Cardiac Performance
Introductory Human Physiology
In this course, students learn to recognize and to apply the basic concepts that govern integrated body function (as an intact organism) in the body's nine organ systems.
Welcome back! In this module we consider how the circulatory system works to deliver oxygen and nutrients to the specific organs. We start with a discussion of the electrical and mechanical functions of the heart which enable it to generate a pressure gradient. This pressure gradient propels the blood through the blood vessels, in a unidirectional manner. The following session considers the factors that govern delivery of gases and nutrients at the tissue level. The last session considers the entire reflex loop, its control, and its response to daily demands (rest and exercise) and how pathology affects these responses. This is a busy week! The things to do this week are to watch the 5 videos, to answer the in-video questions, to read the notes, and to complete the CV problem set. It will be most effective if you follow the sequence of videos. The notes provide a more detailed summary of each topic. We encourage you to find which resource (videos and/or notes) works best for you and to try the problems sets. The problem sets are not graded. Both your understanding and retention will increase with application of the new learned information.
can generate up to a 100, is now generating 180 millimeters of mercury.
So that by simply filling the same heart with more blood,
we're able to get a better contraction,
better force from that particular heart and we have a higher systolic pressure.
So that's an advantage and that's why the heart will in fact,
meet their increased demand by
increasing volume within the system, and that is the filling of the heart.
But in this particular case the stroke volume of the two loops that is A and
B, we kept as 40 milliliters.
So what if we calculate the ejection fraction form loop A, that is the heart at
rest before we started to fill it with more blood, then what we find is
that 40 divided by 90 will give us an ejection fraction which is about 44%.
But what about the injection fraction from loop B.
It's the same heart but we've added more volume, more blood to the ventricular and
we've maintained the stroke volume at 40 and what we see then is it's 40,
divided by 140, which is its end diastolic volume.
And so, now, that heart has only about 28% ejection fraction.
So although it can give us more pressure, or can generate more pressure,
the heart is, in fact, not as efficient at doing so.
Now under normal conditions, [COUGH] excuse me, under normal conditions when
the heart is filling with more volume, the stroke volume is also increasing and
this is due to our Frank Starling relationship.
Remember when we said that the heart
is not able to recruit more muscle fibers such as the skeletal muscle,
because as the heart is pumping it's using all of the fibers.
They're all connected through gap junctions, and
they're synchronously pumping.
So we can't recruit more fibers to generate more power.
But instead, when we stretch the heart and
we stretch the myocytes, then they will give a better contraction.
And this we said was due to
the differences in the molecular arrangements within the fibers themselves.
This is known as the Frank-Starling effect and
effectively what it's saying is that the volume that's coming in to a normal heart
is the volume that will be ejected by that normal heart.
So let's consider this particular figure.
On the x axis, there is the left ventricular and diastolic volume, or EDV.
And on the y axis is the ejection volume and as you know, that's the stroke volume.
So we have stroke volume then versus the end diastolic volume.
And if we start our heart here at rest and
it has an end diastolic volume of 100, then as we fill this normal heart,
we fill it and move it to an End Diastolic Volume of a 150, notice that we now have
moved the stroke volume has increased, the stroke volume has gotten bigger.
So when the heart had an end diastolic volume of a 100,
we have a stroke volume that was about 70.
But at 150, that same heart, the end diastolic volume of 150 milliliters,
that same heart will give us a stroke volume that's now at about 90.
So, we can increase the stroke volume by filling the heart, and this filling of
the heart is referred to as venous return, and it's also referred to as preload.
Preload increases the ability of the heart to eject blood.
It's increasing it's contraction and it's power.
It's able to generate more force by stretching the ventricles.
By filling the ventricles and this is called preload.
Okay, so how does the body adjust preload?
So there's several mechanisms by which preload can be increased and
that's what's noted here.
So the first is what's called the skeletal muscle pump.
As an individual starts to run let's say,
they are requiring more blood to be delivered to the muscles,
to deliver more oxygen to the contracting muscles.
The contraction of the muscle itself is squeezing against
the veins that are within that tissue.
And as it squeezes against the veins,
it Is helping to propel the blood out of the tissue, and back towards the heart.
And so that simply, the local effect, and it is called the skeletal muscle pump.
The second way that we can increase the return of blood to the heart or
increase venous return, is what's known as the respiratory pump.
So again as we're running and we're taking bigger breaths,
then the expansion of the thorax, as you're taking a larger breath,
decreases the pressure that's around the heart.
And that means that the heart can actually expand easier, and so
the blood then can flow back into the heart faster.
So this inspiration, that is taking in a big breath, like this,
will lower the thoracic pressure.
Fourth, and I'm gonna skip three, and we'll come back to it in a second, but
fourth, we have what's called vasoconstriction.
So this is, is that the skeletal muscle that's around the blood vessels on
the arterial side, will constrict when we have a sympathetic drive.
These are through the alpha one andrenergic receptors.
As these cells constrict, they will force the blood then from
the arterial side to the venous side of the circulation.
And so this then, augments the return of blood to the heart.
In addition, we have smooth muscle that's located along the long axis of the veins,
and this smooth muscle also can contract and as it contracts due to the sympathetic
drive, then we will again augment the flow of blood back to the heart.
So vasoconstriction or sympathetic drive will increase venous return or
it aids in the filling of the heart.
Then what about this number three?
This is called an increase in blood volume due to doping.
Doping is a concept where an individual will take blood or
donate blood, takes the blood from his own circulatory system.
Let's say a half a liter, and he stores it.
And then, just before a race, that blood is given back to the individual.
The individual has five liters of blood within his circulation and
he's getting back another half a liter to the circulation, so
he now has onboard five and a half liter's of blood.
This obviously increases his ability to carry
oxygen because there's more red blood cells within the circulatory system, and
it also is increasing the volume within the circulatory system.
So we have more volume then that can be delivered to the heart.
So this aids then in the delivery of blood to the tissues.
It is illegal, and it is illegal partly because it
gives an unfair advantage to these individuals in an athletic event.
But most importantly that by giving this extra blood
back to the individual we're increasing the viscosity of the blood.
You're changing the pressure within the system.
By giving more blood cells to the body,
what happens is that as the individual dehydrates.
So they lose fluid as the during the athletic event through sweating then this
individual's blood actually becomes higher in the hematic increases.
It has more blood cells per unit volume.
And under those conditions the viscosity increases and
this is actually harder on the heart.
So it's more work for the heart to push through a more viscous blood and
can be quite dangerous.
And it is illegal.
The last system that we're gonna consider is that the cardiac
myocytes themselves are sensitive to certain chemicals.
These chemicals are called ionotropic agents and an ionotropic agent
is an agent that can increase the contractility of the muscle
cells themselves, or the muscle fibers themselves.
And that's what's shown here.
So right here we have, again, our left ventricle end diastolic volume
on the x axis, and our ejection volume, or stroke volume, is on the y axis.
Under the resting state where we have normal Individual and
all we've done is increase the volume to this individual.
As we know, by increasing the volume, we will increase stroke volume.
So if we increase end diastolic volume, deliver, preload to the heart,
we increase stroke volume.
But let's keep the end diastolic volume constant at 100.
So, we're sitting here and now, we'll give an ionotropic agent to the individual.
And ionotropic agents are things such as catecholamines.
So norepinephrine and epinephrine are ionotropic agents.
If we give a sympathetic discharge, or norepinephrine, to this individual,
what happens is that the heart now at that exact same end diastolic volume,
can give a better squeeze, and that means that it ejects more blood.
So we move the stroke volume from something like 35 to 70.
So we've greatly improved the ability of the heart then, to eject the blood,
and that's by changing the contractility of the muscle cells themselves.
These effects are multiple effects,
they're occurring at the level of the myofibrils themselves and
also sarcoplasmic reticulum as well as within the plasma membrane itself.
So the entire cell becomes more sensitive to calcium.
By doing so, we're able to have a faster off rate, on rate for
the calcium and the contractual event is actually improved.
So sympathetic stimulation then is a way the heart can effect not only
venous return as we said it aids in the constriction of blood vessels and
so by doing so we move the blood back to the heart faster, but
it increases the contractility of the heart itself, the myocyte itself.
The contraction of the myocyte is more forceful.
And then lastly, as you know, it increases heart rate.
So cardiac output, which is, cardiac output equals to stroke value times
heart rate, the sympathetic nervous system not only increases heart rate,
but it also can increase stroke volume, and therefore can increase cardiac output.
Okay, so what's our key concepts then?
So the general concepts are first, that the volume of the blood
which is ejected with each beat is called the stroke volume and
that the sum of the stroke volumes ejected in one minute is the cardiac output.
Third, that the ejection fraction is the percentage of blood
which is pumped from the heart in each beat.
Fourth, cardiac output increases with increased filling of the ventricles,
and this is referred to as venous return, and also as preload.
And the cardiac output can increase with an increase in sympathetic
stimulation or by giving an ionotophc agent to the heart.