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Hey guys, my name is Brad and welcome to nursing.com. And in today's video, what we're going to be doing is we're going to be discussing hemodynamics. Some of the more advanced cardiac hemodynamics surrounding cardiac output, preload, afterload, stroke volume, contractility, a lot of these fun, ambiguous words that we're going to bring some clarity to. Let's dive in.
So hemodynamics is a direct measurement of how well our blood is moving forward. How well our heart has the ability to pump our blood forward in our body. And we'll recall, this all really starts with the cardiac cycle. I really recommend that you go check out our heart tones and cardiac anatomy video, as these are going to really help bring more clarity to this topic. But remember it all starts with the cardiac cycle, S1 and S2, also meaning systole and diastole, or also meaning ventricular contraction, S2 meaning ventricular relaxation. All of our hemodynamics start with the heart.
So whenever we're talking about cardiac output, we have a little equation that we use to understand what cardiac output is. And that is SV times HR, right? (CO = SV X HR) What the heck are we talking about? SV is also known as stroke volume. This is something that's going to be crucially important for you to know. Stroke volume is essentially the amount of blood ejected out of that left ventricle per one beat, right, per one beat. And we multiply that by our heart rate. We know that heart rate is the amount of times that your heart beats per minute. So if stroke volume is the amount of blood ejected per one beat, and our heart rate is the amount of beats per minute. That's going to give us the total amount of blood ejected out of that left ventricle per minute. And that is what our cardiac output is. Our cardiac output is simply reflective of the amount of blood ejected per one minute.
So why is this important? Our heart rate is usually a constant, right now, granted this variability, but our heart rate is defined as “X” number of beats per minute. But what is our stroke volume? We know that the amount of blood ejected out of that left ventricle per one beat, but it begs the question, what are some of the factors that actually affect our stroke volume?
From the previous slide, I'll let you guys know that the normal cardiac output is four to eight liters per minute. I think it's also important that I let you know here, regarding stroke volume, that a normal stroke volume is 60 to 120 mLs of blood per beat. Remembering stroke volume is the amount of blood ejected from that left ventricle per one beat. But it's important to know what are the factors that are actually affecting stroke volume?
Well, there are three. The first one here is preload. Okay. Preload is often defined as the amount of stretch on that left ventricle at the end of diastole. Whenever that ventricle is at its most full, the amount of stretch. You may see that on an exam. But that was always confusing for me. The best way that I was able to visualize that is whenever we're talking about the heart and we've got these ventricles down here, instead of saying the amount of stretch on that myocardium, let's just say that our preload is the amount of blood in that left ventricle at the end of diastole. Okay. That's what your preload is. What are some things that could affect that. Let's say a patient was in a motor vehicle accident and they sustained a hemorrhagic shock. They are volume depleted. They've lost a lot of volume. That is going to affect the amount of blood that is returning back into that heart, and that is then going to be able to be ejected out of that left ventricle. That's going to affect your preload. And if your preload is down due to a hemorrhagic shock, you can imagine your cardiac output is going to be down as well.
Afterload is the second component that affects stroke volume. And essentially this is defined as how hard this heart right here, this left ventricle, particularly, how hard or what resistance that that heart has to pump against in order to get blood out of that left ventricle to the rest of the body. Imagine that a patient was in a hypertensive crisis. And so all of the vessels of the body are incredibly clamped down, incredibly narrow. And so that left ventricle is pumping blood out through the aorta, to the rest of the body, and imagine that all the vessels in the rest of the body are incredibly clamped down. That's going to provide an incredible amount of resistance that that left ventricle has to pump against. That's what afterload is. It's the amount of resistance that the LV has to overcome to eject blood out of the body or out of the heart. And you can imagine that it's going to affect your cardiac output, the amount of blood you're actually able to eject per minute.
And contractility, of course, this is going to affect your stroke volume as well. This is going to affect how much blood you're able to eject out of the blood during systole right? Imagine that a patient had sustained a myocardial infarction. So a portion of that heart is now damaged, diseased on that left ventricle and it's stunned. It is going to have an incredibly difficult time. It's going to be so loose to contract. So blood, the amount of force that it's going to be able to squeeze to get blood out of the heart is going to be greatly impaired. Any kind of issue with our preload or with our afterload or with our contractility, as we just discussed here, is going to affect our stroke volume, and therefore affect our cardiac output.
So whenever we're talking about therapeutic management, different kinds of pharmacological medications that we may use to assist somebody with impaired cardiac output, we're pretty much going to be using medications that are directly going to affect the three different factors that affect stroke volume: preload, afterload, and contractility. And then of course the other component that affects cardiac output heart rate.
So, in instances, let's say your preload is down, right? We're in that hemorrhagic shock state where we've lost too much blood. We don't have enough volume in that left ventricle to pump out. What might we see given? Well, in those kinds of instances, of course we could see fluids given. We may also end up seeing things like albumin, which is actually a large plasma protein given intravenously to pull fluid from your interstitial tissues back into the vessels, a way to try and increase preload.
Or, let's say that your preload is too high. You've got too much volume, your volume overloaded, congestive heart failure, for instance. In this situation, you may see diuretics given. Things to deplete that intravascular volume to reduce that preload.
Afterload. Same kind of thing. If your afterload is too high, in those instances of hypertensive crises, where all of your vessels are so narrowed and clamped down that your left ventricle was having to push against so much resistance. In those instances, what might we see given? We could see vasodilators or antihypertensives given right? All with the idea in mind to dilate those vessels, to allow the LV, to not pump against such resistance, right? To allow the LV to relax and not have to push against so much force.
Or let's say that our afterload is greatly reduced. We are systemically vasodilated in instances, such as septic shock. And instances with septic shock, your vessels are dilated to the point that blood is just pouring out. You know, you require some level of arterial resistance to allow blood to continue to move forward. You know, we've said previously, the more dilated your vessel is the more blood that's allowed to reach your end organs. But if you don't have some level of resistance, and in instances like septic shock where you're just massively dilated, blood is just falling out basically, and it's not able to reach the end organs. So in these instances, we may see things such as vasopressors given.
Now, contractility is another thing that actually affects your stroke volume, as we've already mentioned. So usually we're dealing with impaired contractility, poor contractility. The heart has become stunned for one reason or another. And we need to increase that contractility. And these instances, we're pretty much looking at positive inotropes, right? Medications that are going to increase the contractility of the heart. Maybe like milrinone, for instance.
And then we're going to be looking at, of course, the one other component up here that affects cardiac output, our heart rate. Medications that can increase or decrease your heart rate. If you needed your heart rate increased, for instance, in patients who were bradycardic, you may use something like atropine. Or, if you had a patient who was tachycardic and that's impairing your cardiac output, you could see something like a beta blocker given, right, ending in -olol, like metoprolol.
So to summarize some of our key points related to hemodynamics, we'll recall that hemodynamics are pretty much a measurement of how well our heart is able to push blood forward throughout our body. Recalling that this all begins with that cardiac cycle of S1 and S2. Now cardiac output equals stroke volume times heart rate (CO = SV X HR). Remember stroke volume is the amount of blood ejected from that left ventricle per one beat. And our heart rate is the amount of beats per minute. So our cardiac output is going to be measured in liters per minute. And you'll remember that a normal cardiac output is four to eight liters per minute of blood ejected out of that left ventricle per minute. Stroke volume. We're going to remember that there are three factors that affect stroke volume, right? Preload, afterload, and contractility. We’ll recall what preload, afterload, and contractility mean. And also knowing that all of our therapeutic management, our pharmacological interventions, are directly geared at affecting or altering a lot of those factors that affect our stroke volume. Also don't forget a normal stroke volume is 60 to 120 mLs per beat.
Guys, I really hope that this video helped bring some clarity to hemodynamics. I hope that this information really helps you as you move forward throughout nursing school. I hope that you guys go out there and be your best selves today. And as always, happy nursing.
So hemodynamics is a direct measurement of how well our blood is moving forward. How well our heart has the ability to pump our blood forward in our body. And we'll recall, this all really starts with the cardiac cycle. I really recommend that you go check out our heart tones and cardiac anatomy video, as these are going to really help bring more clarity to this topic. But remember it all starts with the cardiac cycle, S1 and S2, also meaning systole and diastole, or also meaning ventricular contraction, S2 meaning ventricular relaxation. All of our hemodynamics start with the heart.
So whenever we're talking about cardiac output, we have a little equation that we use to understand what cardiac output is. And that is SV times HR, right? (CO = SV X HR) What the heck are we talking about? SV is also known as stroke volume. This is something that's going to be crucially important for you to know. Stroke volume is essentially the amount of blood ejected out of that left ventricle per one beat, right, per one beat. And we multiply that by our heart rate. We know that heart rate is the amount of times that your heart beats per minute. So if stroke volume is the amount of blood ejected per one beat, and our heart rate is the amount of beats per minute. That's going to give us the total amount of blood ejected out of that left ventricle per minute. And that is what our cardiac output is. Our cardiac output is simply reflective of the amount of blood ejected per one minute.
So why is this important? Our heart rate is usually a constant, right now, granted this variability, but our heart rate is defined as “X” number of beats per minute. But what is our stroke volume? We know that the amount of blood ejected out of that left ventricle per one beat, but it begs the question, what are some of the factors that actually affect our stroke volume?
From the previous slide, I'll let you guys know that the normal cardiac output is four to eight liters per minute. I think it's also important that I let you know here, regarding stroke volume, that a normal stroke volume is 60 to 120 mLs of blood per beat. Remembering stroke volume is the amount of blood ejected from that left ventricle per one beat. But it's important to know what are the factors that are actually affecting stroke volume?
Well, there are three. The first one here is preload. Okay. Preload is often defined as the amount of stretch on that left ventricle at the end of diastole. Whenever that ventricle is at its most full, the amount of stretch. You may see that on an exam. But that was always confusing for me. The best way that I was able to visualize that is whenever we're talking about the heart and we've got these ventricles down here, instead of saying the amount of stretch on that myocardium, let's just say that our preload is the amount of blood in that left ventricle at the end of diastole. Okay. That's what your preload is. What are some things that could affect that. Let's say a patient was in a motor vehicle accident and they sustained a hemorrhagic shock. They are volume depleted. They've lost a lot of volume. That is going to affect the amount of blood that is returning back into that heart, and that is then going to be able to be ejected out of that left ventricle. That's going to affect your preload. And if your preload is down due to a hemorrhagic shock, you can imagine your cardiac output is going to be down as well.
Afterload is the second component that affects stroke volume. And essentially this is defined as how hard this heart right here, this left ventricle, particularly, how hard or what resistance that that heart has to pump against in order to get blood out of that left ventricle to the rest of the body. Imagine that a patient was in a hypertensive crisis. And so all of the vessels of the body are incredibly clamped down, incredibly narrow. And so that left ventricle is pumping blood out through the aorta, to the rest of the body, and imagine that all the vessels in the rest of the body are incredibly clamped down. That's going to provide an incredible amount of resistance that that left ventricle has to pump against. That's what afterload is. It's the amount of resistance that the LV has to overcome to eject blood out of the body or out of the heart. And you can imagine that it's going to affect your cardiac output, the amount of blood you're actually able to eject per minute.
And contractility, of course, this is going to affect your stroke volume as well. This is going to affect how much blood you're able to eject out of the blood during systole right? Imagine that a patient had sustained a myocardial infarction. So a portion of that heart is now damaged, diseased on that left ventricle and it's stunned. It is going to have an incredibly difficult time. It's going to be so loose to contract. So blood, the amount of force that it's going to be able to squeeze to get blood out of the heart is going to be greatly impaired. Any kind of issue with our preload or with our afterload or with our contractility, as we just discussed here, is going to affect our stroke volume, and therefore affect our cardiac output.
So whenever we're talking about therapeutic management, different kinds of pharmacological medications that we may use to assist somebody with impaired cardiac output, we're pretty much going to be using medications that are directly going to affect the three different factors that affect stroke volume: preload, afterload, and contractility. And then of course the other component that affects cardiac output heart rate.
So, in instances, let's say your preload is down, right? We're in that hemorrhagic shock state where we've lost too much blood. We don't have enough volume in that left ventricle to pump out. What might we see given? Well, in those kinds of instances, of course we could see fluids given. We may also end up seeing things like albumin, which is actually a large plasma protein given intravenously to pull fluid from your interstitial tissues back into the vessels, a way to try and increase preload.
Or, let's say that your preload is too high. You've got too much volume, your volume overloaded, congestive heart failure, for instance. In this situation, you may see diuretics given. Things to deplete that intravascular volume to reduce that preload.
Afterload. Same kind of thing. If your afterload is too high, in those instances of hypertensive crises, where all of your vessels are so narrowed and clamped down that your left ventricle was having to push against so much resistance. In those instances, what might we see given? We could see vasodilators or antihypertensives given right? All with the idea in mind to dilate those vessels, to allow the LV, to not pump against such resistance, right? To allow the LV to relax and not have to push against so much force.
Or let's say that our afterload is greatly reduced. We are systemically vasodilated in instances, such as septic shock. And instances with septic shock, your vessels are dilated to the point that blood is just pouring out. You know, you require some level of arterial resistance to allow blood to continue to move forward. You know, we've said previously, the more dilated your vessel is the more blood that's allowed to reach your end organs. But if you don't have some level of resistance, and in instances like septic shock where you're just massively dilated, blood is just falling out basically, and it's not able to reach the end organs. So in these instances, we may see things such as vasopressors given.
Now, contractility is another thing that actually affects your stroke volume, as we've already mentioned. So usually we're dealing with impaired contractility, poor contractility. The heart has become stunned for one reason or another. And we need to increase that contractility. And these instances, we're pretty much looking at positive inotropes, right? Medications that are going to increase the contractility of the heart. Maybe like milrinone, for instance.
And then we're going to be looking at, of course, the one other component up here that affects cardiac output, our heart rate. Medications that can increase or decrease your heart rate. If you needed your heart rate increased, for instance, in patients who were bradycardic, you may use something like atropine. Or, if you had a patient who was tachycardic and that's impairing your cardiac output, you could see something like a beta blocker given, right, ending in -olol, like metoprolol.
So to summarize some of our key points related to hemodynamics, we'll recall that hemodynamics are pretty much a measurement of how well our heart is able to push blood forward throughout our body. Recalling that this all begins with that cardiac cycle of S1 and S2. Now cardiac output equals stroke volume times heart rate (CO = SV X HR). Remember stroke volume is the amount of blood ejected from that left ventricle per one beat. And our heart rate is the amount of beats per minute. So our cardiac output is going to be measured in liters per minute. And you'll remember that a normal cardiac output is four to eight liters per minute of blood ejected out of that left ventricle per minute. Stroke volume. We're going to remember that there are three factors that affect stroke volume, right? Preload, afterload, and contractility. We’ll recall what preload, afterload, and contractility mean. And also knowing that all of our therapeutic management, our pharmacological interventions, are directly geared at affecting or altering a lot of those factors that affect our stroke volume. Also don't forget a normal stroke volume is 60 to 120 mLs per beat.
Guys, I really hope that this video helped bring some clarity to hemodynamics. I hope that this information really helps you as you move forward throughout nursing school. I hope that you guys go out there and be your best selves today. And as always, happy nursing.
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