All right, today we're going to cover key concepts of the heart. So we're going to look at path of blood through the heart. I want to talk about cardiac output.
I want to talk about the cardiac cycle. And I want to talk about EKGs. So we have a lot to talk about today. So if you have not yet looked at your heart anatomy, This might seem a little overwhelming here at first.
So let me give you kind of a brief overview of the heart, and then we'll talk about path of blood through the heart. So four chambers. The top two chambers are called the atria. The bottom two chambers are the ventricles.
With our anatomical position, this is the left side of the heart, and this is the right side of the heart. So this is the left atrium. dude this is sloppy let me try again left atrium and this is the right atrium and then the bottom chambers are ventricles so this here is the left ventricle this chamber here is the right ventricle.
All right, let's look at our blood vessels then. So, blood vessels that come into the right atrium are the superior vena cava or vena cava and the inferior. vena cava or vena cava in the coronary is also drains in here okay then coming out of the right ventricle we have the pulmonary trunk and you can see it splits here and this is the left pulmonary arteries pulmonary artery.
And then over here on this side is the right pulmonary artery. And so you can see everything on the right side of the heart is blue, which represents deoxygenated or oxygen-poor blood. So blood that has low oxygen, high carbon dioxide. And this is the pulmonary circuit. So this is going to pump blood to the lungs for that gas exchange to dump off the carbon dioxide and pick up oxygen.
Okay, so then on the left side, you'll notice all the vessels are red. So these are the left pulmonary veins that come into the left atrium. And over on this side are the right pulmonary veins.
Okay, they also go into the left atrium. They go around the back side, the posterior side of the heart and drain into the left atrium. Okay, and then here we have our aorta, which comes, again, this is a little tricky to see because it's a three-dimensional structure. But the left ventricle comes behind here and the aorta, blood flows from the left ventricle to the aorta.
So the left side of the heart is oxygen rich or oxygenated blood. So lots of oxygen. oxygen, low carbon dioxide.
This is the systemic circuit. This is going to pump blood out to the body. Okay. So that's our chambers and our vessels. So then the next thing is our valves.
So we have four valves. So two of them are AV or atrioventricular valves. And so they separate the atria and the ventricles. And then the other two are our semilunar valves, which separate the ventricles from the vessels.
So on this side, this is the right AV valve, atrioventricular valve, or it's called the tricuspid valve. And then over on the other side, we have the left AV valve, or it is called bicuspid or the mitral valve. And then our two semilunar valves. are here which is the pulmonary semi-lunar valve and then right this is hard to see but right up here right up here between the left ventricle and the aorta right if we remove the pulmonary trunk so right here is the aortic semi-lunar valve okay so that's our heart and our vessels and our valves.
So path of blood through the heart. So this is the first question. This is the very first question on your exam.
Okay. So we're usually start at the right atrium. If you Google this and there is, um, this is also in the PowerPoint, they may break it down in slightly different numbers.
Okay. It's a cycle. We usually just start at the right atrium, but the importance is that you understand the pathway. So this is one of those things that I would recommend drawing or taking this drawing and walk yourself through it. Okay, so we're going to start at the right atrium.
Then blood will pass through the right atrioventricular valve or it's called my tricuspid valve and that's fine to the right ventricle. the right ventricle will then pump the blood through the pulmonary semilunar valve to the pulmonary trunk pulmonary trunk then splits off into left and right pulmonary arteries okay so pulmonary is lungs so the next place that this is going to go is to the lungs where we're going to get gas exchange, both sides. Okay. So now we have oxygenated blood. It's going to come back to the heart.
So it's going to come back to the heart through the left and right pulmonary veins. Remember the right pulmonary veins empty into the left atrium here and the left. pulmonary veins and turn to the left atrium.
So our next stop is the left atrium through the left atrioventricular valve, or it's called bicuspid or mitral valve, to the left ventricle through the aortic semilunar valve. Go up here through the aortic semilunar valve and then through the aorta. And then it's going to continue on through a whole series of blood vessels to go to some tissue in the body. Where again, we're going to get gas exchange.
okay so we're going to give the oxygen to the organs to the tissues and we're going to pick up the waste products right and then it's going to come back into the superior or we'll go all over here oops or inferior vena cava vena cava into our right atrium and then we start over again right atrium through the right AV or tricuspid valve to the right ventricle, through the pulmonary semilunar valve to the pulmonary trunk, splits to either the left or the right pulmonary artery. And then we go to the lungs where we pick up oxygen and get rid of carbon dioxide. The oxygenated blood comes back to the heart through the left.
and right pulmonary veins into the left atrium, through the left atrioventricular valve or bicuspid valve or mitral valve to the left ventricle, through the aortic semilunar valve to the aorta, through a whole bunch of vessels to the body where we again have gas exchange. So we're going to give the tissues and the organs the oxygen and pick up carbon dioxide. And now the deoxygenated blood will return to the heart again through a series of vessels, right? Ultimately ending up in the superior or inferior vena cava back to the right atrium. Okay, you got to just practice this.
Okay, practice it over and over and over. Make sure that you are, again, you can do a silly drawing or you can use this drawing, whatever you want to do, but you need to make sure that you are practicing it. Okay. All right.
So moving on then to cardiac output. So the formula for cardiac output is cardiac output. equals heart rate times stroke volume. Okay.
So cardiac output is the amount of blood that's coming out of the heart in a minute. So cardiac output is... Basically blood per minute.
So you can measure this is like milliliters per minute. Heart rate. Heart rate you should be probably are familiar with, but heart rate is your beats per minute. And stroke volume is the volume of blood per ventricle. Remember the ventricles are the pump.
So this determines our blood, the volume. So this is going to be measured in milliliters. Okay.
So altering heart rate or stroke volume can alter our cardiac output. So like when you're exercising, people will talk about maximal cardiac output, right? So when you're exercising, your heart rate and stroke volume will all increase to help increase your cardiac output. When you're resting, they will both decrease to help reduce your cardiac output. Okay.
And we can alter one or both of them. So let's start with heart rate because I think you're a little bit more familiar with that. Okay.
Heart rate can be altered by factors that are called positive chronotropic. Making C's on here is hard for me. Okay. Chrono. tropic agents or negative chronotropic agents.
So positive chronotropic are going to increase your heart rate and negative chronotropic are going to decrease the heart rate. So if we increase heart rate, we're going to increase cardiac output. If we decrease heart rate, we're going to decrease cardiac output. So what? things that are positive chronotropic would be like epinephrine, thyroxine, so your thyroid hormones like T3, T4.
Chronotropic would be like acetylcholine. Okay. So increasing heart rate increases cardiac output, decreasing heart rate decreases cardiac output.
Okay, so let's look at stroke volume. So again, stroke volume is the volume of blood in the ventricle. This is how much we're getting pumped out of the heart, right? Blood that stays in the heart is not helpful to our tissues.
So we've got to get it pumped out of the ventricles. So there are three things that affect stroke volume. The first one is preload. So for preload, what I like to think of is the stretch. The degree of stretch.
So how another way of thinking about this maybe is like the elasticity of the muscle. If it can stretch, then we can put more fluid in there. So we will have a larger volume.
Right. So if we have increased preload. we're going to have an increased stroke volume and an increased cardiac output. Okay. So this is, you know, cardiovascular exercise helps increase your preload, helps increase that elasticity of the heart muscle.
Okay. But things that can reduce preload. So the opposite is also true here, right? So reduced preload reduces stroke volume and reduces cardiac output. So things that can reduce.
preload would be like fibrous scar tissue. or reduced, you know, stiffening of the pericardial sacs where it creates more friction, okay? Those types of things are going to reduce that stretch and that preload and make it harder to fill the chambers with blood, which then means it's harder to, there's less blood in the chamber, so there's less blood coming out, okay? The second factor that influences stroke volume is contractility.
And I like to think of this as like the strength. So the strength of the contraction, how much blood can we squeeze out of the heart? Okay.
So again, your heart is a muscle and you exercise it, that increases that strength, right? So that can increase contractility. So increasing contractility is going to increase the stroke volume and increase cardiac output.
It works the other way too. Reduced contractility will reduce stroke volume and reduce cardiac output. The factors that the agents that can alter contractility are called inotropic agents.
So we have positive inotropic agents. And they're going to, again, increase contractility, which will increase stroke volume and increase cardiac output. Or we have negative inotropic agents, which do the opposite, which will reduce contractility. and reduce stroke volume and reduce cardiac output. Okay, then we have afterload.
We're going to talk about here in just a second when we talk about the cardiac cycle, that blood is going to move based off of pressure. So it's going to move from high pressure to low pressure. Okay, so afterload, what I think of with afterload is I think of the pressure.
So if the pressure is not, if the pressures are the same, we have no movement. Okay, and blood's going to go from a high pressure to low pressure. So afterload specifically refers to the pressure between the ventricles and the blood vessels, so the pulmonary trunk and the aorta. And the bigger pressure difference is between the left ventricle and the aorta.
So the pressure in the left ventricle has to be higher than the pressure in the aorta. Otherwise, blood is going to stay in the heart. Okay. And so what we're talking about is we're talking about pressure gradients here. So if, so let's just say a normal, so I'm sort of just making these up.
Okay. So we're going to say the aortic pressure is, no, that's not what I want to say. We're going to say you have normal blood pressure.
So your aortic pressure is 120 millimeters of mercury. Okay. So that's normal. Let's say you have hypertension. So your aortic pressure is 160 millimeters of mercury.
Okay. And let's say that the pressure in the left ventricle only gets up to 180 in both cases. Okay, so simple math.
The pressure difference here when you have normal blood pressure is 60 versus over here it is 20. Okay. So this, when you have hypertension, so this is hypertension here because you have elevated blood pressure. This has an increased afterload. So increased afterload because it has that increased pressure that the ventricle has to overcome. Well, that means that there is less of a pressure difference, right?
Lower difference here than here, right? So that means that. With this elevated hypertension here, we're going to reach equilibrium quicker, which means less blood is going to flow through.
So increasing afterload will actually reduce the stroke volume because they're going to reach equilibrium faster. Therefore, it reduces cardiac output. Okay, so this is part of the reason why it's important to maintain a normal blood pressure so that we can get adequate volumes of blood out of the heart.
Okay, if your blood pressure is too low, it also creates problems. All right. Other things that can affect contractility or preload are things like fibrous scar tissue.
So if you have a heart attack. Cardiac cells are not replaced with healthy cardiac cells. They're replaced with fibrous scar tissue.
Fibrous scar tissue has no elasticity and no contractility. So that would reduce both preload and contractility. Okay, so lots of things that influence stroke volume, preload, contractility, afterload, right?
Pay attention to your terms here, chronotropic influence heart rate, inotropic influences contractility and stroke volume. Okay. Remember like when you're exercising, both of these are going to increase when you're resting, both are going to decrease. Okay. The next thing that I want to talk about is the cardiac cycle.
So the cardiac cycle are all of the events that are happening in one complete heartbeat. So there's a lot of things that are happening here. Okay.
Now we started, when we started, we would do this path of blood through the heart. So that was like, if you shrink down magic school bus style so that you're on a red blood cell and you're going. through the heart as a single red blood cell. Okay. If you're doing that, you're going to go through that loop this way.
Okay. You're going to go through that loop heart to the lungs, to the heart, to the body, heart, to the lungs, to the heart, to the body. That's the path of blood through the heart.
Okay. However, when we're talking about the cardiac cycle, we're talking about the heart as a two-sided pump. So we're talking about the left side and the right side, and they should be doing the same thing at the same time.
So when we talk about the atria are contracting, we're talking about both atria are contracting and relaxing at the same time. Both ventricles are contracting and relaxing at the same time. Okay. So let's put some words, let's put some terminology.
So systole or systole. the same thing as contraction so this is when that chamber will contract that's going to increase the pressure and move blood out okay remember blood has to move from high pressure to low pressure then we also have diastole or diastole which is going to be when that chamber relaxes when that chamber relaxes it's going to lower the pressure okay and so blood is going to want to move in all right So the cardiac cycle starts with ventricular filling, which is subdivided into two phases. Okay, so we have ventricle filling, but really we're going to start with this first phase, which is called diastasis.
And this is when the atria are relaxed and we're going to get passive filling of the blood from the atria to the ventricles. So this is like a super cheap sketch, right? But here's our our blood is coming in. And it is just passively going.
There's our AV valve. They're going to be open. Okay. And the blood is just passively coming from the atria down into the R ventricles. Okay.
So we will make a note that our AV valves are open. So on both sides, right, left and right AV valves are open. And this makes sense.
The AV valves have to be open for blood to get. from the atria to the ventricles. Okay. And this passive filling is about 80% of the blood moves this this way okay after that though we need to flip to our second sub phase of ventricle filling here which is atrial systole so remember systole or systole means that the chamber is going to contract so now so now our Atria are going to contract in.
Our AV valves are still open. And the blood is going to move from the atria to the ventricles. So atria systole, atria contract. And they're going to push the other.
Atria contract, which will increase the pressure, right, in the atria. So atria has a high pressure. Ventricles have a lower pressure.
So that's going to cause the rest of the blood is pushed, forced into the ventricles. So that's the other 20-ish percent. It's not going to be 100%, but. You get the idea. Okay.
So now the atria are contracted and the blood is in the ventricles. All right. That's where we're at. Atria contracted, blood is in the ventricles. So now we're going to go to our second phase, which is isovolumetric contraction.
Okay, so again, here we are starting out, right? Our atria, our atria are contracted. Okay, our blood is down here and our, our blood is gonna be down here.
Why is it not laying me right? Here we go, okay. Blood is down here in our ventricles. At least right now, our AV valves are still. Okay.
So this is where we're at, at the beginning of isovolumetric contraction. Okay. So let's look at, break down the word.
Iso means same, same what? Same volume. Okay. So we're not moving any blood, but we're having contraction. Okay.
So the atria are already contracted, so we can't be contracting them. Okay. So what has to be happening here is we have to have ventricle. contraction. Remember that ventricle systole.
Okay. But remember, as we contract a chamber, it increases the pressure in the chamber. It's going to force the blood out, but we just said it is isovolumetric. So we don't want to change the volume.
The ventricles are going to start to contract. The atrio, okay? So if we don't want to change the volume of the blood here, we need to shut our AV valves. When the AV valves close, this creates our first heart sound, which is the love sound.
It's basically the valves are like, okay, like shutting. Okay. So now ventricles are contracting, AV valves are shut.
So we have contraction and we have the same volume. We haven't moved any blood. Okay.
So this is where that afterload comes in. Why are we contracting this chamber and not moving any blood? Because blood can only move from a high pressure to a low pressure. So the whole purpose of this phase is to increase the pressure in the ventricles. Okay.
Once we do that, then we'll move to this. So this is like 2A. So then we'll move to like 2B phase, which is the ejection phase. Ejection phase only happens if pressure in the ventricles has to be greater than the pressure in the vessels. So again, we're really talking about left ventricle pressure in the aorta because that's the pressure difference.
When the pressure in the ventricles is greater than the pressure in the vessels, pressure in the vessels in the aorta that will open the semilunar valves. Okay. So ventricles will contract.
Okay. Aorta, pulmonary trunc. So what's going to happen are Semilunar valves are open, okay, and the blood is going to move into our vessels. All right, ventricles continue to contract to push the blood up by increasing the pressure.
Okay, once the pressure becomes stabilized, then right equal, then we are going to go into our third. phase which is iso volumetric relaxation okay so at this point right our ventricles have contracted we have pushed up The blood is in, most of the blood is in our blood vessels. Okay, so my lunar valves are still open at this point.
Okay, but now we need to start getting ready for the next heartbeat. So we have to lower, the ventricles are out of blood, not completely. Okay, we don't push out all of the blood, but they're out of blood.
push the blood into the blood vessels as much as we can. Okay. And we need to start filling up the ventricles for the next heartbeat. Okay.
So we want to relax the ventricles. So we want the ventricles to undergo that diastole or diastole. Right.
But remember when we do that, we do that. Then, okay, when we do that, the pressure is going to start to come down. And so the blood is going to want to come back into the heart. And so we have to shut our semilunar valves. So we close the semilunar valves.
That creates... our second heart sound, which is the dub sound, okay? The ventricles relax.
Blood is going to stay in the vessels and go to the body or go to the lungs, okay? Because the semilunar valves are shut. So now we're going to start over again, okay? Blood's going to come into the atria passively, into the ventricles.
AV valves we're going to open so the blood can flow from the atria to the ventricles. We're going to have atrial systole where we're going to contract the atria down and force the rest of the blood into the ventricle. During isovolumetric contraction then we're going to start increasing the pressure in the ventricles through ventricle contraction.
Ventricle systole where we want to shut the AV valves creating our first heart sound so that the blood does not go back into the atria because the atria are relaxing so that they can be reset. Once the pressure in the ventricle is higher than the pressure in the, in the left ventricle is higher than the pressure in the aorta, the semilunar valve is going to open and the blood is going to go into the vessels in the ejection phase. Then we're going to start to relax the ventricles. That's going to lower the pressure in the ventricles.
Blood's going to want to come rushing back into the heart. So we're going to shut those semilunar valves, creating our second heart sound, the dub sound. Okay, so this is the cardiac cycle. Okay, this shows you how the valves, how the chambers, you also have your two heart sounds here. Okay, and you can see how this is all driven by pressure.
Blood moves from a high pressure to a low pressure. You have to build up pressure and isovolumetric contraction. so that we can move blood from a high pressure to a low pressure into the vessels.
When we start to relax, lowers the pressure in the ventricles, so we have to shut the valves. Okay, this is another one of those good things that you want to practice walking through and explaining. All right, the last thing then that I want to talk about is EKGs. Okay, so the EKG is the electrical activity of the heart.
It is not a single action potential. It is all of the action potentials. It's an accumulation of all of the action potentials that are happening in the heart at one time.
Okay, we typically do a 12 lead EKG, which is actually sort of getting a picture of the electrical activity from 12 different views. If you will, it's kind of like if you take, you put an object in front of you and rotate it around, it doesn't look the exact same on every side. That's what a 12 lead EKG is. Okay. It's kind of looking at it from different angles, which is super, super helpful to a cardiologist in diagnosing and those types of things.
Okay. Most often the EKG that you see is the lead, is the second lead because that follows, it flows the same direction as. the heart cycle, the cardiac cycle that we just did. That's the one that we see that looks like this. Okay.
That's the only one we're going to look at. We're going to do very basic EKG stuff. So your EKG has P, Q, R, S, and T, and you'll see.
on lab that you can measure these different intervals and segments. Okay. And though that also tells you, so you measure them based off of, so this scale horizontally is prime. So that is also another way that we can use to diagnose. Okay.
Well, we're just going to talk about the electrical activity. So the electrical activity is going to trigger the muscle. reaction, right? So hopefully you remember that from bio 201. So depolarization is going to then cause contraction, whereas repolarization is going to cause relaxation. So the P wave, okay, so the P wave here represents atrial depolarization.
So that's the electrical activity that you see, which will then trigger that atrial systole or systole that we saw in our cardiac cycle. The next section then is the QRS complex. The QRS complex represents ventricle depolarization. which then leads to that ventricle systole or systole, which we saw during that isovolumetric contraction phase.
Okay. Now, remember, this has to get reset. Remember your action potentials and your nerve and muscle signals, it has to get reset. So during this time, we also will have atrial repolarization.
So it's kind of hidden in this QRS complex, okay? And that atrial repolarization is going to cause that atrial relaxation or diastole or diastole. And that happens during that isovolumetric phase of the cardiac cycle.
Remember, we saw that. See how it's all piecing together, okay? And then last, we have the T waves.
So the electrical activity triggers the cardiomyocytes, okay? so the t wave represents then ventricle repolarization which is going to trigger the ventricle diastole or diastole, which is that ventricle relaxation that we saw in the isovolumetric relaxation phase of the cardiac cycle. Okay.
So you can see how the EKG, the electrical activity follows the same pattern and rhythm of the circuit. cardiac cycle, which is telling those chambers to contract or to relax. And that's based off of this electrical activity, which drives the pressure changes of the cardiac cycle, which drives the blood movement within the heart.
Okay. So lots of things happening there. And then we also have our internal conduction system of the heart that kind of sets the pacemaker. It's going to set this rhythm.
So it starts with the SA node, then the AV node, then the AV bundle or the bundle of His, and then the bundle branches that go down into the ventricles and the Purkinje fibers, which branch into the ventricles too. So this is that, this is the order of that electrical. conduction through the heart. Okay. And that's kind of what's going to trigger.
That's what's going to trigger your heart rate. Okay. Specifically this SA node, that's the pacemaker. That's what tells your heart how fast to beat. Right.
And then that ties us back to our cardiac output, which changing heart rate or our stroke volume alters our cardiac output. All right. That is it.
for the heart