00:01
The patient with
pain here would be once again substernal,
may be pressure sensation. That is how they
would describe it if they were to feel the
pain. Why do we say if? Because can you have
a patient who has a silent MI? Of course,
what may happen then? Well how did that occur?
It is the fact that the nerves has been shot,
maybe there was diabetes mellitus resulting
in diabetic neuropathy. And so at that point,
the nerves are not able to properly feel the
pain and that is very scary and you know for
a fact the patient with diabetes has what?
Increased VLDL, which contains triglyceride
and this may then accumulate in your blood
vessels. The pain, how long does it last? Approximately
20 minutes to hours, but it is not a fleeting
pain. Versus what? Versus your anginas. Remember
in exertional. It was exactly that exertional,
stable. Unstable, maybe about 30 minutes, even
at rest. But eventually, remember that is
not an MI. This is, so we will find cardiac
enzymes. It radiates to the neck, jaw and arm
and associated with diaphoresis, right.
01:12
Physical examination, your sympathetic activity
has kicked in once again. If your heart is
beginning to die, it decreases your cardiac
output because it's refers to as being what?
Cardiogenic shock. If it is a cardiogenic
shock, then what branch of the autonomic nervous
system is going to be stimulated? The sympathetic
nervous system. If it is the sympathetic nervous
system, it is doing everything in its power
to restore heart function, isn't it? It may
then function on your beta-1 receptors excessively
resulting in tachycardia. Now if there is
enough damage taking place with the heart,
at some point, the left ventricle becomes
large. Pay attention here, please. So now,
the left ventricle becomes enlarged, association
with CHF, congestive heart failure from AMI,
acute myocardial infarction. Whenever there
is congestive heart failure, I want you to
think about the heart sounds that we will
discuss. And when we do in great detail, then
you know that S1 is the closure of what? Mitral
and tricuspid in that order. S2 is the closure
of what? Closure of aortic, pulmonic in that
order. And when does your aortic valve close?
I want you to pay attention to aortic valve
right now, specifically. It closes doing diastole,
doesn't it? Yes, it does. If it closes during
diastole, then what then opens? Mitral valve.
Are you with me? If you don't, make sure that
your physio is strong here. See the only way
that you are able to properly understand this
and this information will never leave you
because it is a permanent part of your heart
and brain and soul. So now the mitral valve
opens and this left ventricle is rather large
and I will say this blood is rushing into
the left ventricle, are you here? Stay with
me. The blood is rushing into the left ventricle.
Are you going to create a heart sound? Of
course, you are. What is this called? S3 gallop.
You’re with me? And that's why S3 comes after
S2. S2 is a diastolic type of heart sound
because that is the only time that you have
aortic, pulmonic valve closure. Subsequently
thereafter, the mitral valve is then going
to open during diastole and if you have a
large ventricle, you are going to create an
S3. Pulmonary rales may be present, why is
that? While let us go backwards, mean to
say that earlier we just talked about
S3 and if the heart is not able to move forward
because of acute myocardial infarction, then
perhaps there might be congestion. If there's
congestion is taking place from the left ventricle,
then you are going to back up into where?
Good, left atrium. After that what are you
going to back up into? The pulmonary veins.
03:58
And then where are we going to back up into? Increased
hydrostatic pressure in the pulmonary capillaries
may result in pulmonary rales. A new systolic
murmur due to papillary muscle rupture, is
that a complication that could occur? Of course.
Worse case scenario, what if there is a ventricular
septal rupture? May result in something like
a VSD perhaps and when you have that type of
rupture, my goodness, you are worried about
things like cardiac tamponade especially if
it is a ventricular wall rupture. So that
rupture be careful, please. This is ventricular
septum and here we are looking at physical
findings of new systolic murmurs. You should
know already that VSD is the systolic murmur.
On EKG. Now here let put things together I have
repeated this. I have introduced this already
to you. Let's just make sure that we are
clear about what kind of EKG changes you are
expected to see, please focus upon transmural
MI. We have a peaked, a hyperacute T-wave. Next,
ST elevation. That by far is the most important
point. The ST elevation is found with transmural.
Once again you tell me what kind of coronary
blood vessel, an artery or an arteriole? You
answer that question. Artery, right. And if
you have that picture anatomically once again
you will remember that as soon as the artery
has been occluded, there is complete draping
of infarction over the entire transmural tissue.
05:31
There is something called Q-waves and I am
not going to focus upon that so much, but it
if the fact that normally the Q-wave, at least,
tell me this. What is a Q-wave? Is it a negative
or positive deflection? It is a negative deflection.
It is the first negative deflection that you
would find in normal EKG. If you find that
Q-wave to be exaggerated in terms of its negativity,
that is referred to as being your Q-wave. Just
keep that in mind. It doesn't mean that it
is absent. It just means that it might be
exaggerated especially if it is a chronic
type of MI. Let us continue. ST segment elevation
is the classic infarction pattern and this
is what you have to pay attention to. If
it is greater than 1mm, which is one box,
remember dissecting an EKG and what a box
means to you? So that one box whether 1 mm
in 2 or more contiguous leads, by definition
an ST elevation. What about an EKG and its
T-wave? Now it could be peaked or it could
be inverted. The development of new Q-waves
then indicates a transmural MI. What that
means is that they are usually part of late
finding in AMI. Your focus right now, should
be on ST elevation. Once you have understood
that and if you have got that firmly embedded,
then you move on to take a look at these other
waves that are relevant when dealing with acute
myocardial infarction, transmural type. MI
here new conduction system abnormalities and
that we have already known. Whenever there
is a myocardial infarction, my goodness you
are now compromising the conduction systems.
07:09
So, therefore, you are introducing what? New
types of arrhythmia. There might be a new
left bundle-branch block and how do you know
that on your example? What would they give
you? A left bundle-branch block. Now close your
eyes and think of the following. We have bundle
branches. So you have just moved from your
AV node through the bundle of His and you
are moving through your interventricular septum,
are you not? Are you there? Good. Now you
have a left bundle branch and a right bundle
branch normally. Now you tell me what is it
that permits the aortic valve to close? Don't
you need a depolarization event? And so, therefore,
the left bundle branch is going to depolarize
first, always physiologically, so that the aortic
valve closes and then followed by the right
bundle branch and the pulmonic valve. Is that
clear? We have A2, P2, collectively
what heart sound please? The second heart
sound, good. Now, what if there is a left bundle-branch
block, what happens? It means that you have
decreased conduction through the left bundle
branch, yes. So does that mean that you have
conduction passing the right bundle branch?
That is exactly right. So that results in
what kind of split? Paradoxical split, excellent
okay. EKG changes maybe there is a left bundle-branch
block resulting in a paradoxical split of
your second heart sound.