Preload vs Afterload |Hemodynamics | Blood Pressure

preload vs afterload
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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.

Measuring 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.

Conclusion

This is a basic introduction to preload and afterload to help clarify the difference between the two.  Please post any questions or thoughts below.

 

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PODCAST TRANSCRIPT:



So 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 the episode, you will be hearing my son Taz and my daughter Kai in their first guest appearance on the 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 that 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 picture?



So basically preload and afterload, they are contributing factors to stroke volume. What’s stroke volume? Stroke volume is the blood ejected with each contraction from the heart.



So every time the heart beats, it’s pumping out a specific volume of blood. That is the stroke volume. So basically every beat, we should be ejecting about 60 to 120 milliliters of blood every beat. That is the stroke volume.



So there are three things that come into play to create stroke volume. 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. They’re preload, afterload, and contractility. So today we’re just going to discuss preload and afterload. So preload, the best way for me to remember what preload is, is to kind of think of it as a volume. So preload essentially is our end-diastolic volume within the ventricles.



So 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 or your wedge pressure.



So preload is really the volume at the end of diastole, how much volume is in that ventricle, and it’s measured in pressure. It’s measured in the amount of stretch on the ventricles.



So preload is our end-diastolic volume really and preload in your right ventricle is measured with CVP, your central venous pressure, and preload in left ventricle is measured indirectly with pulmonary artery occlusion pressure or wedge pressure is another word for that.



All right. So again, preload is really just kind of 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 that pressure within the ventricle? So that’s what preload is.



Once the ventricles are fully filled, end-diastolic volume, what’s the pressure within there? So then what is afterload? OK. Afterload, it’s best for me to think of afterload as a pressure. So afterload is the pressure required for the ventricles to open the semi lunar valves.



So we have all that volume within our ventricles. Afterload is the pressure required to open the semilunar valves and get that volume out. So afterload is the pressure required to open our aortic or pulmonic valve and to push the blood either into the aorta or into the lungs. So that’s afterload. Afterload is that pressure. You have all that pressure pushing against the semilunar valves. The amount of pressure that the ventricles have to exert in order to open those valves, that is your afterload.



That’s really kind of measured through either your systemic vascular resistance or your pulmonary vascular resistance. So that resistance that your vessels are exerting, the systemic vascular resistance, that essentially is your afterload. It’s that pressure against which the ventricles have to pump in order to get that blood moving.



So 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 and 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? So preload, with our understanding of exactly what it is, it’s essentially affected by volume, how much volume you have going throughout 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 either vasoconstriction or vasodilation. How tightly contracted or dilated those vessels are either in your systemic vasculature or in your pulmonary vasculature is going to determine how much pressure you’re – the force your ventricles are going to have to exert in order to move that blood forward.



So with our preload, again it’s our end-diastolic volume. So like I said, that’s kind of determined by the amount of volume status we have going throughout our system. So 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 like bradydysrhythmias. So your heart is not beating fast enough to move the volume forward. That’s going to increase the preload.



Some things that would decrease our preload are going to be hypovolemia or vasodilation in diseases such as shock and things like that. That’s going to decrease how much volume is going to actually be within our system.



Also if your heart is beating too fast, it’s not going to be able to kind of fill the way that it needs to. So our end-diastolic volume is going to decrease, which is our preload.



So if we need to increase our preload, there are a couple of things that we can give to increase our preload. We can give fluids. We can give blood. We can increase that volume to kind of get more volume within the system and increase our end-diastolic volume.



We could also – if we needed to either increase our heart rate or decrease our heart rate in order to affect the preload, we could do that as well. In order to decrease our preload – so in an example of like heart failure, we have too much volume in there. We need to decrease that 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 to decrease the amount of volume filling the heart with each beat.



So with afterload, afterload like we said again, afterload is that pressure required in the ventricles to open those valves and get the blood moving throughout the system.



So if we need to increase our afterload, that’s going to mean that there’s – 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 that the heart is using to open those valves. So we can give things like vasopressors.



So 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, things like that. That’s a possible reason for giving vasopressors.



Now, if we need to decrease our afterload, we can give things like vasodilators, ACE inhibitors, ARBs. Those things are going to decrease our afterload.


So for example if we need to get the pressure down a bit, 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.



So if we had like 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. The intra-aortic balloon pump is going to help get the volume moving forward as well and it’s going to decrease our afterload.



So those are some of the possible things that we could give to affect preload and afterload. That’s kind of the difference between it. So just to touch on it really quickly, preload and afterload are components of stroke volume.

Podcast Transcription

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

picture?

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

stroke volume.

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.

Preload

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?

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

our preload.

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

beat.

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

one.