So taking a closer look at the regulation of stroke
volume, we find that our stroke volume is equal
to the end diastolic volume
minus the end systolic volume.
Our end diastolic volume is going to be affected by the
length of ventricular diastole as well as our venous pressure.
Our end systolic volume is going to be affected by arterial
blood pressure and the force of our ventricular contraction.
A normal stroke volume is
approximately 70 ml per beat.
There are three main factors
that can affect this stroke volume.
First, we have preload followed
by contractility, and then afterload.
Starting with preload, preload is the degree to which a
cardiac muscle cell is stretched just before it contracts
and so the preload can cause changes in stroke
volume by affecting the end diastolic volume.
The relationship between preload and stroke volume is
referred to as the Frank-Starling law of the heart.
Our cardiac muscle fibers exhibit a
length-tension relationship and at rest,
the cardiac muscle cells are going
to be shorter than their optimal length.
Because of this, this is going to cause a dramatic
increase in the contractile force of the heart.
The most important factor in this
preload stretching of our cardiac muscle
is going to be venous return so blood
that is returning to the heart from the veins.
A slow heartbeat as well as exercise is
going to affect or increase this venous return.
And this increase in venous return or this increase
in the amount of blood the coming back to the heart
is going to distent or stretch the ventricles and
thus is going to increase the force of contraction.
So next we have contractility.
And contractility is going to mean the
contractile strength at the given muscle length.
Contractility is going to be independent of stretch
and also independent of end diastolic volume.
So an increased contractility
will lower the end-systolic volume.
Think about it, if I'm more
contractile then there's less that is left.
This is caused by sympathetic epinephrine release that's
going to stimulate an increase in that calcium influx
and leading to more cross-bridge
formations during depolarization.
Also, positive inotropic agents
can increase contractility as well.
These include things like thyroid hormone
thyroxine, glucagon, epinephrine, digitalis
as well as high extracellular calcium ions.
The contractility of the cardiac muscles can
also be decreased by negative inotropic agents
such as acidosis or increased extracellular potassium or by
the blocking of calcium channels with calcium channel blockers.
The third factor that can
regulate stroke volume is afterload.
Afterload is the pressure the ventricles must overcome in
order to eject blood out of the ventricles into circulation.
Back pressure from the arterial blood is pushing on
our semilunar valves and this is a major pressure.
The aortic pressure is around 80 mmHg and
the pulmonary trunk pressure is around 10 mmHg.
Also, afterload can be affected
by things like hypertension.
So for example, hypertension or high
blood pressure will increase the afterload
which is gonna result in an increase in the the end
systolic volume and that increase in end systolic volume
will result in a reduction of the stroke volume.
So now, let's look at these
factors and put them all together.
So first, the factors that can help determine
our cardiac output include things like exercise,
ventricular filling time, bloodborne
epinephrine or thyroxine or excess calcium
or central nervous system output in responds
to exercise, fright, anxiety or blood pressure.
All of these are initial stimuli that will
have an effect on our cardiac output.
With exercise and ventricular filling time, if
these are happening so first if you're exercising
or if there is a longer ventricular filling time, this is
going to increase our venous return of blood into the atria.
This increase in venous return is gonna
increase our end diastolic volume or our preload.
When it comes to bloodborne epinephrine and other factors,
these are going to increase the heart's contractility.
And an increase in contractility as
going to decrease the end-systolic volume
Next, the central nervous system outputs in response to
exercise can either be sympathetic or parasympathetic.
If it is sympathetic, if we are increasing sympathetic
activity, then this is going to increase cardiac output
and if we're decreasing sympathetic
activity or increasing parasympathetic activity,
then this can decrease cardiac output.
Also, sympathetic activity can
directly affect contractility as well.
When it comes to an increase in end diastolic
volume or decrease in end-systolic volume,
both of these factors will lead to
an increase in our stroke volume.
Sympathetic activity and parasympathetic activity
both can lead to an increase in the heart rate.
When we put these together, all of these
different factors will affect cardiac output.