Let us take a look at the two parameters of
dysfunction in further detail. In systolic
dysfunction, it is the fact that well the
heart is not pumping. Now with that said, there
is the all important graph in physio that
explains the pathology beautifully. Along
with this, well, you want to start thinking about
what kind of pharmacologic agents you want
to plug in here. So, with this graft that
you seen in every single medical text book,
clinicians and professors of all type have
been discussing this matter for years. Let
us put all this together so that you have
a firm understanding as to how this graph
operates. Well before we do any of this, take
a broadside view of the cardiovascular system.
It is the only way that any of this graft
will make any sense to you and not sitting
there just memorizing like you would perhaps
with physics because that is not what medicine
is. Yes sure you can incorporate it but ultimately
it is what is going on in the body. So three-dimensionally,
broadside view of the heart, is a continuous
circuit, isn't it? A continuous circuit, what does that
mean? From the left ventricle, blood is being
ejected out, but it is completely dependent
on the amount of blood that is returning to
the heart, isn't it? So, therefore, the venous
return to the heart, let it be from the pulmonary
veins for the left side or the superior vena
cava and the IVC for the right side, is then
going to equal the amount of blood that is
being ejected out and that then gives you
your steady state, doesn't it? How in the
world could you possibly have an increase
in ejection of the blood of cardiac output
if you don't have enough blood that is returning
to the heart? How is that even possible? It
is not. So, therefore, the fact that you are
looking at the cardiovascular system as being
a circuit, in which everything is just a perfect
circle of flow return is our
graph. You will see exactly what I am referring
to as we dissect this graph in great detail.
First and foremost, on the X-axis, remember
any graph that you get in pathology, in physiology
what have you to do? You have to dissect and
take a look at the parameters. The X-axis
represents what? Atrial pressure. In other
words, this will be volume. Whereas the Y-axis
here would represent two different things.
It would represent the cardiac output. Number 2, represent
the venous return. It has to. Remember I told
you what blood comes into the heart is equal
to the blood that is ejected from the heart.
How do you increase venous return? Simple
question, how do you increase venous return?
By getting more blood out. So the more that
you increase the cardiac output, the more
that you increase venous return. Do you see that
now as being an objective, as being a bird’s
eye view as to what is going on in the circuit?
Let's dived into this further so that you will.
Next, the three questions that you want to
ask yourself with this graph or the three
parameters that you truly want to get a firm
handle of from physio is performance is equal
to changes in cardiac output or contractility
and you have your volume. Is that clear?
Where does performance come in on this graph?
It is the Y-axis. You keep it separate from
contractility, please. What do I even mean?
I want you to take a look at that cardiac
output curve versus normal. You see that.
Well, that cardiac output versus normal. Anywhere
that you would be on that particular curve,
answer this question for me, are you changing
contractility if you move to the top of that
curve by the plateau perhaps or down at the
bottom? Are you changing contractility? No.
As long as you are on that curve and only
on that curve without shifting of that curve,
then contractility remains exactly the same.
Is that understood? If it hasn't, then make
sure that you understand it now. Does that
curve where it represents cardiac output is
that venous return? Not at all. It is strictly
cardiac output. It is strictly contractility.
Now, performance. As we go up and down that
curve, contractility remains the same, but
then what changes? Performance, interesting.
Remember that from physio. So performance
will change as it moves up and down, but contractility
remains the same. So what is the other parameter
that you need to add in here so that all of
this makes further sense. It is your vascular
function curve. It is your venous return.
Isn't it? So your vascular function curve
would be represented by what you are seeing
here as an intersection point. So where is
this normal that your vascular function curve
and that represents the venous return. And
your cardiac output is only equal to the amount
of blood that is returning to the heart and
that gives you approximately a pressure of
2 mmHg. And that is normal, isn't it? Think
about that for a second. In your atria, aren't
you supposed to have low, low pressures? Of
course, you are. And even if it rises to 2, that
means that is high enough pressure where it
is allowing for cardiac output to continue.
So that is perfect at steady state.
So now I want you to take a look at vector A.
Vector A represents what? It causes a decrease
in your Y-axis. So what are the three things
that we were looking at? Performance, contractility,
and volume. Performance equals contractility
and volume. So, now, vector A shows a decrease.
A downward movement on your Y-axis, what happen
to performance? It decreased. How do the performance
decrease? Was it due to volume? I am sorry.
Where was the volume on this graph?
It was the X-axis and as we move from
left to right, what happens to volume? It
increased. If you increase volume, how
in the world is I am going to decrease performance?
What do you mean? Take a look at vector A
then look at me yet. Everyone is smart perhaps,
but vector A represents a decrease in performance,
but that is not due to an increase in volume.
That doesn't make any sense because you know
if you increase the volume, you should increase
the stretch. If you increase the length, then
you might increase the tension. Welcome to
Mr. Frank Starling relationship. So what then
cause a decrease in performance please, in
vector A? Was there a shift in that contractility
curve? Yes, there was. What kind of shift?
A clockwise shift. Isn't that how they have
described it? A clockwise shift. A negative
inotropic effect. What causes this? Maybe
myocardial infarction. And myocardial infarction
has what type of effect on your heart? A negative
inotropic effect. Is that clear? So a decrease
in performance due to decreased contractility.
Stop there for a second. Now look at me because
we are going to predict a few things before
you take a look at the graph. If your heart
starts failing and it does not want to move
forward, it doesn't want to eject the blood forward,
what kind of dysfunction is this? What is
the category? What is the topic? A systolic
dysfunction, isn't it? It is a systolic dysfunction
because it doesn't want to move forward. The
blood doesn't. It can't because it lost the
ability to contract. So now what do you do?
What happens? There is increased amount of
blood in your heart, isn't there? There is
an increased amount of blood in your heart
and when there is an increased amount of blood,
what then happens to the pressures? It increases
doesn't it? When there is increase in amount
of blood and there is increase in pressure
and it does not want to leave, then what happens
to venous return? The blood is stuck in the
heart. How could you possibly have more venous
return? You don't. You have a decrease in
Let us take a look at the three changes that
are taking place with vector A. Number 1, a decrease
in performance due to decrease contractility.
How can you confirm that? An actual shift
of the cardiac output curve. Number 2, there is
more blood left in the heart. How can you
confirm that? The pressure in the heart should
increase. Take a look at the X-axis moved
from 2 and in which direction are you moving?
From 2mmHg, you move to the right. That is
number 2. You have increased the pressure. And what's
number 3? Venous return. Think about this. More blood
is left in the heart. So what happens to venous
return? It decreases. Where is venous return?
On this graph, on the Y-axis and if you take
a look at vector A and you move down what
happens to venous return? It decreased. You
see that. Good. What are we referring to here?
A systolic type of dysfunction.
Now we are going to skip over into compensation
a little bit and where is my actual fluid?
"What do you mean Dr. Raj?" I mean to say that
if you have congestive heart failure and you
have left-sided heart failure where might
my fluid be? You have heard of edema, have
you not? Increased hydrostatic pressure, pulmonary
edema and we will talk about signs and symptoms.
What if there is right-sided heart failure?
Then what are you looking for? Once again
edema. Where am I? Positive JVD and then what
might you have done in the lower extremity?
Pitting edema. Transudate.
What is my point? The point is this, it is
the fact that when you have a negative inotropic effect
and that fluid is being shifted out,
then how the kidneys are going to respond?
If the fluid is moving out into the interstitium,
there is less effective circulatory volume,
isn't it? So when there is less effective
circulatory volume heading through towards efferent
arteriole, what is going to be released from
juxtaglomerular apparatus? It is called renin.
And then we have the RAAS system, which is
going to kick in and here comes mild aldosterone.
Why? This is the compensation we are paying
attention to. Not the neural reflex, this
is congestive heart failure. The neural reflex
is at this point for all intentented purpose,
it is null and void. So we get into aldosterone
system. How could you confirm that? I will
just show you the patient conceptually. So
with this aldosterone, what is it trying to
do? It is trying to restore some of that contractility.
Let us ask the same questions again with aldosterone.
With aldosterone, where are we working? Working
in the collecting duct. What is the name of
that cell? It is the principle cell. What
is it doing? It is stimulating sodium-potassium pump
or maybe ENaC. Are you picturing that? In
the collecting duct of your nephron, way distally
in nephron, where are the principle cell? On the
basolateral membrane with sodium-potassium
pump. It will stimulate it so that we absorb
sodium. On the luminal membrane or the apical
membrane, it stimulates ENaC or epithelial
sodium channel on the hopes of doing what?
Reabsorbing your sodium. Is that what the aldosterone
does? Of course, it does. It reabsorbs the
sodium. In addition, what are you going to
do with volume? You are going to retain it,
aren't you? Then you have it. Now you have
your volume that is increased. When you increase
your volume, then now what will happen?
Take a look at vector B. So now with vector
B, we have an upward swing, we have an upward
movement of your Y-axis. So what happen to
performance? Increased, because it is the Y-axis.
Performance increased, why? Was an increase
in contractility? My goodness gracious. Take
a look at that curve from vector A. As you
go from vector A and where we just move down
to a negative inotropic curve and we have
moved up through vector B, have we changed
or shifted your cardiac output curve? No, you
haven't. So contractility remains the same.
If you want to confirm that, go back and take
a look at physio. This must be understood.
So what in the world increase the performance
in vector B? It is the fact that you increase
the volume. How can you confirm that? Take
a look at the X-axis. Vector B, you moved
further to the right. You increase the volume
thus you increase the performance. How can
you confirm that further? Once again in physiology.
Isn't this amazing that you were able to integrate
all this now, in the setting of systolic dysfunction?
With all of this when we have an actual change,
X intercept. When you have an actual change
physically of the X intercept, then you know
that you have an increase in volume because
you shifted to the right. Thus in the process
in this patient with what is known as compensatory
congestive heart failure. We do have restoration
for this time being of some of this performance.
But the contractility is still pretty much,
overall contractility compared to normal?
Decreased. What do you want to do now at this
point? This patient has come in, maybe we
starting thinking about giving? Drugs. What
kind of drugs? Well, you want to try to give
those drugs in which it decrease in mortality,
it inhibits remodeling and that would be your
point. So later on, at some point, we will
do a little bit of pharmacology. We will take
a look at those drugs depending as to what
are they going to ask you? Maybe they will
ask you well what kind of drug will increase
inotropy and you will correctly say digoxin.
What kind of drug was going to take care of
your preload because of pulmonary edema? Isn't
that a symptom that you want to take care
of? My goodness. My patient cannot breathe
properly, especially at night, wakes up and
says "Doc, I have to run to the window, open
up the window, gasping for air." So you want
to take care of some of the pulmonary
edema, one are our diuretic such as furosemide.
Or maybe perhaps you want to decrease mortality,
increase survival. Welcome to metoprolol,
beta-blockers? Be very careful and the reason
I say that is because if you have decompensated
type of congestive heart failure, you might
kill your patient. So strict supervision is
Let us take a look at diastolic dysfunction.
Now there is a lot there with systolic dysfunction.