Welcome back to our next lesson on hemodynamics.
In this lesson we are going to be talking about our cardiac output as well as the different
factors that go in to determining what our cardiac output is.
Just for a little refresher let's go ahead and throw up our cardiac output equation.
We have our cardiac output (CO) is equal to our heart rate (HR) times our stroke volume
(SV).
And again, lets just hit on our normals again.
Stroke volume normal is going to be 60-120; heart rate is going to be 60-100; cardiac
output is going to be 4 to 8 unless you are looking at our cardiac index then it will
be 2.5 to 4.
Now one really important thing to know about our heart rate and our stroke volume in this
equation is that they work together almost in a seesaw like manner.
So let's say we have our heart rate over here and our stroke volume over here, our heart
rate is going to change to compensate for changes in our stroke volume.
So if our stroke volume is high we are going to have a lower stroke volume as a result.
And by the same token, if our stroke volume were to decrease then we would see our heart
rate increase in an attempt to compensate for that decreased stroke volume.
Let's go ahead an move on to the first component of our cardiac output which is going to be
our heart rate.
Like we just talked about, the big important thing with the heart rate is it's goal, its
job, is to compensate.
It's going to compensate in changes in our stroke volume.
Let's say for example we have decreased stroke volume, this is going to lead to an increase
in our heart rate, which often times we refer to as tachycardia.
Again, that heart rate is trying to speed up in order to give us more beats per minute
because our stroke volume is now a smaller volume.
Some of the things that are going to contribute to tachycardia are going to be hypovolemia,
and this could be as a result of dehydration, fluid loss, or even blood loss.
Another thing would be low blood pressure.
Also if we think about our sympathetic nervous system.
This is going to be our fight or flight.
So if you think about in those situations the body releases the catecholamines which
are going to increase your heart rate.
And also other things like fever, and even something as simple as, and I know I don't
do enough of this, exercise.
These are all going to be things that are going to increase our heart rate.
One important thing to know when we are talking about tachycardia as a form of compensation
is there are limits to how much we can compensate for decreased stroke volume by increasing
our heart rate.
If we have a normal health person, typically a heart rate that is greater than 180 beats
per minute, if you have a rate that is faster than that, you are not going to have enough
time to fill the ventricle between each beat and as a result, if you continue to increase
your heart rate, you're not going to see an increase in your cardiac out as a result,
and therefore it's no longer going to be able to compensate.
Now this is in a healthy heart, so if you have someone that has a deconditioned heart
or a diseased heart, oftentimes anything that is greater than 120 beats per minute is no
longer going to be able to compensate.
Important things to keep in mind as your patients are becoming increasingly tachycardic, at
some point, and depending on the health of their heart, its no longer going to be doing
them any good, and it may be hurting them.
Now on the flip side of tachycardia, if we are in a situation where we have an increased
stroke volume this is going to lead to a decreased heart rate and this is what we refer to as
bradycardia.
One great example of this we often see in our athletes.
If you think about with these patients, they have very strong cardiac muscle so they have
great stroke volume and as a result their heart rate is going to compensate and lower.
A lot of times you will see these patients with heart rates in the 40's and 50's and
they are totally fine.
Now the last important thing to talk about when we are talking about our heart rate are
things that can lead to alterations.
Either alterations in the regularity, or alterations in the physical beating of the heart.
For example, if we talk about patients that have arrhythmia's.
So if they are in afib, aflutter, lets say they are in a junctional rhythm or even an
idioventricular rhythm, this is going to have an effect on both our heart rate, in the examples
of either slow rates with junctional or idioventricular rates, or fast rates such as afib or aflutter.
These arrhythmia's can also cause asynchrony between atria and ventricle which can also
impact our cardiac output.
Another thing that is going to have an impact on our heart rate is if we have different
heart blocks.
This is primarily going to be our second degree and third degree blocks, but these are going
to impact our heart rate and again will have an effect on our cardiac output.
Also if a patient has had an MI, this can also have an impact on our heart rate.
And finally if our patients are on either beta or calcium channel blockers.
These medications are all going to have an impact on our patients heart rate as well
as their ability to compensate in situations where their heart rate may need to increase
in order to make up for decreased stroke volume.
Alright so that covers everything with our heart rate.
Let's go ahead and move on to our next component of our cardiac output which is going to be
our stroke volume.
So once again for a refresher we will put our cardiac output equation.
Cardiac output (CO) is equal to our heart rate (HR) times our stroke volume (SV).
And if you remember we talked about our stroke volume is primarily composed of three factors.
Those three factors are our preload, contractility, and afterload.
So let's go ahead and talk about these different factors.
To start off, we are going to talk about our contractility.
To put it simply, contractility is simply the squeeze that your heart is able to do.
This is going to be the force of the contraction that the heart, or the ventricle is able to
beat with each time it contracts.
As an example, if we have an increased contractility this is going to lead to an increased stroke
volume.
If we think about it, the more squeeze we have the more blood that we are going to eject
with each contraction.
As a result of that, this is going to lead to an increase in our myocardial oxygen demand.
By having that increased squeeze, its going to take more energy, more force from the heart,
so as a result its going to require more oxygen to do so.
Things that can lead to increased contractility would be things like our sympathetic nervous
system.
Again like we talked about, that fight or flight system will not only increase your
heart rate but will increase your contractility.
And also things like exercise.
Now again, on the flip side of this if we have a decrease in our contractility that's
going to lead to a decrease in our stroke volume.
But as a result we are going to have a decrease in our myocardial oxygen demand.
Some of the things that can lead to a decreased contractility would be if your patient has
had an MI, if they've had cardiac surgery, things such as hypoxia, hypercapnia, hyperkalemia,
or hypocalcemia are all things that can lead to decreased contractility.
And finally, metabolic acidosis can also have a negative effect on the contractility of
your heart.
Moving on to the next factor in our stroke volume is going to be our preload.
Preload is often referred to as our filling pressure.
Essentially the preload is the amount of blood that is in the ventricle prior to contraction.
Often times you will hear this referred to as "how full the tank is."
Essentially it's that filling pressure; how full, how much volume do we have in order
to aide in contraction.
Now with our preload, there are three main factors that play a role in determining what
our preload is going to be.
The first of these is going to be our blood volume.
Essentially if you don't have any blood you are not going to have any volume for your
preload.
Next is going to be the distribution.
This is referring to the distribution of fluid volume in your body.
Is it in your vasculature, is it inside your cells, or is it in your third space?
What is the availability of that volume to be able to contribute to preload.
The last factor that we hit on just briefly when we were talking about the heart rate
is going to be our atrial contraction.
Really, what we are asking is, is the atria beating in conjunction with or in synchrony
with our ventricle?
As we know, when the atria contracts it forces that last bit of blood in to the ventricle
really filling it prior to contraction, and this "atrial kick' can actually account for
as much as 20% of our stroke volume.
So if our atria is not beating in synchrony with our ventricle, for example in afib or
aflutter, then we are not going to get that good atrial kick and it will have an impact
on the preload.
In order to really understand preload and have an idea of how it impacts stroke volume,
you need to understand something called the Frank-Starling Law.
The basic concept behind the Frank-Starling Law is an increase in preload equals an increase
in our stretch of cardiac muscle and this equals a stronger contraction.
The best way to really understand this, or visualize this is if we imagine a rubber band
here.
If we take that rubber band and we stretch it out, when you let go, that rubber band
is going to snap back with more force.
So again, if we stretch it out even further and we let go of that rubber band, again it's
going to snap back with even more force.
And that's the basic principal behind the Frank-Starling Law.
As we increase that preload it's going to stretch the ventricles more and by stretching
those ventricles more they're actually going to be able to have a stronger, more forceful
contraction in ejecting the blood.
Now there is a caveat to the Frank-Starling Law and this concept of stretching and stronger
contraction and that is that there are times that you can over-stretch the heart so that
it's not able to contract as forcefully.
And this is when we are going to be talking about congestive heart failure.
It is going to be important when we are talking about preload and the Frank-Starling Law that
we do talk about a concept called compliance.
And with compliance there are two different things that we worry about with compliance.
We can either have an increase in our compliance or we can have a decrease in our compliance.
An increase in our compliance is often what we refer to as over stretch.
This you are going to see in our patients that have CHF or a dilated cardiomyopathy.
Essentially the heart has too much compliance; it's able to stretch too much and as a result
you're not able to get that forceful strong contraction that you need.
Now on the opposite end, a decrease in compliance is not going to be able to stretch or accommodate.
You might see this in patients that have had an MI and patients who have a restrictive
cardiomyopathy and also in patients who have stunned myocardium.
Examples of this would be trauma or cardiac surgery.
Again that compliance will play a role in the hearts ability to effectively deal with
the volume or the preload that it is receiving.
Alright so let's go ahead and move on to the last factor that impacts our stroke volume
and that is going to be afterload.
Now afterload can be simply summed up as resistance.
So essentially, how hard does the heart have to beat in order to eject its blood.
This is also something that you will commonly hear referred to as "how clamped down is the
patient."
And just to give you a little visual representation.
If we have our heart and let's say we have a nice big wide aorta to beat in, it's going
to be a bit different that if we have one with tighter or more restricted aorta because
essentially afterload is that resistance that our heart is having to overcome each time
its beating trying to eject it's blood.
Now with this as well, we are going to have three factors that are going to impact our
afterload.
The first of these is going to be the compliance of the aorta.
The compliance of the aorta is talking about its ability to stretch with each beat, so
if you have a more compliant aorta, when the heart beats it's more able to stretch as opposed
to a non-compliant aorta which is going to be a stiffer aorta and as the heart beats
each time it's going to be beating up against a stiffer vasculature.
The next factor that plays a role in our afterload is going to be just that, the vascular resistance.
And that's exactly what I just drew above with the pictures there.
It's the amount of resistance that the heart is beating against, how wide or how clamped
down are those vessels that the heart is having to beat against.
Obviously the wide larger vessels, the easier the heart is going to be able to beat, and
the more constricted those vessels are the tougher it is to beat against that.
One thing to note with this here is if you have a patient who is hypoxic this can actually
lead to an increase in vascular resistance.
The final factor that is going to play a role in our afterload is going to be viscosity
of the blood.
Essentially how thick or how thin is that blood.
Thicker blood is going to be heavier and tougher to move as opposed to thinner blood which
is going to be able to flow more freely.
And those are the three factors that determine our resistance or our afterload.
At this point we've covered all the different factors that go in to determining our cardiac
output from our heart rate and stroke volume, to breaking our stroke volume down in to our
preload, contractility, and afterload, as well as talking about some of the basic principals
of each of those.
This concludes this lesson on hemodynamics and our cardiac output component.
In our next lesson we are going to talk about how we monitor our hemodynamics.