in a state of bleeding why would
you want to use a thrombolytic? That is just going
to exacerbate the issue. It might actually
kill your patient. Who are my patients? Hemorrhagic
strokes, non-hemorrhagic stroke past three
months, intracranial neoplasia, active internal
bleeding, aortic dissection, closed head or
facial trauma, once again for three months.
Now take a look at some of these. If the patient
is already at risk for severe bleeding, by
adding a thrombolytic, these are absolute
contraindications for then using a thrombolytic
now. This is absolute for any licensing exam.
In clinical practice, you might always
find that attending who might be extremely
confident in his or her ability to still give
a thrombolytic in such situations, but that
is not being asked here nor is it going to
be asked on your boards. Relative, severe
hypertension, proliferative diabetic retinopathy,
what does that mean to you? You are thinking
about the eye and when undergoes proliferation,
you want to be careful though because what
might you do? By thrombolytic, you might then
cause bleeding take place. Known bleeding
diathesis, for example von Willebrand disease,
prolonged CPR, allergic reactions, pregnancy,
blood pressure, ulcers be careful there,
please. Very careful actually, for example,
when you use a thrombolytic at some point
with that ulcer, there might be so much bleeding
that you might actually bring about perforations.
So please be careful when using such drugs.
Contraindication for thrombolytics, absolute
versus relative. Now, management continues.
All patients with AMI should undergo intensive
treatment for modifiable risk factors. What were they again?
Aspirin, ACE, beta-blockers, secondary prevention. So
you want to continue taking baby aspirin,
ACE inhibitors always a good thing, beta-blockers
all these are then for secondary prevention.
Treatment of hyperlipidemia, statins. I had
another drug in there for you that is very
relevant. That's your, once again proprotein convertase
subtilisin kexin 9 inhibitor, and those of
some of your monoclonal antibodies, we have
referred to that earlier known as alirocumab
or your evolocumab, locumab is their suffix
you pay attention to please. diabetic control,
smoking, and diet and exercise. If you are
able to do this and if you are able to educate
your patient properly where you are exercising
prevention is not the best medicine.
Mechanical complications that we are worried
about. Weakened infarcted cardiac tissue.
the timeline that we walked through with myocardial
infarction and at some point with that scar
formation, it might become weak and may result
in a ventricle aneurysm or rupture. Oh my
goodness we have either septal or wall rupture
may result in papillary muscle might have
a new type of murmur that has been introduced.
A mitral valve regurg or if you had a septal
rupture, it kind behaves like a VSD. What
kind of murmurs are these please? Close your
eyes. You got theses. Systolic murmurs that
are being introduced newly. If it is a wall
rupture, you're worried about death from what? Sudden
accumulation of blood within your pericardial
cavity and say that you have tachycardia and
have hypertension, you have what is known
as kussmaul sign mean to say positive JVD
and you have muffled heart sounds. Worried about
pericardial tamponade, don't you? What is your
next step in management? My goodness gracious
get in there, do a pericardiocentesis and get
that fluid out. Mechanical complications require
emergency type of surgical issues. Papillary
muscle rupture can present with acute hypotension,
acute pulmonary edema. Understand that everything
is being backed up. Here is our mitral valve.
Are you with me? And you have regurg back into where?
Left atrium. Back into where? Pulmonary veins.
Pulmonary edema acutely, new systolic murmur.
Chronically what kind of issues are you worried
about? Conduction system big time and if that
is the case my goodness gracious you plant
a pacemaker, arrhythmias due to scar formation.
That's what we'd talk about over and over again and
major complication that you are worried about
resulting in sudden death is the fact that
you are messing up the conduction chronically.
Mechanical failure, your left systole or should
I say your left ventricle is dying. So, therefore,
the systolic function on the left side is
also not working. And so therefore, now I
want you to pay attention to this statement,
there is a lot of clinical importance for
this particular stanza. When I walk you through
this, if your heart dies on the left side
and that is which you focus upon here, please.
If the heart dies on the left side, it cannot
pump forward. What is the active process of
your heart phase? Systolic. What kind of dysfunction
would you call this if the left ventricle
is not functioning properly? A systole dysfunction,
stop there. If I can pump my blood forward
into the aorta, where is all my blood? In the
left ventricle. It is stuck in the left ventricle.
How are you going to measure this? On the
left side, a central venous pressure or you
are going to use a PCWP, a pulmonary capillary wedge
pressure. You are correctly telling me PCWP,
pulmonary capillary wedge pressure. Where
is my blood? In the left ventricle. Why? It
is not moving forward. Are you seeing this?
Close your eyes and conceptualize, the only
way that you get all the questions right.
There is my blood lying in my left ventricle,
increased preload and your PCWP is increased, correct?
Yes. Now the mitral valve wants to open, the
blood wants to rush into the left ventricle.
But the problem is there is blood still remaining
there residually from the previous systolic
dysfunction. So could that systolic dysfunction
then give rise to a diastolic dysfunction? Yes, it can.
What does that mean to you? Pay attention here. What
kind of heart sounds are you going to find
here? If it is a systolic dysfunction, what
does that mean? The blood is not moving forward.
So, therefore, my left ventricle could be
rather large and it could result in what kind
of heart sound? An S3. We talked about that
earlier, an S3 gallop, what is happening?
It is the fact that because of the systolic
dysfunction, you have a large left ventricle,
as soon as a mitral valve opens, it create
an S3, stop there. Well what if the blood starts accumulating
in your left ventricle? Right.
So now that's a diastolic dysfunction because
you cannot properly fill up the left ventricle
and that blood now that is rushing from your left
atrium, are you seeing this? That blood that
is rushing from the left atrium through the
mitral valve, into the left ventrical,
hitting the blood in your left
ventricle, is going to create a what? A fourth
heart sound. What does a fourth heart sound
mean to you? You have heard of this as
being hitting a stiff left ventricle. But
with all that blood in there, it might as
well be stiff. If you haven’t understood
that, please make sure that you go back and
review what I just told you with that particular
statement. Do you understand how much clinical
relevance there is with each one of these statements?
Some more than others, especially when it comes
to pathology. Continue. Insufficient or significant
damage myocardium, it cannot do what? It cannot
maintain the proper heart function.