Alright Ninja Nerds, in this video we're going to talk about cardiac output. So how do we define cardiac output? Cardiac output is basically your heart rate multiplied by your stroke volume.
So let's go ahead and dig into that a little bit more, because we're going to go ahead and talk about this in a pretty good detail. So first off, we're going to say that cardiac output, we're going to kind of denote that as CO. Okay, cardiac output, CO, is equal to your heart rate, we're going to denote that as HR, multiplied by...
your stroke volume. Okay, so what do we know so far? We know that the cardiac output is equal to the heart rate multiplied by the stroke volume.
Let's go ahead and dig into this little equation a tiny bit more and kind of get a little bit more of an idea of what cardiac output is. Well first off, we need to look at heart rate. What's the units for heart rate? The units for heart rate is actually going to be in beats per minute. So it's in beats per minute.
Whereas stroke volume is the total volume of blood that the actual ventricles are ejecting for every one beat. Okay, so heart rate is the amount of beats that are occurring per minute. Stroke volume is the total volume of blood in milliliters that is being pumped out of the ventricles with one beat. So if you look at it, the actual beats cancels out.
What are you left with here? Milliliters per minute. Now, let's even get into this a little bit more.
So we know that cardiac output is a total volume of blood that's being pumped out of the heart within one minute. How much is that? What's the normal amount?
Well, let's take the average heart rate and the average stroke volume. So then we'd have to say, okay, cardiac output is equal to the heart rate. What's the normal heart rate? Well, it's somewhere in between 60 to 80 beats per minute, right, on average. So let's take in between.
Let's say 70 beats per minute, okay? And let's multiply that by the stroke volume. On average, stroke volume happens to be around 70 milliliters, and we'll see how in a second.
So let's say that's about 70 mLs, all right, per beat. When we multiply these two, 70 times 70 is about what? 4,900, right? Let's round that up. Let's just round that up to about 5,000, what?
5,000 milliliters per minute. So it's approximately about 5,000 mLs per minute. Which if we just kind of like change that to a little easier number, 5 liters per minute.
So what do we know so far? Cardiac output is equal to the heart rate times the stroke volume. Its actual unit is the total volume of blood that can pump out in milliliters per minute. That volume is generally at around 5 liters per minute.
But you know that we can increase that significantly during certain situations like an exercise. Or we can decrease it significantly. due to parasympathetic innervation or other different types of things that we're going to talk about in this video. Okay, so now we got a good idea of what cardiac output is for right now. Let's go ahead now and decipher heart rate and decipher stroke volume.
So over here on the left side, we are going to primarily talk over here about heart rate. So this side over here is going to be primarily focused on heart rate. What we need to do is we need to talk about what...
Things influence heart rate and again what's the units for heart rate? It's right around beats per minute and we said it was an average we said that there was an average heart rate that average heart rate was somewhere around 60 to 80 beats per minute right within that range right we can even bring it up a little bit more we can actually say the normal heart rate is in between 60 to 100 anytime you go greater than 100 then it actually is considered to be tachycardia but for right now I want to talk about this one The reason why is who sets this 60 to 80 beats per minute? Who sets that? That is the job of the SA node. So if you guys remember, the SA node is the one who is setting what's called your sinus rhythm.
So he's the one that's setting the sinus rhythm. He's the one that's generating those what? He's the one that's generating those intrinsic abilities, the action potentials that can be sent out throughout the heart. So he is the one that's generating this nice.
Rhythm. He's generating the sinus rhythm which is right around 60 to 80 beats per minute. Now here's something we have to think about. We know that the heart has the ability to intrinsically depolarize, generate action potentials, and send it out to the myocardium to trigger the myocardium to contract. And that's right around 60 to 80 beats per minute.
But how can we increase that? How can we fluctuate that heart rate? Well one way that we can do that is we can actually cause the production of sympathetic nervous system neurotransmitters.
Well, one way is the sympathetic nervous system. You know the sympathetic... The nervous system is basically the one that is releasing certain chemicals.
What are those chemicals that it's releasing? Remember it's releasing norepinephrine? So norepinephrine was one of the big ones there, acting on the beta-1 adrenergic receptors. What was another one? Another one was epinephrine.
Remember epinephrine? Epinephrine was actually released by the adrenal medulla. And this also was influencing the heart rate by acting on the beta-1 adrenergic receptors. We already went through that mechanism in extrinsic innervation of the heart.
So what kind of action do we say it had? If I draw here a positive, what does that mean? It means it's a positive effector of the heart rate, meaning that it can increase the heart rate. That's called chronotropic action. So really, what is he then?
He's a positive chronotropic agent. So your sympathetic nervous system is a positive chronotropic agent. It can increase the heart rate. That's one thing. But then let's take the flip side.
Let's say that I want to decrease the heart rate. If I want to decrease the heart rate, how do I do that? Well then I can actually target this with acetylcholine.
Remember acetylcholine is a part of the parasympathetic nervous system? So if it's a part of the parasympathetic nervous system, this is releasing acetylcholine onto those muscarinic type 2 receptors, if you remember, which is causing the potassium ions to leave the cell, causing the cell to hyperpolarize. It was also inhibiting the production of cyclic AMP and basically causing the cell to slow down the rate of action potentials.
So this is a negative chronotropic agent. So, so far we know that the sympathetic nervous system is a positive chronotropic agent. The acetylcholine, which is a part of the parasympathetic nervous system, is a negative chronotropic agent.
What else? So, so far what do we have here? Let's write these down here.
We have a positive one, a positive stimulator is the sympathetic nervous system. A negative regulator. or negative chronotropic is the parasympathetic nervous system via the acetylcholine.
So this is the acetylcholine and then the sympathetic nervous system was with the presence of epinephrine and norepinephrine. So norepinephrine and epinephrine. Sweet.
What else? Hormones. Hormones also have a very positive effect too.
You know there's a special hormone who also can come here and actually increase the heart rate too. Let's actually show this guy like this. Look right there.
This guy is called thyroid hormone, so T3 and T4. These also are a very powerful regulator, very, very powerful regulator of the heart rate, and they can increase the heart rate, okay? They can increase the heart rate, okay? So, so far we have hormones.
So what's another positive regulator of this? We're gonna say thyroid hormone, so T3 and T4. This is a good one. You know what else T3 and T4 can actually do?
They can increase your basal metabolic rate. When you increase your basal metabolic rate, what does that do? What is one of the byproducts of metabolism? Heat.
As you start generating a lot of heat, what does that do? It amps up your metabolic rate, so you're actually breaking down substances a lot faster. As you start breaking down substances a lot faster, you generate more energy.
You generate more heat, so it speeds up the metabolic rate. That's another thing about T3 and T4. Whenever you have an increase in the internal body temperature, whether it be due to T3 and T4 or whether it be due to exercise, because you know during exercise you generate a lot of heat. That amps up your metabolic rate. So one of the other things that we can say that actually is going to affect the heart rate here is we can also say it could be body temp.
We can say the body temperature is a huge regulator. Generally, if you want to stimulate it, you want to have an increase in the body temperature. If you want to slow down the heart rate, whenever you're increasing the body temperature, this is increasing the metabolic rate. So again, whenever you increase the body temperature, this is going to stimulate.
and increase the metabolic rate, increase the speed of the actual heart rate. So again, what we say here, if you increase the body temperature, this is another positive chronotropic agent of the heart. Now let's talk about something else.
What about ions? Ions are very critical here. What kind of ions are really important in this area?
You know there's calcium? Calcium is super important. Calcium is a very important regulator. You know whenever you have calcium levels there's two situations I say that you have high calcium levels and let's take that the opposite of this and let's say low calcium levels so calcium is a very important regulator of the heart rate if you have high calcium levels this tends to speed up the heart rate there is conflicting evidence on this but for the most part most literature supports that it's going to be hypercalcemia drives an increase in the heart rate because more calcium is coming into the cell triggering the increase in the actual depolarization and the action potential sent out to the heart muscle. So that's one thing.
So really, we can actually, let's separate these. Let's say that this one here is actually the high calcium. So high calcium would do what?
It would act as a positive chronotropic agent. But let's take The actual opposite and let's say that we have low calcium levels. Low calcium means that less calcium is coming in from the extracellular fluid.
This is going to be a negative chronotropic agent. Okay, so so far we have calcium being an effect there. What else? Potassium.
Potassium has another influence on the heart rate. So if we have potassium, let's say that our blood is really high in potassium. What do you call when you have high potassium levels in the blood?
They're called hyperkalemia. What happens is... Imagine here for a second I draw a cell. Let's say I draw a small cell here, and I just want you to understand something just about the cell.
Our cells are basically filled with a ton of potassium. And if you have a blood vessel circulating nearby here, let's say here's a blood vessel and it's circulating nearby, and the potassium levels are higher out here in the extracellular fluid and lower here in the cell, what's going to happen? It's not going to move against its, it's not going to move down its concentration gradient, it's going to have to move against it.
That means less potassium will leave the cell. Why is this so bad? Because this can actually cause the heart to go into cardiac arrest. So hyperkalemia is very, very, very dangerous, okay?
So that's one of the really, really important regulators here, is that high potassium levels can significantly negatively inhibit the heart rate. It is one of the more important ones because it's going to affect the heart from being able to send action potentials and cause the person to go into cardiac arrest. And the same thing though, um... Other things that actually get affected is the low potassium.
Low potassium allows for the potassium to leave more quickly. And so again, potassium ions can actually cause arrhythmias. So any change in these ions can have negative, negative effects.
They even say, you know what else is really weird here? So what else do we have here? Let's actually put over here just in general. We said that if we have high potassium levels, high potassium levels are going to be a negative inhibitor. They're going to be an inhibitor, right?
And if we have high calcium levels, High calcium levels are going to be a stimulator. We said that if we have low calcium levels, low calcium levels is going to be an inhibitor. Now there's something else that's kind of interesting.
Let's say here, I draw quickly, the another component, which is going to be right here. Let's say that I have here the aorta. So here's just a little small aorta here. And you know, coming off the aorta, you have what's called that brachiocephalic trunk, which splits into the Common carotid, which goes into the subclavian, and then this common carotid here, right, which splits into the internal carotid artery and the external carotid artery.
Right there at that bifurcation point, we have these specialized cells right here. What were these cells here called? They were called the chemoreceptors. They were chemoreceptors.
There were some there, and there were also some here. Whenever our partial pressure of oxygen is really low, or the partial pressure of CO2 in the blood is really high, or our pH is really low, It stimulates these chemoreceptors. And what do these chemoreceptors do?
They carry this information to the central nervous system. And when they take it to the central nervous system, what does the central nervous system do? It integrates that information, right, within the medulla and tries to increase your respiration rate.
But you know what else it can do? Let's say here I have a small little cross section here of the brain. Just a small little one here. And I draw here like this.
Here's my midbrain, here's the pons, here's the medulla, and here's the spinal cord. Real quick, right? Right here, what will happen is these chemoreceptors will take the information into the medulla.
And in the medulla, we have that nucleus of tractus solitarius, right? What will happen is he can stimulate the cardiac acceleratory center. As a result, what will the cardiac acceleratory center do?
It'll send out these impulses to what? It'll send out the impulses to the heart. And what will it try to do to the heart?
It'll try to result in an increase in the heart rate because it's going to have sympathetic effect. Okay, so I want you guys to realize what is another effector of this. Any type of situation in which there is hypoxia, there's an increase in the partial pressure of CO2, there's a decrease in the pH, they can activate the chemoreceptors and try in an attempt to increase the heart rate.
But again, it's not as significant of an effect as it is on respiration, okay, because really the more powerful effect that you need to realize is it goes to the respiratory centers. And these respiratory centers go to your actual lungs. And then try to do what? Increase the actual respiration rate and the depth. Just so we're clear, this is the more potent effect.
All right? But there is a minor effect here for the heart rate. So what can we say then?
We can say stimulation of these chemoreceptors, these peripheral chemoreceptors, due to some type of situation where there is a decrease in the oxygen, increase in the CO2, decrease in the pH, these things... can try to increase the heart rate. So again, we said stimulation of peripheral chemoreceptors. will act as due to what?
What are the stimuli here? Low partial pressure of oxygen, increased partial pressure of co2, and a decrease in the pH. These are going to get stimulated here and they do what to the heart rate? They stimulate the heart rate. So stimulation to the peripheral chemoreceptors due to these things stimulate an increase in the heart rate.
Okay? Alright, sweet deal. So we covered that.
Now I want to talk about something else. What about just general things? What about Me being like a generally like I say that a child what about a child's heart rate in comparison to my heart rate?
So you know fetus the fetuses have an extremely extremely fast heart rate. Their heart is pumping like no other. So when you talk about age, age is also another factor.
So let's compare here if we were to compare let's say that we have like a fetus or an infant so fetus you know slash infant they have super super high heart rates. Okay, so they can go from like 120 to 140 beats per minute. Okay, that's like the fetus.
Then let's take like adults. Again, adults should range. Adults should range anywhere from 60 to about 100 beats per minute.
That's a good range for it. Now, let's even get into this a little bit more. Adults, obviously there's two different types of sexes, right? Hopefully, there's going to be males and females. So if we look here and we split this out, let's say that we look here at males.
And we look here at females. What's the difference here? Do you know that females actually have a faster heart rate?
So females heart rate ranges because we said it's between 60 to 100. Well really if we take the intrinsic ability it's really 80. Anytime you go above 100 is tachycardia. So males they have a kind of a slower heartbeat. Theirs is right around 64 to 72 beats per minute.
And again this is at rest. When we talk about females theirs is a little bit higher. Theirs can go from about 72 to 80 beats per minute. Okay, so theirs is a little bit higher than ours. Last thing, so I guess it's like the circle of life.
So for the fetus and the infant, it's really high. For the adults, it's kind of low, right within this age. And as you start to get a little older, as you get a little older, it actually can go back up sometimes. This fluctuates. This obviously varies.
But generally, theirs can actually increase a little bit as you get older, okay? So that's kind of the factor of age. So we said that with age, fetus has a very high heart rate. Adults, we can say they try to keep a heart rate around 60 to 80 beats per minute, but in females, okay, I'm sorry, males, it's right around 64 to 72. Females is a little faster, 72 to 80 beats per minute, okay?
So we talked about that. Wow, a lot of things that are affecting the heart rate, isn't there? A significant amount of things.
Now, last thing I want to talk about is what is this thing that we talked about with tachycardia and stuff? So there's two terms that we need to get straight here. One is called bradycardia, bradycardia, which is basically defined as whenever the heart rate is less than 60 beats per minute. So this is a situation in which the heart rate is less than 60 beats per minute. It's a terrible situation, right?
For certain things, what could be causes of bradycardia? There could be many causes of bradycardia. Could be due to... Like a parasympathetic nervous system is activated there. Could be due to other things such as certain drugs.
Certain drugs could even slow it down. Could be due to another thing. You know, really weird in endurance runners.
People who run excessively. They put their heart through a lot of work. And that's kind of a good thing in a way. But as they're actually exercising and they're doing these long endurance activities, the heart starts getting really strong.
Very, very strong. And so it doesn't require as much high of a heart rate because their stroke volume and their actual cardiac. So you know let me explain like this. We know that cardiac output is dependent upon heart rate and stroke volume.
Because these endurance runners are working so hard, okay, so these endurance runners, people who are doing like marathons and stuff, we can split up cardiac output we set into heart rate times the stroke volume. These people their stroke volume is so high. Why?
Because the myocardium is really strong. They're having good preload, they're having good contractility. So for these people, they have good, a lot of preload, and a lot of contractility.
So that's increasing their stroke volume. Because of that, the heart rate can slow down because the stroke volume is taking over the primary effect of cardiac output. So we can bring the heart rate down a little bit, okay, to allow for the heart to have time to rest.
So again, cardiac output we said. It's dependent upon heart rate and stroke volume. In endurance activities, people who are doing this consistently, their heart rate will start to drop really, really low.
Because their stroke volume is so high because their myocardium is very strong. Okay? So that's something you might see in people who are bradycardic.
But then if you take the opposite side of that, you take someone who's actually going to be on the opposite scheme. So now we say that the person is tachycardic. So now that we say that the person has tachycardia, in other words, they're having a heart rate that is greater than 100 beats per minute.
And obviously there could be many causes of this. Could be sympathetic nervous system activity. Could be due to high T3 and T4. Could even be due to certain drugs.
Could even be due to anxiety. So certain types of emotional factors. If you ever notice someone who's having certain psychological disorders or are very anxious, they have a very, very, very fast heart rate. So that covers that part for heart rate. Now what I want to talk about is I want to go into the actual stroke volume.
I want to talk about stroke volume a little bit. So let's come over here now. Let me get all my markers over here.
Let's make this nice and colorful. All right. Now we're going to talk about stroke volume. So we said that stroke volume is basically, what did we say? We said it was basically the milliliters that is being pumped out of the ventricles per beat.
But let's actually dig into this a little bit. So there's actually an equation for stroke volume. There's actually an equation.
The equation for stroke volume is you can take the total volume of blood that's coming to the heart and filling the heart. So let's say that I have blood coming from the inferior vena cava, I have blood coming from the superior vena cava, and I have blood coming from the coronary sinus, and it's emptying into the right atrium. I have blood coming from the pulmonary veins, from the right side and the left side, and these are emptying into the actual left atrium, and then it's emptying into the...
ventricles as a result, right? Whenever the atrium goes systole, they push it down. But if you remember, we talked about this in cardiac cycle, about 70 to 80 percent of the blood passively flows down without contractile activity.
So let's say that the blood is sitting here in the heart, just accumulating there, right? So the blood's just sitting there in the heart and accumulating. That volume of blood that is sitting in the heart before the heart even contracts, it's during the relaxation period when the heart is in diastole. This is called the end diastolic volume.
Okay, on average, The EDV is approximately around 120 milliliters. It could range from about 120 to 140. We're going to put down 120 for right now, okay? Then, if I take the EDV and I subtract it from what's called the ESV.
So, how do we define EDV? We should actually write this out. EDV is defined as end diastolic volume. Okay, so EDV is basically defined as the end diastolic volume.
I like to think about it as basically like the pre-pumping volume. So it's the volume of blood that's in the heart before your ventricles are going to contract. So EDV is basically the end diastolic volume. ESV stands for end systolic volume.
So this is the volume of blood that's remaining in the heart after the ventricles have contracted or undergone systole. So let's say that after this, you take the blood and you eject it up through into the pulmonary trunk and out to the lungs, or you eject the blood from the left ventricle up into the aorta and out into the actual peripheral and systemic circulation. The blood that's remaining, so we said originally, let's say it was like 120. Now let's say that we just decrease this a little bit.
Now the amount of blood that's sitting in here after that time, there's less blood now here, right? That volume of blood that's remaining after the contraction is called the ESV. This is on average about 20%. 50 milliliters.
It can range from 50 to like kind of like 70. So now what I'm gonna do is I'm gonna take and subtract this. So if I take and subtract this, that's my stroke volume. My stroke volume is equal to 120 minus 50. That's 70. So 70 milliliters.
Okay, and then again how much per beat? So this is what we can say is equal to the stroke volume. Now, we gotta even go into a little bit more depth unfortunately, because now we can actually say the stroke volume is divided into three other subcategories. So let's say that we take stroke volume and we we divide this. Take stroke volume here and I'm going to take and divide stroke volume into three categories.
Let's actually bring it down here so we have plenty of room here. Actually bring it down here. So right here. Stroke volume is actually broken into three categories. One of the categories is called preload.
Okay so this is stroke volume. One is dependent upon preload. The other one is dependent upon what's called contractility. So contractility.
And the last one is dependent upon a term called afterload. Afterload. Alright, let's go ahead and decipher each one of these things and what affects them and how that affects stroke volume and how that affects cardiac output. Okay, so first off, preload. How will we define preload?
Preload is basically the degree of stretch of the cardiac muscle. So we can really just, the simplest way of defining preload is how much the actual myocardium of the heart is stretching when it's getting filled with blood. Okay, that's how we define preload. So we can really just say that this is kind of like the stretch of the heart. So the stretch of the heart.
More stretch, the more preload there is. The less stretch, the less preload it is. Okay, well how do we stretch the heart out? How do we do that? Get a lot of volume in there.
So what's the volume of blood that's accumulating in the heart when the heart is actually in diastole or relaxation? EDV, end diastolic volume. The more of that I have, the more it's going to push on the heart and stretch the heart, and that's going to increase the preload. Okay, so one of the things I can say right away for this is if I increase my end diastolic volume, I'm gonna increase my preload. I'm gonna stretch the walls even more.
Okay, well that leads to a next question. How in the heck do I increase my end-hystolic volume? One way that you can do it is to get a lot of venous return. What is that?
You know how we actually have here, let's say I make a tiny little heart here real quick, tiny little one. Okay, let's say here, okay, I have, let's say I have here this vein here. This is my inferior vena cava, right, inferior vena cava.
Let's say down, I have some veins in my legs here. Okay, you know veins have valves. We talked about this in blood vessel characteristics.
We said that veins are very low pressure though. Veins are very low pressure. They have a hard time being able to get blood up on their own. So one of the ways that we can increase that is you know we have some muscles nearby. And we can actually have these muscles, we said, contract.
And when they contract, they squeeze on the veins and help to pump some of the blood upwards. We call that that muscular milking activity, right? We call it the milking activity.
It sounds weird, but that's one of them. One of the ways that we can increase this venous return. is by increasing the muscular milking.
That's one way. Another one, whenever you're breathing, let's imagine I take in some good breaths, right? I'm changing my thoracic cavity volume, and I'm changing my abdominal pressure. So whenever you're breathing, during that breathing process, the abdominal cavity pressure actually goes up, and that compresses some of the veins within the abdominal cavity. When you're breathing your thoracic cavity volume is going to increase so the pressure in there is going to decrease.
So what did I say? Abdominal cavity pressure is going to increase, thoracic cavity pressure is going to decrease. What happens is, you can kind of think of it like this.
Let's say that I actually get rid of, let's say I make another little heart here. And let's say I kind of do it like this right here. Okay. Let's say here is actually going to be where my diaphragm is. Let's say here's the diaphragm.
The pressure in the abdominal cavity is going to be very high, so high abdominal pressure. But the thoracic cavity pressure above the diaphragm is going to be low. Where do things like to move? Why did I put TBB?
The thoracic cavity pressure, so I put TCP. If this is high, things like to go from high pressure to low pressure. So what it does is it sucks the blood upwards.
If it sucks the blood upwards, it's kind of acting like a nice little vacuum or pump. That's called the respiratory pump. So the respiratory pump is whenever you're breathing, you increase the abdominal cavity pressure, decrease the thoracic cavity pressure, and suck blood up like a vacuum.
And that helps to increase the actual respiratory venous return here. Sorry. So this would be the respiratory pump. Another thing is your sympathetic nervous system. They have control over your venomotor tone.
So your sympathetic nervous system, can actually come over here and do what? It can act on the smooth muscle in this area by releasing what chemicals? Neuroepinephrine. And this can actually stimulate the contractility of the smooth muscle to cause small little increases in the contractility to push the blood upwards. So we can also say another positive regulator of this is going to be what's called venomotor tone.
Venomotor tone, or just venoconstriction. So we can actually subclassify this as vino. constriction.
So this is kind of helping to squeeze some of the blood upwards. Alright, one more thing is the filling time. That's another thing that's important. If you don't give the heart enough time to fill with blood, that's not going to stretch the heart.
So giving the heart adequate time to fill with blood. What does that mean then? You really, this is where that heart rate thing can actually be very, very devastating.
If you have an increased heart rate, you don't give the heart enough time to fill with blood. Because you just keep causing it to push and push and push as much blood as it can out. It's not relaxing enough. So because of that, if you increase the heart rate too much, that can actually decrease the actual filling time.
And if you decrease the filling time, you're going to decrease your actual preload. Okay? And that's not good. Okay?
One other thing is just related to the stretch. What if you actually, what if your heart can't stretch very well? Because of myocardial infarctions.
So let's say that for whatever reason, you've had many myocardial infarctions, MIs. What happens to the heart muscle? It gets replaced with fibrous tissue. Does fibrous tissue stretch very well? Not really.
It's not going to, it's not, it doesn't have a lot of give. So because of that, it's going to affect the preload. So that's what we know about preload.
We know that preload is the stretch of the muscle. If there's an increase in the EDV due to increased venous return from muscular milking, respiratory pump, venomotor tone, right? Or there's a lot of, there's enough time to fill the heart.
So you're going to have to increase the diastole. By doing that, you're not going to want to have the heart rate too high because if the heart rate's too high, it doesn't have enough time to fill with blood. And the last thing is you want the heart to be healthy.
You don't want it to be not able to stretch. So you don't want there to be a lot of fibrous tissue from MIs. All right? That kind of covers that thing.
Last thing I want to relate with this is a law. And laws are important. Okay?
Laws are important. This law here is a really important law. Let's actually make it a different color. This law is related to this.
It's called Frank Starling's Law. And what Frank Starling's Law says... is that whenever you have an increased stretch on the heart, so whenever there's increased stretching of the heart, it allows for this length-tension relationship, more cross-bridges to be active. So whenever there's stretching of the heart, and there's optimal cross-bridge connections, that increases the preload. If you increase the preload, you're going to significantly increase the stroke volume.
So Frank Starling's Law of the Heart, just in basic terms here, says The greater the stretch, the greater the force of contraction. So how will we say Frank Starling's Law? Just to sum it up here, greater stretch, there's more cross bridges, and the more cross bridges within the optimal length is the best. Greater stretch equals greater contraction. That's the relationship between this.
So greater the stretch, the greater the actual force of the contraction. Alright, sweet deal. That's that part.
Next thing we have to talk about is contractility. Contractility is super, super crucial. This is a really, really important one. So one of the things about contractility is that we can actually say that contractility is actually dependent upon, one of the big things, is the sympathetic nervous system.
So contractility is super, super dependent upon the sympathetic nervous system. How? Because if you release the chemicals like epinephrine, and norepinephrine.
What are these guys doing? They're acting on those beta-1 adrenergic receptors. If they're acting on these beta-1 adrenergic receptors, what was their overall effect?
They were increasing the calcium levels in the cell. As you increase the calcium levels in the cell, what starts happening to the actual cross bridges? They increase. This increases the actual contractility.
So you're gonna have more frequent contractions and that increased the stroke volume. What else? Hormones.
Same thing. But this is interesting. Some people kind of get like a little messed up with this one. Let me get this over here so we don't confuse this one here.
Okay, so we know that the norepinephrine acts on the beta-1 adrenergic receptors and basically increases the calcium, which increases the contractility. Okay. Hormones are an important one.
What kind of hormones? T3 and T4. These guys are crucial. But how do they do it?
This is a real weird one. We've already talked about it in the thyroid hormone video, but what happens here, let's say I have a cell here. Let's say that's a myocardial cell, and let's say here's my T3 and my T4, okay?
And it comes into this cell, and it acts on basically an intranuclear receptor. And when it binds onto this intranuclear receptor, it stimulates these genes. And what these genes can do is they can produce a bunch of different types of proteins. One of the proteins is it increases the expression of those beta-1 adrenergic receptors.
So T3 and T4 can act on the myocardial cells by increasing the expression of beta-1 adrenergic receptors. So that's a beautiful thing. If you have more of these, you have more receptors for norepinephrine and epinephrine to bind to. If they bind on to this, they're gonna have a more amplified effect.
Okay, so that's one thing. Another really interesting one is glucagon. Glucagon also has the ability to do this too. So increase in the actual glucagon.
So glucagon can actually also increase the actual contractility. Something else here is drugs. Obviously certain drugs can do this too, like digitalis.
Digitalis Actually has that effect. Dopamine has that effect. Epinephrine has that effect.
There's so many different drugs here. Epinephrine, I'm not even gonna try to spell that because I always butcher that one. I'm gonna put epi. Okay, so you guys get it.
There's a lot of different types of drugs that you could use here. You can even use what's called dobutamine and isoprenolene. There's a lot of different drugs here.
Atropine. But these are trying to increase. So I'm gonna put here on the side here, they're trying to stimulate the increase in contractility through various different mechanisms. Like digitalis is a sodium potassium ATPase inhibitor which increases the calcium levels inside of the cell.
Dopamine, he actually works through different weird ways. Dobutamine acts on the beta-1 adrenergic receptors and atropine actually blocks the acetylcholine on the M2 receptors. Basically, it's trying to increase the calcium levels inside of the cell to increase the contractility.
But at the same time, you have to have those that oppose, right? So you even have those who can block certain channels. You can use beta blockers, okay? Like metoprolol, atenolol.
propanolol. You can even use calcium channel blockers. And these calcium channel blockers, you could use like verapamil, you can use diltiazem, nifedipine.
So calcium channel blockers are also really good ones too. Okay, there's a ton of different things that you could use to try to be able to inhibit the contractility. All right, sweet. So these guys here are inhibitors.
So beta blockers and even some calcium channel blockers, right? All right, so that covers that part. Now, one other thing though is ions.
Ions also have an effect here too. So ions, it's kind of interesting here. We could say, same thing here, things like calcium.
If you have increasing calcium levels, this is actually a stimulator because there's more calcium that's going to be coming into the cell. If there's less calcium, hypocalcemia, this is an inhibitor of contractility. If there's actually high amounts of potassium, this is actually an inhibitor of contractility.
And if there's high amounts of sodium, hypernatribia, this is actually an inhibitor of contractility. So certain situations, ions can actually have a negative effect here too. You know what else has a really negative effect?
Protons and acidosis. So when someone has really high amounts of protons during acidosis, this is also a very, very powerful inhibitor of the actual heart, the contractility. Leads me to another term.
Whenever you're trying to increase the contractility of the heart, It's dependent upon what's called inotropic action. So if something is trying to stimulate the contractility of the heart, they're called a positive inotropic agent. So for example, calcium is a positive inotropic agent if it's in high levels. Epinephrine or epinephrine are positive inotropic agents. T3 and T4 and glucagon are positive inotropic agents.
Digitalis, dopamine, dobutamine, atropine, epinephrine, all those guys are positive inotropic agents. But things like beta blockers. or calcium channel blockers or other different types of drugs, those are negative inotropic agents. And if you think about it like this, potassium, high amounts of potassium is a negative inotropic agent.
High amounts of sodium is a negative inotropic agent. High amounts of protons like acidosis is a negative inotropic agent. Okay?
I think we beat the dead horse there for the inotropic agents. Let's do the last thing here. Let's bring Afterload over here a little bit.
Okay, let's bring this Afterload over here a little bit. So afterload is kind of a really interesting one because it has a lot of clinical relevance here too. Because this is one of the common things that people suffer with a lot is hypertension, which means that they're going to have a lot of afterload coming up.
So if we come over to this last one, this last one here is afterload. How do we define afterload? Afterload is basically defined as the amount of resistance that must be overcome in order for what?
In order for the ventricles to eject blood into the actual aorta or into the pulmonary trunk. So for example here, let's say I draw another little mini heart here real quick here. So I have another little mini heart here and I show it like this. Let's say here's my actual right ventricle here.
So here's my right ventricle. I'm trying to pump blood out. As I'm trying to pump blood out, let's say that this valve here is stenotic. I'm having a hard time to be able to push the blood out.
So if there's a stenotic valve, it's going to be really, really hard to push blood across that stenotic valve. That's a lot of resistance. That's a lot of resistance that I have to overcome to push the blood out.
What about if I look at the other side? Let's say that I look at the left ventricle, because this is more common with the left ventricle. Let's say that I draw here this tiny little heart here, and here's my aorta. And there's the aortic valve there.
What if that's stenotic? Or what if I have, by some terrible situation here, I have some type of plaque there? Some type of coronary atherosclerotic plaque or whatever it might be that's occluding the blood flow in that area. That's another negative thing.
That's also going to increase the amount of resistance I'm gonna have. overcome. What if I have, you know how when your vessels, they come down here, they go to capillary beds and then these, they branch out here.
And we said that one of the most important guys for resistance here is your arterioles because your arterioles have that smooth muscle that respond to like apprehension. and norepinephrine. So whenever these guys, these different types of vasoconstrictors here, I'm going to put here for positive for the vasoconstrictors, they're going to act on that smooth muscle and cause the smooth muscle to contract.
As the smooth muscle contracts, what happens to this blood flow? It's impinged. heated from moving through there. And so what can happen is this pressure can actually move this way, backwards.
So because you're constricting this, the pressure is backing up behind it. As this pressure is backing up behind it, then look what happens to the pressure within the aorta. It increases. If the pressure in the aorta increases, that's going to be harder for me to be able to push blood out.
Let me explain it another way. Let's say, here's my aortic valve, there's my mitral valve. Let's say that I have the pressure in this area.
So here's the pressure in my ventricles right the pressure in the ventricles is normally you want it to be about a hundred and twenty millimeters of mercury that's what you want it to be generally the diastolic blood pressure is around 80 millimeters of mercury if I increase this pressure let's say I increase it to like 100 I increase it to a hundred millimeters of mercury before it was a difference of 120 to 80 but now I'm going from 120 to 100 that's a 20 millimeter mercury difference so going from 120 millimeter mercury to 80 gave me a 40 millimeter mercury difference. When I go from 120 to 100 that only gives me a 20 millimeter mercury difference. That means I'm going to have to move from high pressure to kind of like a little bit higher pressure than normal. If I move from this it's a little bit lower so more blood is going to go out.
So if I increase that pressure that's increasing the afterload. I'm increasing the amount of resistance that I have to overcome to push blood from this ventricle into that vessel there. And again what things could change that?
One is plaques. That could be one. One is whenever the aortic valves are kind of stenotic and sclerotic. Another thing is because of that vascular resistance.
So now, you remember how we have the capillary beds right here? And they branch out here into like the arterioles we said, right? We said that they control that smooth muscle contraction.
So if these guys are actually contracting, they're increasing the systemic vascular resistance. That's backing that pressure up. That pressure starts backing up and guess what it does?
It's one of the things that also can contribute to this change. from it going from 80 to 100, for example, in this situation. So again, one of the things could be some valve stenosis.
Another one could be plaque buildups. Another one could be hypertension due to this high systemic vascular resistance. There's a lot of things that can contribute to this.
But the whole point here that I really need you guys to understand is, is that as compared to these two, whenever there's an increase in afterload, there's a decrease in the stroke volume. Whereas, whenever there's an increase in the preload, there's an increase in the stroke volume. Whenever there's an increase in the contractility, There is an increase in stroke volume. This is the only one that's inversely proportional to afterload.
So again, what things could actually inhibit the afterload or cause a lot of problems? One is aortic valve dysfunctions, primarily that of like stenosis or sclerosis, where it's hard to open up the valve. Or another negative influence is going to be some type of plaque buildup. So maybe some type of plaque or occlusion, so an occlusion of the blood vessel.
Or it could be due to hypertension, so high blood pressure, okay, due to the high systemic vascular resistance, okay? So that's the idea here. One other thing I want to mention because I forgot to mention it real quick is with respect to this heart rate. There's this weird reflex. This reflex here is called the atrial.
Bainbridge Reflex. It's one of the other regulators here of the heart rate. It actually can stimulate the heart rate, so it's actually kind of a positive effect on the heart rate. There's an increase in the venous return, that means it's going to cause an increase in the stretch. Increase in the stretch is going to stimulate the cardiac acceleratory center, which is going to go to the SA node and that's going to increase the heart rate.
Okay? So that's that little tidbit on the atrial bain-bidge reflex. Ninja Nerds, we covered so much information in this video on cardiac output.
I really hope that you guys liked it. I really hope it made sense. I truly do. If it did help, if it did make sense, if you guys liked it, please put some comments down in the comment section. Subscribe, hit that like button, maybe even share the video if you can.
Alright Ninja Nerds, as always, until next time.