What is Preload?
The best way to think of preload is as a volume.
Essentially, preload is the VOLUME of blood in the ventricles at the end of diastole. This is termed End Diastolic Volume (EDV), thus at the very end of diasotole, if you look at that volume of blood sitting in the ventricles . . . that is your PRELOAD.
That volume is measured as the pressure that it exerts on the walls of the ventricles in mmHg.
There are two numbers that we can use to indirectly measure or estimate preload: CVP and PAOP
CVP is central venous pressure and provides an indirect measure of the EDV in the right ventricle. This is a parameter that a nurse can view using a flowtrac or other system that allows this number to be viewed.
PAOP is pulmonary artery occlusion pressure provides an indirect measure of the EDV in the left ventricle. This number can aid in evaluating preload status of the left side of the heart.
Preload Highs and Lows
Preload is essentially (in basic terms) a measure of volume status within the body. In states that lead to low volume (shock, hypotension, tamponade) you will also see decrease preload. In states that create excessive volume ( heart failure, brady-arrhythmias) , you will notice increased preload. Therefore treating the underlying cause should result in alleviating the problem. If preload is low due to a volume issue volume can be added through fluids or blood. If preload is high due to poor pump function diuretics or alternative medication therapy might be considered.
What is Afterload?
The best way to think of afterload is pressure.
Essentially, afterload is the PRESSURE that ventricles must exert to open the semilunar (aortic/pulmonic) valves. Vessels distal to the ventricles exert a pressure due to vasoconstriction or vasodilation. This pressure maintains the valves closed. In order to open the valves a specific pressure within the ventricles must be reached . . . this pressure is the AFTERLOAD. This number is represented by SVR and PVR (systemic and pulmonary vascular resistance respectively).
Afterload Highs and Lows
While afterload can be effected by volume status it is basically a result of vascular resistance within the aorta and lungs. These numbers are further a result of vasoconstriction and vasodilation. So if afterload is too high (HTN, aortic stenosis, SNS stimulation) the patient may benefit from vasodilators. In cases of decreased afterload, overdilation of the vasculature (sepsis, hypotension), the patient might benefit from vasopressors.
This is a basic introduction to preload and afterload to help clarify the difference between the two. Please post any questions or thoughts below.
As a quick heads-up with this episode, I do have two kids who are going to make a guest
appearance on this episode. So about halfway through this episode you will hear my son
Taz and my daughter Kai, making their first guest appearance on this podcast.
Hello, this is Jon with NRSNG.com – the NRSNG podcast.
Today I just wanted to briefly discuss preload versus afterload. I remember in nursing
school, this was kind of a difficult concept to grasp exactly what it was, what it meant,
what the difference between the two were. So I just wanted to briefly discuss that.
So what is preload and afterload and how do they fall into the whole hemodynamic
Basically, preload and afterload are contributing factors to stroke volume. What is stroke
volume? Stroke volume is the blood ejected from each contraction from the heart. Every
time the heart beats its pumping out a specific volume of blood – that is the stroke
volume. Basically, every beat, we should be ejecting about 60 – 120 mL of blood every
beat. That is the stroke volume. So there are three things that come into play to create
First is contractility – how hard the heart is beating, how strong it’s beating with each
beat. And then you have preload and afterload. So you have three determinants of
stroke volume: preload, afterload and contractility. Today we’re just going to discuss
preload and afterload.
The best way for me to remember what preload is, is to kind of think of it as a volume.
Preload essentially is our end-diastolic volume (EDV) within the ventricles. Really, it’s
the volume of blood in each ventricle at the end of diastole. It’s measured as a pressure
– it’s measured as either your CVP or your pulmonary artery occlusion pressure; your
wedge pressure. Preload is really the volume at the end of diastole, how much volume is
in that ventricle, and is measured as pressure – measured in the amount of stretch on
the ventricles. Preload is our end-diastolic volume really. Preload in your right ventricle is
measured with your CVP (central venous pressure) and preload in the left ventricle is
measure din directly with the pulmonary artery occlusion pressure or wedge pressure is
another word for that.
Again, preload is really just a volume measurement of what’s in the ventricles at the end
of diastole. So after the ventricles have completely filled at that moment of maximum fill,
how much volume is in there, what’s the pressure within the ventricle. That’s what
preload is. Once the ventricles have fully filled, end-diastolic volume, what’s the pressure
within there. Then what is afterload?
The best for me to think of afterload is a pressure. Afterload is the pressure required for
the ventricles to open the semilunar valves. We have all that volume within our
ventricles, afterload is the pressure required to open the semi-lunar valves and get that
volume out. Afterload is the pressured required to open our aortic or our pulmonic valve
and to push the blood either into the aorta or into the lungs. That’s afterload – afterload
is the pressure. You have all that pressure pushing against the semi-lunar valves, the
amount of pressure that the ventricles have to exert in order to open those valves – that
is your afterload.
That’s really measured through your systemic vascular resistance (SVR) or your
pulmonary vascular resistance (PVR). So that resistance that your vessels are exerting,
that’s a semi-vascular resistance, that essentially is your afterload. It’s your pressure
against which the ventricles have to pump in order to get that blood moving.
That’s really preload and afterload, that’s essentially what they are. Preload is the end-
diastolic volume – it’s the amount of stretch that the ventricles have experienced at the
end of diastole once they’re completely filled. Afterload is the amount of pressure that
the ventricles have to exert in order to move blood throughout the vasculature.
So, what essentially affects preload? Preload, with our understanding of exactly what it
is, it’s essentially affected by volume – how much volume you have going through the
system and how well that volume is able to move; that’s going to affect your preload.
Afterload is also affected by volume but even more directly it’s affected by
vasoconstriction or vasodilation. How tightly contracted or dilated those vessels are,
either in your systemic vasculature or your pulmonary vasculature, is going to determine
how much pressure or force your ventricles are going to have to exert in order to move
that blood forward.
With our preload, again, it’s our end-diastolic volume – so like I said that’s kind of a
determined by amount of volume status we have going throughout our system. Some
things that would increase our preload could be heart failure, as that blood isn’t able to
move forward because of our weakened ventricles that could increase our preload. Also
hypervolemia – if we have too much volume within our system then that’s going to
increase our preload. Or if you have bradydysrhythmia, so your heart is not beating fast
enough to move the volume forward, that’s going to increase the preload.
Some things that will decrease our preload are going to be hypovolemia or vasodilation,
and diseases such as shock and things like that is going to decrease how much volume
is going to be in our system. Also if your heart is beating too fast, it’s not going to be able
to fill the way that it needs to. Our end-diastolic volume is going to decrease, which is
If we need to increase our preload, there’s a couple things that we can give to increase
our preload – we can give fluids, we can give blood, we can increase that volume to get
more volume within the system and increase our end-diastolic volume. We can also, if
we needed to, either increase our heart rate or decrease our heart rate to affect the
preload – we can do that as well.
In order to decrease our preload – in an example of heart failure, we have too much
volume in there, we have to decrease the volume within the ventricles, we can give
diuretics, ACE inhibitors, you can give vasodilators, things like Nicardipine and things to
dilate those vessels will help decrease the amount of volume filling the heart with each
With afterload, like we said again, afterload is that pressure required of the ventricles to
open those valves and get the blood moving throughout the system. If we need to
increase our afterload, that’s going to mean that the pressure isn’t great enough that the
ventricles need to overcome, so we need to increase that squeeze. We need to increase
the amount of pressure the heart is using to open those valves. We can give things like
vasopressors. For example, if our patient is experiencing shock and their pressure has
dropped drastically, we would need to give pressures in order to increase that pressure.
Things like Norepinephrine, Vasopressin, Epinephrine, Neo-Synephrine, and things like
that. That’s a possible reason for giving vasopressors.
If we need to decrease our afterload, we can give things like vasodilators, ACE
inhibitors, ARBs, and those things are going to decrease our afterload. If for example we
need to get the pressure down a bit that the ventricles are having to exert, we can give
those things to help open the vasculature, decrease the amount of pressure required to
open those valves and potentially fix the problem. If we had overstimulation of the
sympathetic nervous system that was driving our pressure up, we could correct that. If
it’s just hypertension, we could do that as well. Also, another therapy that is used is the
Intra-aortic Balloon Pump (IABP). The Intra-aortic Balloon Pump is going to help get the
volume moving forward as well as it’s going to decrease our afterload.
Those are some of the possible things that we could give to affect preload and afterload.
That’s kind of the difference between it. Just to touch on it really quickly; preload and
afterload are components of stroke volume. Stroke volume is how much blood is being
pushed out of the heart with each beat, and that is affected by how much blood comes
into the heart, which is preload, and how easily it is for blood to move out of the heart,
and that’s afterload. So preload is our end-diastolic volume – it’s what amount of volume
is sitting on a ventricle at the end of diastole, how much blood is put in the ventricles and
how much is sitting there at the very end of diastole. Afterload is how easily it is for the
blood to move forward through the system – how much vascular resistance we have.
That’s really kind of what our systemic vascular resistance is, is that afterload. It’s how
easily for blood to move out through the ventricles. How easily we can open those semi-
lunar valves and get blood moving.
So that’s just a quick overview of the difference between preload and afterload, what
they are, and a couple of the easy therapies that are used to increase or decrease either
Date Published - Oct 27, 2014
Date Modified - May 1, 2019