Afterload and BP...So Confused!!

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So I have looked all over this site for information regarding afterload...and everywhere else!!! I have been trying to get this question answered for a while now and I can't seem to get it to where I'm satisfied with the answer.

There is a burn pt. his propane tank exploded burning the face, arms, and chest. He has mixed burns to most areas except his hands and face where he has 3rd degree burns. His BP is 65/45 and his HR is 200 bpm. He was unconscious in the ER but regained consciousness the next day.

Now I have to explain why his BP is so low using the BP equation and why his HR is so high using the BP equation.

Now my book says the BP equation is: BP = CO x PR. TPR is the total resistance for the systemic circulation, so TPR is often referred to as SVR. Now the equation for CO is: CO = SV x HR. SV is determined by preload, afterload, and contractility. HR is mainly regulated by the PNS and the SNS. Now the patient has burns so he is going to have fluid shifts (third-spacing), which leads to hypovolemic shock. As a result the BV decreases. The decreased BV causes decreased venous return to the heart, which means preload decreases. With less blood coming back to the heart, the heart contracts less because it has less blood to push out. Therefore, less blood to eject means that SV decreases. Since CO is a product of SV and HR, as a result of a decreased SV, CO will decrease. Also, CO is the amount of blood ejected from the heart per minute (per cycle). Therefore, if the heart beats less times per minute, less blood is leaving, which results in a decreased CO. Since BP is the product of CO and PR, a decrease in CO will result in a corresponding decrease in BP. However, the body quickly responds to the decreased BV and BP by activating the SNS, which leads to an increase in HR and contractility, and causes peripheral vasoconstriction (so blood is shunted from the less-vital areas - like the skin and GI tract - to the more vital areas - like the heart and brain). This should cause BP to increase back to normal. Because again, CO is the product of HR and SV. An increase in HR causes CO to increase. The peripheral vasoconstriction causes afterload to increase, which causes SV to increase. BP is the product of CO and PR. Therefore, BP increases to normal.

However, the patient's BP is so low that this tells me that the compensatory mechanisms are no longer working. I get kind of lost here. Because his HR is high, so it makes me think that his compensatory mechanisms are still working. Also, he was unconscious in the ER, but regained consciousness the next day. That tells me that the perfusion to his brain decreased enough to make him unconscious, but the perfusion increased enough for him to regain consciousness. I'm not sure if that's right - if that's why he lost consciousness and regained consciousness again? OK back to the HR. I know that when the HR is excessive enough - like 200 bpm - it decreases the amount of filling time (time in diastole). the heart does not remain relaxed (in diastole) long enough to allow the cardiac chambers enough time to be completely filled before the next contraction. This causes EDV to be decreased, which results in a decrease in preload. The decreased preload leads to a decrease in SV. As a result, CO no longer increases but falls. Also, with such an excessive HR resulting in less diastolic filling time and decreased EDV, there is less ventricular wall stretch. According to Frank-Starling mechanism, less wall stretch means that you have less contractility. So you have increased HR, but you have myocardial depression (poor contractility). I think that's right. OK so you have an excessive HR - I think due to the SNS trying to raise the BP, but eventually the compensatory mechanisms become detrimental to the person. The increased HR, vasoconstriction (increased afterload) cause more harm than good. So the HR becomes too high and results in the CO decreasing. The decreased CO causes the BP to decrease.

So the HR is so high and the BP is low because the HR increases as a compensatory mechanism to maintain BP, however it eventually starts to do more harm than good. The HR increases to an excessive amount, where the heart does not have enough time to fill properly. This causes the CO to decrease, which leads to a corresponding decrease in BP.

OK sorry...I seem to have gotten off the point of my question. I actually have 2 questions I guess. To see if I am right regarding this case and regarding afterload. Now on to afterload.

So my teacher in his lecture said that afterload is the force that the heart has to push against. So he gave 2 examples. I think I get it but want to make sure

For example, if you have a mean pressure in the aorta of 100 mmHg, you must generate what is known as the afterload - you must generate a force in excess of 100 mmHg in order to open up the aortic valve.

So I understood this as - He said that afterload is the force the heart has to push against. So if the mean pressure in the aorta is 100 mmHg. The blood is in the left ventricle. So in order for the aortic valve to open up and for the blood to be pushed through and into the aorta and out to the rest of the body a force in excess of 100 mmHg must be generated. He said that you must generate what is known as the afterload - you must generate a force in excess of 100 mmHg to open up the aortic valve and get the blood through to be dispersed to the body. So for example, so a force of 150 mmHg is generated in order to open up the aortic valve. Then what he is saying is that the 150 mmHg, for example, would be the afterload.

Second Example:

If we're talking about the pulmonary circuit, in the pulmonary trunk, the mean BP is about 20 mmHg, so that would be the afterload in the pulmonary system. So you have to generate a force in excess of 20 mmHg to open up the pulmonary valve.

So I understand this as - Again, he said afterload is the force the heart has to push against. So if the mean pressure in the pulmonary artery is 20 mmHg he is saying that is the afterload. He said "the mean BP is about 20 mmHg, so that would be the afterload in the pulmonary system." So the heart would have to push against the 20 mmHg in order to get the pulmonary valve open and get the blood through to go to the lungs. This is what I think is afterload. If it is the force the heart has to push against. If the pressure in the pulmonary artery is 20 mmHg, unless a force in excess of 20 mmHg is generated that will fight that 20 mmHg and get that valve open, the 20 mmHg of the pulmonary artery will be able to keep that valve closed. So if, for example, the heart generates a force of 40 mmHg, that would be enough force to overcome the force of the pulmonary artery (20 mmHg) and get the pulmonary valve to open and get the blood through to the lungs.

Am I getting this right?

Thanks so much for any help!!!

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Specializes in ICU.

Sorry, you only get 140 characters for your questions here. :sneaky: I started skim reading about half way through, but it seems that you understand it correctly. What EXACTLY is your question? I got lost between the relationship of the burn guy and the after load scenarios. If you've got a sick patient like this, then that's when a Swan-Ganz Catheter is really useful. You can measure filling pressures directly, then calculate the cardiac output and SVR and determine exactly how to treat this patient. You will weigh him every morning so you know that he's third spaced say 25 lbs of fluid, but still his filling pressures (wedge pressure, CVP, and PA pressures) are still low, so maybe he needs MORE fluids? Or maybe a plasma expander (such as 25% Salt Poor Albumin which helps draw that 3rd spaced fluid back into circulation by osmosis). If his filling pressures are reasonable, but BP is still in the 60's/40's and his SVR is low, then he needs a pressor, such as Vasopressin to tighten up the vascular system and bring that bp back to normal. You wouldn't use Dopamine, because it's also a positive chronotrope, makes the heart beat faster, and at 200 already you don't want that! OKay, so now he's got a Swan Ganz catheter and associated electronics, is on vasopressors (blood pressure is okay now), and in the ICU. He's up 25lbs of fluids, but because his blood pressure was low for so long, his kidneys went into shock and now he's not peeing (you know this because he has a foley catheter). You tried to coax his kidneys with Lasix, but his BUN and Creatinine are really elevated and he's still not peeing. WHat now? Now you need to get ANOTHER line placed (Mahurkar) and begin CVVH or CVVHD to take fluids off for him until the kidneys recover. Yada yada yada, and the ICU dance begins. I think you've got it. :yes:

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LOL...Sorry it was really long!! I carried on a little much ;) For the question I don't need to know what medications to give him or measurements to take. I need to explain why his BP is so low using the BP equation - BP = CO x PR (the equation from my book) and I also need to explain why the HR is so high using the BP equation. Regarding the burn patient why his BP is so low with such a high HR is immediately when the BV decreased and the BP decreased the body sensed this and activated the compensatory mechanisms - SNS, baroreceptors - these mechanisms work up to a point, but eventually become detrimental to the patient. I get that the HR is so excessive at 200 bpm that the filling time (diastole) is shortened so much. With the heart not filling properly, the CO decreases. I think I'm getting that part. But I guess what I don't understand is at what point does the compensatory mechanisms for hypovolemic shock stop working and start being harmful to the patient? I read that the baroreceptors have a threshold and when the MAP falls below that threshold they are no longer activated. At this point the chemoreceptors become activated - they sense that the patient is in lactic acidosis because the patient has low oxygen so switched to anaerobic metabolism and lactic acid built up. The chemoreceptors sense low oxygen, low pH, and high carbon dioxide - all which occur. The vasoconstriction that occurs as a compensatory mechanisms causes the blood flow to decrease even more, which decreases the amount of oxygen going through the body even more? Is that right? So at some point the compensatory mechanisms become harmful to the patient and the BP can no longer be maintained and starts to decrease. I'm guessing the excessive HR at 200 bpm is one way the compensatory mechanisms become harmful to the patient. The body is trying to increase the HR to raise the BP, but the BP is not increasing and the HR is going to high which is decreasing filling time causing the CO to decrease. Sorry this is getting long again. So to end - I don't need any medications the patient needs or what to do with the patient. I just need to know if I am correct on why his BP is decreasing and the compensatory mechanisms are becoming harmful to the patient. At what point does the compensatory mechanisms become harmful in hypovolemic shock? What occurs to make them harmful?

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OH....also thank you very much for your help!! It is greatly appreciated!!!! :)

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Oh also...one other thing I am a little confused about...Can the contractility be decreased with a high HR? I would think that the contractility would increase with a high HR. However, I believe that when the HR increases to such an excessive amount and the filling time decreases, so there isn't as much blood getting into the heart (which is why the CO decreases because there isn't much blood coming out - is that right?) so the contractility is decreased? Is that right? Or would the contractility increase to try and get that little amount of blood out to the body better?

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Specializes in ICU.
LOL...Sorry it was really long!! I carried on a little much ;) For the question I don't need to know what medications to give him or measurements to take. I need to explain why his BP is so low using the BP equation - BP = CO x PR (the equation from my book) and I also need to explain why the HR is so high using the BP equation.

I can't do your work for you, but given the information known, I don't think you can fully explain his low blood pressure from just that simple equation. It's much more complex than that.

Regarding the burn patient why his BP is so low with such a high HR is immediately when the BV decreased and the BP decreased the body sensed this and activated the compensatory mechanisms - SNS, baroreceptors - these mechanisms work up to a point, but eventually become detrimental to the patient. I get that the HR is so excessive at 200 bpm that the filling time (diastole) is shortened so much. With the heart not filling properly, the CO decreases. I think I'm getting that part. But I guess what I don't understand is at what point does the compensatory mechanisms for hypovolemic shock stop working and start being harmful to the patient?

It happens when the body tires and can no longer keep up. It's not a machine, it's a living organism that requires energy reserves. Younger patients can survive longer than older, and children who aren't fully grown, will crash very quickly.

I read that the baroreceptors have a threshold and when the MAP falls below that threshold they are no longer activated. At this point the chemoreceptors become activated - they sense that the patient is in lactic acidosis because the patient has low oxygen so switched to anaerobic metabolism and lactic acid built up. The chemoreceptors sense low oxygen, low pH, and high carbon dioxide - all which occur. The vasoconstriction that occurs as a compensatory mechanisms causes the blood flow to decrease even more, which decreases the amount of oxygen going through the body even more? Is that right?

So at some point the compensatory mechanisms become harmful to the patient and the BP can no longer be maintained and starts to decrease. I'm guessing the excessive HR at 200 bpm is one way the compensatory mechanisms become harmful to the patient. The body is trying to increase the HR to raise the BP, but the BP is not increasing and the HR is going to high which is decreasing filling time causing the CO to decrease. Sorry this is getting long again. So to end - I don't need any medications the patient needs or what to do with the patient. I just need to know if I am correct on why his BP is decreasing and the compensatory mechanisms are becoming harmful to the patient. At what point does the compensatory mechanisms become harmful in hypovolemic shock? What occurs to make them harmful?

The exact point of when the patient can no longer sustain life is going to be different in each case. Stop thinking about it as a machine ... if this, then that. It's more like ... if this, then maybe this, maybe that , or the other. Maybe all three!

I can't look at it in a textbook point of view that you're looking for. It's called the 'Art of Medicine' for a reason. It's not black and white by any means. I'm an ICU nurse, so I have to worry about how to stop the processes that are going to kill the patient. At what point is the patient going to stop breathing? When is the heart going to go into a lethal rhythm? Also, what I do to correct problems as they occur, will have side effects that may cause other problems. These can not be ignored.

You'll just have to work out how to answer your questions in a way that's acceptable to your class. You've got a grasp of the mechanics. :yes:

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Is it possible that the patient has an increase in preload, causing the actin and myosin fibers to stretch so far apart that the heart has to work overtime to try to realign the fibers leaving less time for contraction which would cause a decrease in SV?? I am not a nurse, just curious.

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Eagle78 - I know that the preload decreases initially, when the patient's BV first decreases. However, due to the compensatory mechanisms the SV is maintained, which keeps the CO maintained and therefore the BP maintained. Eventually, the compensatory mechanisms no longer work and the CO decreases which causes the BP to decrease. I believe that the preload stays decreased the whole time because of the decreased BV.

Biffbradford - Thanks so much for all of your help! I really appreciate it! I understand each person is going to be different. I think I get how to explain it that will be acceptable to my professor. As long as I am getting the concepts right? Is what I believe about afterload correct? This is what I think is afterload. If it is the force the heart has to push against. If the pressure in the pulmonary artery is 20 mmHg, unless a force in excess of 20 mmHg is generated that will fight that 20 mmHg and get that valve open, the 20 mmHg of the pulmonary artery will be able to keep that valve closed. So if, for example, the heart generates a force of 40 mmHg, that would be enough force to overcome the force of the pulmonary artery (20 mmHg) and get the pulmonary valve to open and get the blood through to the lungs. - So the force in excess of 20 mmHg, for example the 40 mmHg, would be the afterload?

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Your way of thinking about afterload is correct. It is the pressure that the chambers of the heart must generate in order to eject blood out of the heart into the aorta or pulmonary artery. The greater the aortic/pulmonary pressure, the greater the after load on the left/right ventricle. This tension in the ventricle is largely dependent on the pressure in the ventricle, the thickness of the myocardial wall and the volume in the ventricle.

Now, the F-S mechanism basically just states that functional cross-bridge formation in the sarcomeres increases as the heart dilates due to an increase in the filling volume of the heart (as in pump failure). You can have increases and decreases in contractility independent of the EDV.

You have a good understanding of the problem you presented. Perhaps a burn victim wasn't the best way to go as there's a lot more going on physiologically than just "the patient is hypovolemic". They should have chosen a more straightforward BV is low, therefore SV (EDV - ESV) is low, therefore HR goes up.

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Specializes in Critical Care, ED, Cath lab, CTPAC,Trauma.

It is actually really simple......

Preload is stretch. The amount of volume being returned to the right side of the heart from systemic circulation.

Afterload is squeeze. The amount of resistance the left side of the heart has to overcome in order to eject blood.

Preload is about volume. If the water pressure is low, the water output will be a trickle, not enough to water and sustain your pretty garden. If the volume is too much, it will back up your plumbing system (Right-sided heart failure engorged liver, systemic edema, etc, or left-sided failure pulmonary edema.)

Afterload is about pressure or resistance. If there is a link or narrowing in your garden hose, the volume will back up AND the output will drop. Think of it like a garden hose.........

A good analogy is that your hose has gone form a garden hose to a fire hose or developed huge leaks and it will either get more blood to the right places easier (decreasing afterload so the heart doesn't have to work as hard and will therefore work better) ...or you will not get the blood to where it need to go until you "patch it up" (constrict the blood vessels to a more normal size like the vasodilation that occurs with sepsis)or stop the bleeding by sealing the leak(the source of hemorrhage)....OR....

Gross analogy, but it works...Think about flushing a toilet......you flush, and then flush again right away......nothing happens right? This is because the tank doesn't have time to fill....PRELOAD is decreased in the tank.

What if the toilet is plugged up? When you flush, it backs up....this is too much afterload.

Preload = Volume

Afterload = Pressure/Resistance

https://allnurses.com/nursing-student...ad-887678.html

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Specializes in Critical Care, ED, Cath lab, CTPAC,Trauma.

This is a great site....Welcome to Critical Care Medicine Tutorials

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Specializes in Critical Care; Recovery.

Thank you Esme12. I'm a new critical care nurse and this website is very helpful. I was even able to print the information for my new binder I'm putting together for work.

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