Fundamentals of Hemodynamics Explained

Okay, when we talk about hemodynamics, and specifically when we talk about the parameters that are important to know for nurses, it can get very complex and very complicated. So what we're going to do today is we're just going to cover some of the very basic introductory terms for hemodynamics and some of the parameters that you need to know how they all play in together now we are going to have a chart available that will help you build learn hemodynamics and how they all play in together and that charts going to be available at NRSNG.com slash hemodynamics and that chart is we're going to kind of go over uh... because of that chart today that's gonna be available for free you can uh... go to the nars ng dot com slash human dynamics and uh... download that chart for free can share it print it uh... market up to whatever you want with it can be available in a pdf format so you can have it available in your notes and and take to work for everyone okay so what is human dynamics so human dynamics essentially is It's blood flow. It's the motion and equilibrium under the action of external forces. So what we're going to do today is we're going to talk about hemodynamics, and we're going to understand that blood flow just a little bit better, and the motion, and what's creating that equilibrium. Okay, so when we discuss hemodynamics, there's a few key terms that we really need to know. The terms that we're going to focus on today, of course, are going to be heart rate. We're going to talk about cardiac output and cardiac index. We're going to talk about stroke volume. And we're going to talk about preload, afterload, and contractility. Okay, we're going to talk about these several things and how they play in together and how they affect our hemodynamic equilibrium. And how they all interplay together. It's pretty neat how they all work together, and we're going to discuss each of these as we go. So first of all, it's pretty amazing how all these kind of work together. Right now we'll start with our heart rate. So our normal heart rate is going to be 60 to 100 beats per minute. And our heart rate, obviously, is the rate at which our heart is actually beating. So that's an important factor of hemodynamics because the rate at which our heart beats is going to affect how much blood actually moves throughout the system. So heart rate is going to directly affect cardiac output. Okay, so what is cardiac output? Okay, so cardiac output is the volume of blood that leaves the left ventricle. every minute. Volume from left ventricle every minute. And the normal value for that is going to be 4 to 8 liters per minute. Now, as people started assessing cardiac output more and more, they found that that volume that needs to leave the left ventricle every minute is going to vary from person to person. So in order to understand better if someone was getting enough cardiac output or not, we also analyzed cardiac index. And what cardiac index does is it takes cardiac output and divides it by body surface area. And what that does is that gives us a number based on how large the person is, if they're getting enough cardiac output or not. Okay, so cardiac index. So cardiac index is cardiac output divided by body surface area. Okay, and our normal range for that is going to be 2.5 to 4 liters per minute. per meter squared of body surface area. Okay, so that's going to really give us a better indication of cardiac output. Because it really bases it all off of the size of the individual. Okay, so we have our cardiac output, which is going to be the 48 liters per minute. And that's going to be just a generic number. We can use our cardiac index, which is the 2.5 to 4 liters per minute per meter squared. And that's going to give us a better indication of if this person is actually perfusing enough or not. Okay, so now what is going to affect our... cardiac output. Okay, the primary determinant of cardiac output is going to be our stroke volume. Okay, so what is stroke volume? Okay, so cardiac output is the volume that leaves the left ventricle per minute. Stroke volume, on the other hand, is the volume of blood that leaves the left ventricle every stroke. Volume from the left ventricle per stroke or per heartbeat. We'll say per beat. Okay? So there's the difference there. This is a volume per minute is our cardiac output. This is the volume per beat. Okay? So obviously our stroke volume is going to directly affect our cardiac output. The volume that leaves our left ventricular every beat is obviously going to affect the volume that leaves the heart every minute. And stroke volume is measured in. in milliliters per beat. And our normal value for that is going to be 60 to 120 mils per beat. OK? So that's kind of the easy part of this. And now we kind of get on to the more complicated aspect of this. But if we look back at this, so the volume of blood that leaves our heart every beat is going to directly affect the volume of blood that leaves our heart every minute. And that's going to directly affect our heart rate, or be affected by our heart rate. So as we work through this, we can adjust our heart rate to adjust our cardiac output. We can adjust our cardiac output with different things to adjust the heart rate and things like that. So now we're going to kind of move forward to something a little bit more complicated, and we're going to start up here with stroke volume. Okay, so we still have everything above what we just talked about, our cardiac output, cardiac index, and heart rate. But there's three things that essentially affect stroke volume. Again, stroke volume is going to be the volume of blood that leaves the heart with each beat, and our normal amount is going to be 60 to 120 milliliters per beat. Okay, and there's three things that affect our stroke volume, okay? So we'll draw three things here. The first thing is going to be our contractility. Okay. So our contractility is the ability of the ventricles to squeeze. It's the squeeze that those ventricles exert with each beat. And that can also be called our inotropy. And so, you know, when you hear about positive inotropes and things like that, what those drugs are doing is they're directly affecting. our contractility. So stroke volume is affected by contractility. It's also affected by preload. And it's affected by afterload. So what are preload and afterload? We'll just talk about this very briefly and very superficially. Preload essentially is your end diastolic volume. So you have your heart here. You have your atria on top, ventricles on bottom. So preload is going to be the amount of volume, essentially, within the ventricles at the end of diastole. So after the ventricles have filled, there's going to be a volume in there, and that volume is going to exert a pressure against those ventricles. That volume, that pressure, that is your preload. So as these are stretched at the end of diastole, that's going to be your preload. How much volume is in those ventricles at the end of diastole? Okay, so then what is afterload? Okay, so we understand preload. Afterload is going to be the amount of pressure that these ventricles are going to have to exert in order to get blood out of the ventricles. Okay, so here's our left ventricle. We're full of blood. Now, in order to actually open this aortic valve, We're going to have to exert a certain amount of pressure. That pressure is going to be determined by the, how dilated or how constricted our aorta is. And that pressure that we have to overcome to actually get blood into the aorta, that is the afterload. Okay? So our afterload is going to be affected by our systemic vascular resistance on our left ventricle. and our pulmonary vascular resistance in our right ventricle. Okay? So, what afterload is, is afterload is the amount of pressure, amount of force that has to be exerted in order to open the valves and get blood out of the ventricles. Okay? So, we understand that. So, stroke volume is affected by preload, contractility, and afterload. Preload. is the amount of volume, the amount of force exerted on the ventricles at the end of diastole, how full they actually get. Afterload is the amount of force required to open the aortic and the pulmonic valve. Okay? So, how can we affect these values? Okay, so we have preload and we have afterload. Okay, preload, let's draw our heart here. Preload is the end diastolic volume, amount of stretch that these ventricles experience at the end of diastole. Afterload, let's draw our heart here. Here's our aorta coming out of our left ventricle. And afterload is the amount of force required to open this aortic valve. Then we also have our pulmonic valve. So the amount of force required to open these valves and get blood out of there, that's going to be affected more by the vessels on the other side of that valve, how much pressure is being exerted back into those ventricles. Okay, so preload and afterload. So let's say we have an elevated preload. How can we decrease our preload? Okay, so to decrease preload, we can give things like vasodilators or diuretics. Okay, so let's say like in the situation of heart failure, your ventricles aren't going to be pumping as effectively and so the ventricles are just going to continue to fill with blood. And that blood's not going to squeeze out, and so we're going to have an increased preload. So if we want to decrease that preload, we can give something like a diuretic to get rid of that volume. We could also give ACE inhibitors. We could give ARBs, things like that. So let's say we want to increase our preload. We can give things like fluids to increase our volume. We can also give blood, depending on the situation. So In situations, for example, like septic shock or like a vasogenic shock, when we have severe vasodilation, we're not going to be filling our ventricles as much, so we're going to have less volume in here. We can give some fluids to increase that volume. Okay, so that would be how we increase and decrease preload. Now with afterload, let's say we have an increased afterload. Our afterload is really high. So what that's going to mean is we have very tight aorta, so that there's a lot of squeeze on that aorta. It's very constricted, and we're not able to get that open because that constriction causes that pressure required to open the aorta to go up. So we have a high afterload. We can get things like arterial vasodilators. We can get things like ARBs. We can give ACE inhibitors, and we can use other therapies like intra-aortic balloon pumps. So the way the intra-aortic balloon pumps work, let's see here. So we have our heart here. We have our aorta coming up here. Let's say it's coming down here. So an intra-aortic balloon pump essentially... Inserts a little balloon up into the aorta and when the When the ventricles are filling, this balloon in here inflates and it causes, so this is used in situations like ischemia and things like that, or if you really have a decreased aphelogen, you could use this intra-aortic balloon pump, but it's used more for situations of ischemia. So by inflating that, it's not allowing any blood to escape here and it's forcing more blood to fill these cardiac vessels. But then as this... opens up, what it's going to do is this balloon will deflate. So on systole, this balloon is going to deflate. And by deflating, it's actually going to pull some of that blood forward with it. So that's going to decrease our afterload as well. Okay, so that's another therapy that can be used there. Let's see. Okay, so let's say we have... a significantly decreased afterload. So we're opening that aortic valve too easily. So this is the decreases. So let's say we have a, so we need to actually increase our afterload. There's things we can give, mostly what we can give our vasopressors. So you could see this afterload. Maybe you have a patient with a blood pressure of like 60 over 40 or something like that, possibly also in like a shock state or a septic type state. So we can give things like vasopressors. So what vasopressors are going to do, let's say we have an extremely dilated aorta or arteries. What we can do is we can give vasopressors. And what that's going to do is it's actually going to cause these vessels to actually constrict. And that's going to require our heart to increase the force with which it contracts. And that's going to increase our afterload. So there's going to be things like norepinephrine. We can get things like neosynephrine. We can get things like vasopressin, epinephrine. So those things are all going to act in... different areas on the heart, or on the vessels, but they're all going to work in different ways to create vasoconstriction. Okay, so we've gone over that. Let's just look at this chart real quick. So this is kind of the chart that we went over. So we have our heart rate, and our heart rate is going to be affected by our cardiac output and our cardiac index. And then we have our stroke volume. which is our volume per stroke, per beat. And stroke volume is affected by our preload, our contractility, and our afterload. And then there's various therapies that we can do to increase or decrease each of these aspects. And by increasing or decreasing those aspects of our hemodynamics, we can actually manipulate the other variables. So that's really kind of a basic introduction to hemodynamics. We have another video up on preload and afterload, and we'll continue to get more videos up on this, but I hope that that kind of helps you see how they all play into each other. We do have a chart similar to this, but with the values and the therapies available for increasing and decreasing these values available on nrsng.com slash hemodynamics. So if you go to nrsng.com slash hemodynamics, we have this chart available that you can download. for free and it has some of the different therapies and things that you can use to alter these Aspects of the hemodynamics, so we appreciate comments if you have any questions or comments, please feel free to to leave them below and to Keep on getting this show going and getting people learning Please visit us at NRSNG.com And then also go to the hemodynamics page and you can download this chart for free We greatly appreciate you visiting with us, and we'll talk to you soon.

go to the nars ng dot com slash human dynamics and uh... download that chart for free can share it print it uh... market up to whatever you want with it can be available in a pdf format so you can have it available in your notes and and take to work for everyone okay so what is human dynamics so human dynamics essentially is It's blood flow.

It's the motion and equilibrium under the action of external forces. So what we're going to do today is we're going to talk about hemodynamics, and we're going to understand that blood flow just a little bit better, and the motion, and what's creating that equilibrium. Okay, so when we discuss hemodynamics, there's a few key terms that we really need to know. The terms that we're going to focus on today, of course, are going to be heart rate.

We're going to talk about cardiac output and cardiac index. We're going to talk about stroke volume. And we're going to talk about preload, afterload, and contractility. Okay, we're going to talk about these several things and how they play in together and how they affect our hemodynamic equilibrium. And how they all interplay together.

It's pretty neat how they all work together, and we're going to discuss each of these as we go. So first of all, it's pretty amazing how all these kind of work together. Right now we'll start with our heart rate. So our normal heart rate is going to be 60 to 100 beats per minute.

And our heart rate, obviously, is the rate at which our heart is actually beating. So that's an important factor of hemodynamics because the rate at which our heart beats is going to affect how much blood actually moves throughout the system. So heart rate is going to directly affect cardiac output.

Okay, so what is cardiac output? Okay, so cardiac output is the volume of blood that leaves the left ventricle. every minute. Volume from left ventricle every minute. And the normal value for that is going to be 4 to 8 liters per minute.

Now, as people started assessing cardiac output more and more, they found that that volume that needs to leave the left ventricle every minute is going to vary from person to person. So in order to understand better if someone was getting enough cardiac output or not, we also analyzed cardiac index. And what cardiac index does is it takes cardiac output and divides it by body surface area.

And what that does is that gives us a number based on how large the person is, if they're getting enough cardiac output or not. Okay, so cardiac index. So cardiac index is cardiac output divided by body surface area. Okay, and our normal range for that is going to be 2.5 to 4 liters per minute.

per meter squared of body surface area. Okay, so that's going to really give us a better indication of cardiac output. Because it really bases it all off of the size of the individual.

Okay, so we have our cardiac output, which is going to be the 48 liters per minute. And that's going to be just a generic number. We can use our cardiac index, which is the 2.5 to 4 liters per minute per meter squared. And that's going to give us a better indication of if this person is actually perfusing enough or not. Okay, so now what is going to affect our...

cardiac output. Okay, the primary determinant of cardiac output is going to be our stroke volume. Okay, so what is stroke volume?

Okay, so cardiac output is the volume that leaves the left ventricle per minute. Stroke volume, on the other hand, is the volume of blood that leaves the left ventricle every stroke. Volume from the left ventricle per stroke or per heartbeat. We'll say per beat. Okay?

So there's the difference there. This is a volume per minute is our cardiac output. This is the volume per beat. Okay?

So obviously our stroke volume is going to directly affect our cardiac output. The volume that leaves our left ventricular every beat is obviously going to affect the volume that leaves the heart every minute. And stroke volume is measured in.

in milliliters per beat. And our normal value for that is going to be 60 to 120 mils per beat. OK? So that's kind of the easy part of this. And now we kind of get on to the more complicated aspect of this.

But if we look back at this, so the volume of blood that leaves our heart every beat is going to directly affect the volume of blood that leaves our heart every minute. And that's going to directly affect our heart rate, or be affected by our heart rate. So as we work through this, we can adjust our heart rate to adjust our cardiac output. We can adjust our cardiac output with different things to adjust the heart rate and things like that.

So now we're going to kind of move forward to something a little bit more complicated, and we're going to start up here with stroke volume. Okay, so we still have everything above what we just talked about, our cardiac output, cardiac index, and heart rate. But there's three things that essentially affect stroke volume. Again, stroke volume is going to be the volume of blood that leaves the heart with each beat, and our normal amount is going to be 60 to 120 milliliters per beat. Okay, and there's three things that affect our stroke volume, okay?

So we'll draw three things here. The first thing is going to be our contractility. Okay. So our contractility is the ability of the ventricles to squeeze. It's the squeeze that those ventricles exert with each beat.

And that can also be called our inotropy. And so, you know, when you hear about positive inotropes and things like that, what those drugs are doing is they're directly affecting. our contractility. So stroke volume is affected by contractility. It's also affected by preload.

And it's affected by afterload. So what are preload and afterload? We'll just talk about this very briefly and very superficially. Preload essentially is your end diastolic volume. So you have your heart here.

You have your atria on top, ventricles on bottom. So preload is going to be the amount of volume, essentially, within the ventricles at the end of diastole. So after the ventricles have filled, there's going to be a volume in there, and that volume is going to exert a pressure against those ventricles.

That volume, that pressure, that is your preload. So as these are stretched at the end of diastole, that's going to be your preload. How much volume is in those ventricles at the end of diastole?

Okay, so then what is afterload? Okay, so we understand preload. Afterload is going to be the amount of pressure that these ventricles are going to have to exert in order to get blood out of the ventricles. Okay, so here's our left ventricle.

We're full of blood. Now, in order to actually open this aortic valve, We're going to have to exert a certain amount of pressure. That pressure is going to be determined by the, how dilated or how constricted our aorta is.

And that pressure that we have to overcome to actually get blood into the aorta, that is the afterload. Okay? So our afterload is going to be affected by our systemic vascular resistance on our left ventricle.

and our pulmonary vascular resistance in our right ventricle. Okay? So, what afterload is, is afterload is the amount of pressure, amount of force that has to be exerted in order to open the valves and get blood out of the ventricles.

Okay? So, we understand that. So, stroke volume is affected by preload, contractility, and afterload. Preload. is the amount of volume, the amount of force exerted on the ventricles at the end of diastole, how full they actually get.

Afterload is the amount of force required to open the aortic and the pulmonic valve. Okay? So, how can we affect these values? Okay, so we have preload and we have afterload.

Okay, preload, let's draw our heart here. Preload is the end diastolic volume, amount of stretch that these ventricles experience at the end of diastole. Afterload, let's draw our heart here.

Here's our aorta coming out of our left ventricle. And afterload is the amount of force required to open this aortic valve. Then we also have our pulmonic valve. So the amount of force required to open these valves and get blood out of there, that's going to be affected more by the vessels on the other side of that valve, how much pressure is being exerted back into those ventricles. Okay, so preload and afterload.

So let's say we have an elevated preload. How can we decrease our preload? Okay, so to decrease preload, we can give things like vasodilators or diuretics.

Okay, so let's say like in the situation of heart failure, your ventricles aren't going to be pumping as effectively and so the ventricles are just going to continue to fill with blood. And that blood's not going to squeeze out, and so we're going to have an increased preload. So if we want to decrease that preload, we can give something like a diuretic to get rid of that volume. We could also give ACE inhibitors.

We could give ARBs, things like that. So let's say we want to increase our preload. We can give things like fluids to increase our volume.

We can also give blood, depending on the situation. So In situations, for example, like septic shock or like a vasogenic shock, when we have severe vasodilation, we're not going to be filling our ventricles as much, so we're going to have less volume in here. We can give some fluids to increase that volume. Okay, so that would be how we increase and decrease preload.

Now with afterload, let's say we have an increased afterload. Our afterload is really high. So what that's going to mean is we have very tight aorta, so that there's a lot of squeeze on that aorta. It's very constricted, and we're not able to get that open because that constriction causes that pressure required to open the aorta to go up.

So we have a high afterload. We can get things like arterial vasodilators. We can get things like ARBs. We can give ACE inhibitors, and we can use other therapies like intra-aortic balloon pumps. So the way the intra-aortic balloon pumps work, let's see here.

So we have our heart here. We have our aorta coming up here. Let's say it's coming down here. So an intra-aortic balloon pump essentially...

Inserts a little balloon up into the aorta and when the When the ventricles are filling, this balloon in here inflates and it causes, so this is used in situations like ischemia and things like that, or if you really have a decreased aphelogen, you could use this intra-aortic balloon pump, but it's used more for situations of ischemia. So by inflating that, it's not allowing any blood to escape here and it's forcing more blood to fill these cardiac vessels. But then as this... opens up, what it's going to do is this balloon will deflate.

So on systole, this balloon is going to deflate. And by deflating, it's actually going to pull some of that blood forward with it. So that's going to decrease our afterload as well. Okay, so that's another therapy that can be used there. Let's see.

Okay, so let's say we have... a significantly decreased afterload. So we're opening that aortic valve too easily. So this is the decreases.

So let's say we have a, so we need to actually increase our afterload. There's things we can give, mostly what we can give our vasopressors. So you could see this afterload.

Maybe you have a patient with a blood pressure of like 60 over 40 or something like that, possibly also in like a shock state or a septic type state. So we can give things like vasopressors. So what vasopressors are going to do, let's say we have an extremely dilated aorta or arteries. What we can do is we can give vasopressors. And what that's going to do is it's actually going to cause these vessels to actually constrict.

And that's going to require our heart to increase the force with which it contracts. And that's going to increase our afterload. So there's going to be things like norepinephrine. We can get things like neosynephrine. We can get things like vasopressin, epinephrine.

So those things are all going to act in... different areas on the heart, or on the vessels, but they're all going to work in different ways to create vasoconstriction. Okay, so we've gone over that.

Let's just look at this chart real quick. So this is kind of the chart that we went over. So we have our heart rate, and our heart rate is going to be affected by our cardiac output and our cardiac index.

And then we have our stroke volume. which is our volume per stroke, per beat. And stroke volume is affected by our preload, our contractility, and our afterload. And then there's various therapies that we can do to increase or decrease each of these aspects.

And by increasing or decreasing those aspects of our hemodynamics, we can actually manipulate the other variables. So that's really kind of a basic introduction to hemodynamics. We have another video up on preload and afterload, and we'll continue to get more videos up on this, but I hope that that kind of helps you see how they all play into each other.

We do have a chart similar to this, but with the values and the therapies available for increasing and decreasing these values available on nrsng.com slash hemodynamics. So if you go to nrsng.com slash hemodynamics, we have this chart available that you can download. for free and it has some of the different therapies and things that you can use to alter these Aspects of the hemodynamics, so we appreciate comments if you have any questions or comments, please feel free to to leave them below and to Keep on getting this show going and getting people learning Please visit us at NRSNG.com And then also go to the hemodynamics page and you can download this chart for free We greatly appreciate you visiting with us, and we'll talk to you soon.

Transcript for:Fundamentals of Hemodynamics Explained

Transcript for:
Fundamentals of Hemodynamics Explained