Cardiac Output

Cardiac Output


Hello everybody. Once again, welcome. We are going to discuss another important physiological concept which is cardiac
output. So what is actually cardiac output? And what is it’s important? It
measures the ability of the heart to pump enough blood to the different
organs. How do we measure the cardiac output? So it is the volume of blood
ejected from each ventricle per minute. Remember, because we are going to use
another parameter which is going to be per beat and not per minute . How do we
calculate the cardiac output? We multiply what we call stroke volume — we’re going
to learn about this in a minute — by the heart rate. We put in some numbers here
and we come out with around 5 liters per minute. So this should be the normal
cardiac output, around 5 liters per minute. So we’re going to look at stroke
volume alone. We’re going to look at heart rate alone and see how these will
determine the cardiac output. So what is stroke volume? It is the volume of blood
ejected from each ventricle per beat. Every time the heart beats it’s going to
eject some volume of blood. So let’s look here. We are looking at
diastole and remember diastole is when the ventricles are relaxed and filling
with blood. So when we look here the ventricles will start to fill and when
they are absolutely filled with blood we call this the end diastolic volume and
we’re going to put in a number of 120ml. When the ventricle starts to contract in
systole — systole is contraction — some blood is going to start
leaving the ventricle and will be ejected outside. There is going to be a
volume of blood remaining inside. This blood remaining is called the end
systolic volume. So if I subtract the end diastolic volume, 120, from the end
systolic, which is remaining here, 50, I will know how much is ejected in that
beat and this is around 70 ml. This is my stroke volume. Now, are there
circumstances that will change the stroke volume? Is this something that is
constant? Now, there are going to be things, factors that will interfere with
with stroke volume and we’re going to learn these factors together. All right.
We’re going to learn three important factors. Preload, Contractility, Afterload.
What do I mean by preload? I am looking at how much volume of blood I am loading each ventricle with. How much venous return is coming to fill in the
ventricle? And this will definitely make a difference. If I have too much or too
little, it’s going to change my stroke volume. The second factor here is the contractility, the ability of the
ventricular muscle to contract and push the blood out. Again, if there is change
in contractility, it will change my stroke volume. The last factor here is
the afterload. How much resistance or pressure is meeting the blood when it is
trying to be ejected from the ventricles? The more resistance or the less
resistance, this will change my stroke volume. Let’s look at each one of these
individually. This is my preload. So I’m actually looking at the
end diastolic volume. How much blood is in the ventricles over here? If for any
reason there is decrease in this volume definitely the stroke volume will be
decreased. And commonly, if somebody has dehydration or bleeding, there is
definitely less blood leaving the ventricles and this person will have
lower cardiac output. If there is increase in the end diastolic volume,
there is more venous return. This will push on the walls of the ventricle. This
will stretch out the walls of the ventricles. And someone called Mister
Starling studied this phenomenon and he came up with the Frank-Starling law. And he said the more this stretch on the walls of the ventricle, the stronger is
going to be the contraction of this ventricle to push this excess fluid away
from the heart. So for example, if somebody is over hydrated, they’re just
drinking lots of fluid and this ends up in the heart, the heart is going to
contract more and stronger to push this excess fluid out into the system.
Eventually it’s going to reach the kidneys. It’s going to be filtered outside
as urine and this person will excrete this excess fluid. All right. Next we’re
going to talk about the Afterload. So I am looking here. This is the blood that
needs to be ejected. Is it meeting any resistance? Is there any pressure against
it that will impede the normal stroke volume? So, is there is any increased
afterload? So we’re looking at the two main valves here. We’re looking at the
pulmonary valve and the aortic valves. If there is
disease that decreases the diameter, decreases the ability of the valve to
open, definitely this will decrease the ejection of blood and stroke volume will
be decreased. In hypertension, blood vessels that are farther away from the
heart are constricted. And again, this will impede the normal stroke volume and it will decrease. On the other hand, if I if I want to decrease the afterload to
help the blood to be ejected, we can give a person vasodilators, dilate those
vessels up here, and then the ejection is going to be easier and stroke volume will
increase. The third important factor here is Contractility. I am looking at the
ability of my muscle to contract and push the blood out. So if we have
diseases of the cardiac muscle, the myocardium is weakened such as in heart
failure. Or, it is too thickened because of some hypertrophic heart diseases, it
will not accommodate enough fluid to start with or be able to eject to the
outside. So those situations where I have weakness in the cardiac muscle or
stiffness, definitely the contraction, contractility, is diminished and
definitely the stroke volume will be decreased. On the other hand, are there
substances or circumstances where we can increase the contractility? Yes, the
sympathetic stimulation. So every time we go out and exercise this sympathetic
stimulation is going to increase, it’s going to increase the contractility of
the ventricles. So the ventricles are pushing blood quicker
to our systems taking it to the muscles for the exercise that we need to perform.
Also, in situations where people have heart failure we can give them what we
call positive inotropic drugs. These drugs will increase and improve the
contraction of the failing ventricles. All right, we’re going to look at the
other factor which is the heart rate. What are things that will affect the
heart rate? These are pretty simple. We’re talking first about the autonomic
nervous system. We know that sympathetic stimulation will increase the heart rate
while the exact opposite, the parasympathetic, will decrease the heart
rate. Medication. Any medicine that increases the heart rate we call it a
positive chronotropic drug and an example is epinephrine.
Any medicine that decreases the heart rate is called a negative chronotropic
drug. An example of these are beta blockers and we use these in difficult
different clinical settings. Hormones, epinephrine and thyroxine are known to
increase the heart rate. Certain ions will affect the heart rate, particularly
potassium. Very high levels of potassium in the blood will decrease the heart
rate and accordingly decrease the cardiac output. And this concludes our
discussion of cardiac output and thank you.