So, now, let’s get into preload.
Preload is very important for the filling component of the heart.
That is your left ventricular end-diastolic volume.
That's the maximum amount of volume
you have in your left ventricle prior to a contraction.
Interestingly, when you talk about preload,
it’s actually about a fiber length
that we’re most concerned about.
How much stretch is there on the
left ventricle before you contracted again.
Those kind of thoughts can be
easily seen with things like a balloon.
You're filling a balloon until it gets
to a certain point or toughness,
and that's when you know it's full.
But until that point, you have a large space to fill.
When looking at preload,
there are couple of intrinsic mechanisms
associated with the muscle.
let's explain those to a greater degree.
It depends on how much you fill the heart,
how much it's going to be able to contract.
The more it's full,
the harder it can contract.
The less it’s full,
the less hard it can contract.
So, let’s look at that diagrammatically.
When you have a low preload,
you don't fill the heart as much.
at any given left ventricular pressure,
you can only push out so much stroke volume.
If you fill the heart more
at that same level of contractility,
you can push out more blood.
What factors affect preload?
Two of the biggest ones are venous
blood volume and venous compliance.
So, the more blood volume you have,
the more return of blood you have to the heart.
If your veins are less compliant,
meaning that they are constricted,
the more blood you'll be
able to return to the heart.
That has to do with increasing venous pressure,
a lot depends on how compliant your left ventricle is
to accept this new level of preload.
The amount of contractility of
the top portion of the heart
also affects your preload
because it's going to be pushing in
that last little bit of blood.
The harder the atrium contract,
the more preload you get.
Another factor that affects preload,
which is a little bit more indirect
– it’s one of those secondary effects –
if you increase the amount of afterload,
you will not be able to push as much
blood out on any given stroke of the heart.
If you don't push as much blood out,
you have more blood left over after each stroke.
if you have more blood left over,
you can fill it to a greater degree.
So, in fact, if there is an increase in afterload
and you don't get as much blood out per stroke,
on the next time the heart beats
it will contract harder.
Because you filled it to a greater degree.
The last two items that affect ventricular preload
are heart rate and inotropy.
These two items are normally
associated with more cardiac output,
but if you slow the rate of the heart,
you don't have it beat as fast,
it has more time to fill.
So, one way to get more preload is
don't beat the heart as fast
and you can be on diastole
for a longer period of time.
Ventricular inotropy works on a similar principle,
in which if you decrease the strength of the contraction,
therefore you have a greater end-systolic volume.
The next beat of the heart,
you'll fill it to a greater degree
and that increases your preload.
So, let's look at this preload concept on a graph.
Because this will land the principle.
And even though this is a hard one,
you'll get it if you can see it in action.
So, when we look at a graph like this,
let’s talk through the different axes.
The first axes we’re going to have is the x-axis.
It's going to be left ventricular end-diastolic pressure.
On the y-axis,
we’re going to have stroke volume.
So, those are our two variables.
If we start off in a condition,
which is A,
if we move from A to B,
we have increased the left
ventricular end-diastolic pressure.
At that point,
you’ll have a greater stroke volume that will occur.
So, let's go through that
a little bit more in detail.
If you increase left ventricular filling pressure,
that is an index of what preload?
That index of preload will cause
then an increase in stroke volume.
This relationship is called the Frank-Starling mechanism
or Frank-Starling principle.
This principle or relationship
allows for this inherent property of cardiac myocytes.
It's interesting you're not actively using more ATP
to generate this stronger contraction.
You're simply letting the myocytes stretch more
and then they’ll contract back harder.
This is also referred to as
a length-dependent activation.
So, it matters at what length you are,
what level of contraction you'll get.
So how does preload affect pressure-volume loops?
Everybody's favorite, pressure-volume loops.
And with a pressure-volume loop,
we have normal indices,
which stack out at the top and
the bottom portion of the graph.
These are places in
which we cannot go out of.
It provides our minimal and
maximal components in the figure.
A normal pressure-volume loop looks like this,
where you start off filling the
heart along the bottom axis.
You have a vertical line,
which is the contraction of the heart.
You have an ejection portion
and then a relaxation portion.
How does preload change that?
Preload should allow you to
fill to a greater degree.
If you're filling to a greater degree,
you should be what?
Increasing that volume.
As you do that,
you make a bigger pressure-volume curve.
You increase end-diastolic volume
and you increase stroke volume.
All because of the increase in venous return.
Now, let's look at this if we have
a decrease in venous return.
you’re going to have now a shorter curve
that decreases left ventricular end-diastolic volume
and decreases stroke volume.
Nice ways to think of changes
in the pressure-volume loop.
How would you get such pressure-volume loop changes?
Well, a good example of
an increase in venous return
is if you get extra volume added to your blood,
maybe you were hooked up to an IV
and infused in volume through,
let's say, isotonic saline.
A decrease in volume could
be just the opposite.
Maybe you've undergone dehydration
and you've lost body water.
So, those are two examples
of both either an increase
or a decrease in venous return.