Now with dynamic auscultation, things that
you want to pay attention to. Altering heart
sounds by changing circulatory hemodynamics.
We will be spending time with this. You have
heard hard grip. You have heard of watch
this, I am going to disappear for one second.
What did I do? Rapid squat right. So these
are some of the changes or these are some
of the manuevers that we will be conducting
or you will be asked about and depending on
the manuever how is that going to affect or
influence the heart valves and heart sounds,
is that clear? Now this can be separate, but
clinical, we are going to use some of these
depending on what you are trying to confirm
for diagnosis. And once you understand the
physiologic alteration, then you've got your
diagnosis. Let us continue.
Before we even get there though, let us make sure
that we understand the difference between
preload and afterload please. How do you increase
your venous return? We will talk about this
manouveres coming up. But if you were to increase
your venous return to right atrium, to right
ventricle, what have you done to preload? You
have increased your preload. What does preload
mean to you? Preload means that it is the amount
of fluid volume within the heart. So if you
increase the venous return for example, if
you are to constrict the veins, are you
picturing this, not the arteries but the veins,
the veins are a major pooling area. If you
constrict the veins, you are increasing venous
return to the right side. What are you doing
to the preload? You are increasing it. It
is that simple. Preload is the volume of blood
in the ventricle. What if you decrease the
venous return? If you decrease the venous
return, volume of blood into right atrium,
right ventricle such as standing up. If you
go from supine position to standing up, then
where is my blood? In the dependent areas.
It is down in the lower extremity. What happens
to venous return? It decrease, didn't it? So you
have decreased preload. Now, what is definition
of afterload that you want to know here? Because
this is important. Afterload is when you have
increased resistances that the left ventricle
was facing. The left ventricle, when it faces
increased resistance. Give me some examples.
Aortic stenosis, coarctation of aotra and
tell me about the arterials. Take your time. What state are
the arterials in, in which it would then provide
increased resistance to the left ventricle?
Did you listen to my question? What state
is my arterials in providing increased resistance
to your left ventricle? Constriction. Arterials
are the most important component or contributor
to resistance as you know especially TPR,
total peripheral resistance. If you can split
your arterial, what happens with TPR? Increase
your TPR. What then happens to afterload?
You increase the afterload. Are you seeing
this? So afterload is that simple. It is
the resistance that the left ventricle is
facing period. And I just gave you bunch of differentials.
What are they again? Aortic stenosis, coarctation
of aorta and arteriolar vasoconstriction. Continue
Now let us talk about those actual manuvers and
we will go through the pathophysio. Deep
inspiration, so what does that mean to you?
Let's all take a deep breath. You're with me? Good. But then just
happened the diaphragm contracted, which way
did it go? Downwards. What happened to abdominal
pressure? Increased upon deep inspiration.
What happened to the thoracic pressure? It
decreased. It literally became a vaccum. It
is going to suck up like a straw. It is going
to suck up the blood into the heart. What
is my topic? Increased venous return upon
deep inspiration, is that clear? When you
have deep inspiration, increased venous return
to the right side, what then may happen to
the intensity of the murmurs on the right
side? It would obviously increase. Clear? Next. Supine
position versus standing up. If you are supine,
which I hope that you are not in right now
because if you were, there is every possibiity
that you are falling asleep. Supine position
would be lying flat. So, therefore, you are
making it easier or more difficult for blood
to return to the heart? You are making it
easier. And that is our topic increased venous
return, supine position. What if you went
from supine to erect position? The blood then
drops where? Down to the legs. So decreased in venous
return, it is that simple. Passive leg elevation.
You pay attention to the same thing here.
You are going to raise your legs and when
you do so then what happens? You are going
to then return the blood to the right side, clear?
Increased venous return. Rapid squatting,
now this is important. There are two major issues
that you want to pay attention with squatting,
please. Here you gonna do this quickly, okay? Let's just
think of me just rapidly squatting. When I
did so, then it increased the venous return. Here
comes more blood. That is one example here
that you may want to think about clinically.
Now, what about if this was a child. What
do children like to do? They like to
play. They like to go run. "Hey mummy, can I go play?"
"Of course you can." Right? Of course the child wants to play.
Then all of a sudden the child is playing and cannot breathe
or having a hard time breathing, and the child
really instinctively is going to do what? Squats.
What is the diagnosis in this patient in which
after playing for little bit, the child instinctively
knows to squat? It is called the tet spell.
What is happening there? What I am going to
do for you here is make sure that we delineate
the two different type of squatting maneuvers
and depending as to what you are trying to
confirm is going to give you different types
of diagnosis. If it is rapid squatting,
yes, it does bring about
increased venous return but tell me about
the patient, the child who just squatted,
when the child is feeling a little cyanotic
with a little hypoxemia, it is the fact that
there might have been what? There might have been pulmonic stenosis,
number 1. Number 2, there might have been right ventricular
hypertrophy. Number 3, there was what? Ventricular septal
defect. Number 4, there was overriding aorta. What
am I referring to? Obviously tetralogy of
Fallot. Tetra, four. What kind of shunt is
this? It is a congenital cyanotic heart disease,
a right to left shunt, right from the beginning. Because
the right ventricular hypertrophy is then
shifting. What kind of blood is in the right
ventricle? Tell me. Good, deoxygenated. And
that right ventricular hypertrophy is pushing
the blood through the VSD into left side.
What kind of shunt? Right to left shunt. So
what do we have? Cyanosis? Who is feeling
it? The child is. What is the child doing
instinctively? Squatting. To do what? Not to
increase venous return. So why is the child
squatting? To increase TPR. How do you do
that? You increase TPR by constricting arterials.
I just got then telling you what happens when
you increase TPR? You increase afterload.
When you increase afterload, who is facing
increased resistance? The left ventricle. And
so therefore what happens to the shunt? It
gets reversed, instead of right to left shunt
that type of squatting with tetralogy of Fallot
will then turn into a right to left shunt. Is
this the only time we will see it? Not at
all. Talked about this in embryology. We will
talk about this further as we are getting
to congenital heart disease. Why am I bringing
this up? Because you must be very clear about
the issues of squatting.
Let us talk about valsalva. I have closed
my epiglottis phase II, and that's you pay attention
to. So when you are expiring against a closed
epiglottis, what happens to thoracic pressure?
You have increased your thoracic pressure.
Initially in phase I, what
did you do to your pulmonary capillaries?
You close your pulmonary capillaries. Would you
tell me as to what is distal to the pulmonary capillaries?
I believe it is the left atrium. Correct. And
by quickly closing pulmonary capillaries,
you increase venous return to left side, but
that is not the point. The point here is during
phase II. If you continue to squeeze your
pulmonary capillaries, there isn't any more
blood in there. Look, there is no more blood
in there. So what will happen to venous return?
It decreases. Are you with me? If you continue
to squeeze because of that increased expiration
against a closed epiglottis, then at some
point you are going to decrease venous return
and that you must pay attention to because
that becomes important to us as we get into
valvular diseases and at that point I
will repeat this very point. Well, let us go from
supine position to standing up. So you stand
or sitting up quickly, then what then happens?
The blood then rushes down into your legs. What
happens to venous return ladies and gentleman?
It is going to decrease. There is your blood down
in the feet. It is not in your heart. You
take me one step further. What did you learn
in physiology already? You've heard about baroreceptor
reflex. Where are they located in, these baroreceptors?
They are located in your sinuses, aren't they? Which one
is more sensitive? The carotid aortic sinus.
The carotid sinus because that is not accustomed
to large amounts of blood like the aorta is.
The aorta is accustomed to large amounts of
blood. It is not as sensitive. The carotid
has glossopharyngeal. The blood has then gone where?
Down into legs. Then what happens? Stretch,
decreased stretch. When you have decreased stretch, what happens
to pharynx? Decreased pharynx. My blood is then rushed
down into legs. What kind of outflow do you want
from the autonomic nervous system please? Sympathetic,
it is exactly what is happening. It is called
the baroreceptor reflex. You're going to be asked
about this, guaranteed you will, in many places.
Now let us take a look at these other maneuvers
that then will help you diagnose your patient.
I want you to take your hand and I want you to
clench your fist and I want you to come at
me right now. Because "Dr. Raj, you're driving me
crazy. You are frustrating me. You are giving
me all this information. I just want to hit
you." Okay, so you clench your fist. You with me? So is that your
sympethetic system? Of course, it is. When
you do a hand grip, a sympethetic nervous system
because you are angry. Calm down, it's okay. If you have
a stress probably good time to grab. So here you are, you are
squeezing it. And what have you done to your arterials?
You have constricted it. What have you done
to your TPR? You have increased it. Once again when
you increase your TPR, what have your done?
Are you affecting your afterload? Yes, you
are. Then what have you done to your after load?
You have increased it. Why is it important?
You shall see and I will keep coming back
to this point where you have understood, by
increasing that afterload, then where is my
blood? In the left ventricle. It is having
a hard time getting out of the left ventricle
and you shall see and you will understand
why an aortic stenosis? When you do a handgrip,
what happens intensly as a murmur? Decrease.
Don't worry, we will talk about it again.
What about exercise? Well exercise, once again,
you've talk about this in physiology, what is it going
to do to your arterials? It was my question.
What is it going to do to your arterials?
Vasodilate, it has to. Why in the world would
you want to increase your TPR and exercise?
That makes no sense. You want to make sure
that you have vasodilations so that you properly
oxygenate your tissues. Clear? In the meantime, what
is happening to your veins in exercise? Venoconstriction.
The combination of the two. Well, what do you know about
cardiac output? You might go from 5 liters.
You might have increased by 100 percent to
10 liters. That is amazing in exercise, but
what about blood pressure. It doesn't change
much, why? Because the vasodilation and venoconstriction.
And so, therefore, the combination of the
two will keep your mean arterial pressure approximately
normal. Is that clear? It is amazing. Exercise
is a beautiful phenomenon and the more that you
know about it the more number of questions
that you will get right. In this case here,
increased flow across your valves.