Welcome, welcome to the module. We'll be covering the cardiac anatomy and physiology. So what I want to walk you through today are the different portions of our heart anatomy, as well as the way the heart functions with the goal that when we start talking about terminology and start talking about medications and the way we manage things, you'll understand kind of the key concepts that feed into why we do what we do. So we're gonna start with cardiac anatomy. So I just want to do a really quick review of the heart. So you'll see in front of you a schematic, and if you can think about the heart has four chambers. There's two top chambers and two bottom chambers. So the top chambers are referred to as the atria or atrium, and there's a left atrium and a right atrium. And when you start looking at things like echocardiography results and some of our other imaging results, you will see these terms described as far as these chambers. And then the bottom two chambers of the heart are referred to as the ventricles, and there's a right ventricle and a left ventricle. And then you'll see kind of in the middle of these ventricles, there's a section of tissue, and that is considered the septum. So there's a septum between the left atria and the right atria, and there's another septum between the left ventricle and the right ventricle. And then between the four chambers, there's valves. And you can think of the valves as doors that open and close. So when the valve is closed, it doesn't allow any blood flow that direction. When the door is open, it allows for emptying of that chamber. So those four valves are the tricuspid, the pulmonic. So the tricuspid is between the right atria and the right ventricle. The pulmonic is between the right ventricle and then the pulmonary veins, which feed into the pulmonary vasculature, which I'm actually gonna explain that in just a minute. And then there's the mitral valve and the aortic valve. The mitral valve lives between the left atria and the left ventricle, and the aortic valve lives between the left ventricle and the aorta and allows for the emptying. And so again, when you start getting into working with physicians and clinicians and reading reports, these chambers and these terminology terms will become very consistent, and you'll be seeing them over and over again. I do wanna point out though, this is a great graphic for you to kind of think about the flow of the blood through the heart. So when we start to get into the physiology, which I'm gonna talk about in just a minute, I'll describe, or I am gonna describe the heart as a pump. And it's a pump like any other pump in your house, your water pump, the pump in the car. The goal of the heart is to keep everything moving forward. And so as the blood flows through the right side into the lungs, into the left side, it's all moving the blood through into the peripheral vasculature of the body. And I'll explain that here in just a minute. Now that we've covered the anatomy, we're gonna transition into the cardiac physiology. So you can think of physiology as the way things work. And so, like I mentioned, the heart is really a pump, moving the blood forward through the body and allowing the blood to return to the pump in which it then is reoxygenated and moves forward. So if you go back to our graphic, you'll see I described a right side versus a left side. And the right side of the heart is what you can think of as the intake. So the blood returns through the venous system in the body. From above the heart, it comes through the superior vena cava. From below the heart, it comes up from the inferior vena cava. And these both empty into the right atrium. From the right atrium, it crosses into the right ventricle through that tricuspid valve. And then from the right ventricle, it crosses over into the pulmonary vasculature through the pulmonic valve. What you don't see on the graphic are the lungs. So when it goes through the pulmonic valve, the blood then moves into the lung vasculature, and that's where it's reoxygenated through our breathing, and then comes into the left side of the heart. So now you'll see on the left side of the heart, it's all red. So we kind of think about the red as being oxygenated blood, and the blue is the deoxygenated blood that's headed towards the lungs. So once it returns from the lungs into the left atria, the blood crosses into the left ventricle, and then the left ventricle, when it contracts, empties its contents or pumps the blood forward into the aorta. The aorta is the beginning of the arterial system that then sends the blood out into the periphery. So the blood goes into the periphery, it has its oxygen, and it goes to all of our muscles and cells and tissues and organs to provide the oxygen we need in order to maintain life. So again, if you simplify it, you need to think about right versus left. Right side, it is the return from the body intake into the pump. Left is the return from the lungs, and then an output into the body. The blood flows from right to left. And then again, think about that flow in two different circuits, the pre-lungs and the post-lungs. And then remember the valves, they're the things that open and close that allow the blood to work through. They also, when they're closed, they keep the blood from moving backwards. So the goal is we always want that blood moving forward towards the left. So I wanna walk you through three different kind of components of the cardiac anatomy and physiology that feed into the diseases that our patients are being managed for when they come into our clinics. So the first one is gonna be the plumbing, which we kind of describe as the area where we end patients end up with ischemic heart disease or coronary artery disease. And in some cases, you'll hear interventional cardiologists described as plumbers, because that's the part of the heart that they work on. So think about it as the plumbing. And what this really is, it's the arterial bed that feeds the cardiac muscle. So the heart muscles, like any other muscle in the body, it needs oxygen in order to function. So it needs arteries that feed that oxygenated blood down into that muscle. So what I have provided for you here on the left side is coronary for heart arterial tree, which is kind of the schematic of the way the arteries are set up that feed the heart muscle. And if I had a cadaver heart, kind of a regular heart sitting here to show you, these arteries all sit on the outside of the muscle, on the outside of the heart, and then kind of feed capillaries down into the muscle. So that's how our muscle gets oxygen in order to function. This also is the area where when people describe having a heart attack, these arteries get clogged and the lack of blood flow through that artery creates a lack of oxygen to that portion of the heart muscle. That portion of the heart muscle then, for lack of better way of describing it, begins to die because it doesn't get good oxygen. And that's what we term a heart attack or a myocardial infarction. So back to kind of our ischemic heart disease, these coronary arteries are the blood flow that feeds the heart muscle to allow for heart function, which when we get into that portion of the actual pumping mechanism is the contractility or the contraction of that heart muscle. It squeezes to empty the blood or pump the blood forward. The narrowing in these heart arteries create a lack of blood flow and therefore a lack of oxygen to the heart muscle. And with a large enough blockage and enough time, the heart muscle will die, again, termed myocardial infarction or heart attack. So it's really important when you start to look in at reports like cath lab reports, coronary angiogram is another word for that or a heart catheterization, they will describe this arterial tree. And you'll see, I've got on here, and we'll provide this in your handout, but we've got different names for these arteries. So this first big one that comes off is called the left main. And then we've got LAD stands for left anterior descending artery. We've got a proximal, we've got a mid distal, we've got a ramus, which is a branch. There's another heart artery called the circumflex artery. And then there's one called the RCA or the right coronary artery that comes off this side of the heart over here. So again, each of these has names. And so when you start to get into the reports, you'll see these specifically called out into the report where patients may have a narrowing in their heart artery or have a blockage in one of these places. So I mentioned blockages. The blockages can occur in one of two ways, either through chronic narrowing, where again, when we start to talk about ischemic heart disease and the way we manage our patients, things like high blood pressure, high cholesterol, tobacco use or smoking, diabetes can all lead to what we call vascular disease where the arteries start to have plaque that gets laid down in them. And over time, the plaque creates a narrowing and becomes much tighter. So if you look at the second picture over here, that's where that plaque begins to lay down. And over time, the artery, we call a lumen, which is the middle part where the blood flows becomes narrower and narrower. And that's where that blockage begins to occur. So sometimes patients can have just narrowing to the point that there's not enough oxygen. So when they're active and they need a little more blood flow, they have chest pain, which is the heart saying, I'm not getting enough oxygen because of that narrowing. And so the cardiologists go in and they put a stent in there, open that back up. And then they get good blood flow again and their chest pain goes away. In other cases, there's something we describe as an acute blockage, which is something that happens. I was fine one minute, I'm not the next. And that's what we refer to as an acute myocardial infarction or a sudden myocardial infarction or heart attack. And what happens there is that same plaque begins to break. And when it breaks, a whole cascade of events occur and a blood clot forms and a blood clot forms very quickly. And over that period of very quick time, the narrowing becomes to the point that no blood flow gets through and the patient immediately starts having chest pain. And that's where it becomes an emergency. We describe that as an ST-elevated myocardial infarction or a STEMI for short. Patients need to go to the hospital, by ambulance to the cath lab and have that opened up very quickly. In fact, we usually say within two hours, otherwise we start to see heart damage if that's been closed longer than two hours. So in addition to kind of thinking about those heart arteries, we also have the ability to understand based on the artery and the location of that blockage, when people have a myocardial infarction or a heart attack, we can describe that based on the area. So I'm gonna talk about terminology in another module, but there's really four heart walls, if you will, or portion of that heart muscle that can be affected. The anterior wall, the lateral wall, the inferior wall and the posterior wall. So when you start to look at some of our heart reports, cath reports or echo reports, you'll see a description that says left wall or anterior wall abnormality. That suggests that that portion of the heart is not contracting normally and likely may have had a heart attack in that area in the past. So again, as you start to work through our reports and get to know the way the physicians manage the patients, understanding anterior, lateral, inferior and posterior, the whole goal of those terms is to understand what part of the heart muscle was affected with that particular myocardial infarction or where the patient may have had damage. So that's really the plumbing portion. So think about that as the heart arteries and the blockage within the arteries and the ability to get blood flow to that heart muscle or not. The second area I wanna cover is the heart pump. So the way the heart contracts and moves the blood forward out into the body. So when you start to talk about areas like heart failure or structural heart disease, those both refer to the ability of the heart to pump normally and keep blood moving forward and not allowing blood to move back. So what I mean by this is again, the heart is a pump like any other pump. It's the goal is to move forward. When the heart gets to a point where it can't efficiently keep the blood moving forward, it begins to back up into different parts of the body. So sometimes it backs up into the lungs, sometimes it backs up into the body and we start to see symptoms within our patients that suggest that the heart's not working very efficiently. And we describe that term as heart failure. Now there's two important concepts here. The heart is a muscle that contracts. And if that muscle squeezing or contractility is not functioning appropriately, it's not contracting like it's supposed to, we term that systolic dysfunction. So again, when you start to look at diagnosis, you look at reports, you'll see the term systolic and you'll see the term dysfunction, meaning it's not functioning normally. When you see that, it basically means the heart's not contracting in its normal strength. It's weaker than normal. And so the weakness has affected the contractility and it's not pumping effectively. So that's concept number one. Concept number two is diastolic dysfunction. So in addition to a heart that doesn't contract normally, there are abnormalities that create environments where the heart doesn't relax normally. So again, if you think about a pump mechanism, it needs to be able to fill and it needs to be able to empty. That's the function of a pump. So when the heart's not filling appropriately, it's not relaxing appropriately to allow the blood into the chambers to then allow it to contract and move the blood forward, we can see the same heart failure symptoms. But in this case, we term it diastolic dysfunction or lack of appropriate relaxation. The heart is not relaxing appropriately. So again, as you start to look at your reports and see the patients that the physicians and clinicians, APPs that you're working with are providing care, these will be very common terms that you'll begin to see. So another area of this heart pump that's important to understand is a term called ejection fraction. So the ejection fraction or EF as we sometimes call it is the percentage of blood that remains in the left ventricle at the end of systole. Systole is the time in which the heart muscle contracts. And if the heart muscle is not contracting effectively, it won't empty its contents appropriately. So let me just give you a term. So ejection fraction, a normal ejection fraction is somewhere between 50 and 65%. So what that means is when the heart contracts and it empties its contents, 50 to 65% of its contents are being emptied out into the periphery. What I always tell people is it's not a percentage of heart function. It's a percentage of what's being emptied from that left ventricle at the end of contraction. So when you get into patients that have significant systolic dysfunction, remember abnormal contractility or the heart's not contracting very well, you'll see that number fall. Sometimes it's 30%, sometimes it's 20%. And I've even seen as low as 10%. So this is an area that again, when you're looking at reports, you'll see this term ejection fraction, 50% or ejection fraction, 30%. Normal is 50 to 65%. So again, if a patient asks you, what is my ejection fraction? Do not describe it as a percentage of heart function. It's a percentage of the amount of blood that's emptied from the left ventricle every time that ventricle contracts. So that's, and again, if you don't understand this concept, that's a good one to ask your preceptor questions about. This is a really important one to understand. And then the last piece of this pump I wanna talk about are the valves. So remember at the beginning, when I showed you the anatomy, we had four valves. So there was the tricuspid, the pulmonic, the mitral and the aorta. And these are doors that open and close. So what happens, there's two different abnormalities we see with our valves. The first one is stenosis, which means the door is not opening appropriately. So instead of opening all the way, maybe it's only opening 50% of the way or 30% of the way. The less it opens, the worse that it is. So the term is stenosis. And you will see in your patients, things like aortic stenosis is probably the most common, but there is mitral stenosis, tricuspid stenosis and pulmonic stenosis. So we can see this happen in all four of the valves. The other valve abnormality is something termed regurgitation or insufficiency. And this is another area where sometimes we make it more confusing than it needs to be. Both terms for the most part mean the same thing, but it means that it fails to close properly. So instead of that door closing completely, it doesn't come all the way together and the blood leaks backwards. So if you think about that heart contracting, when it contracts and it's supposed to move forward through the open door and there's one door that's closed, if that closed door is open, a portion of the blood will move backwards into the previous chamber. And what we see here, the different terms you'll see is aortic insufficiency, mitral regurgitation, tricuspid regurgitation and pulmonic insufficiency. And again, insufficiency and regurgitation really do mean the same thing. We just over the years have termed, depending on the valve, it's termed a little bit differently. But you can think about this as the valve is leaking, it's not closing effectively and it's allowing for blood to flow backwards. So for those of you that are working in structural heart, this will be a very important concept for you. And then the last section I wanna cover today as the electrical part. So the electrophysiology or the electricity of the heart muscle. And this one I find fascinating for multiple reasons, but basically I mentioned how the heart contracts. Well, the heart has to have a message to tell it to contract and it gets that message through the electrical pathway. So the electrical pathway we describe as a conduction pathway and it's the conduction of the electricity through the heart muscle that tells then the heart to contract. And if you look at a heart that's contracting, it has a very rhythmic look. The top two chambers contract and then the bottom two chambers contract. So it's a really important pathway and if the pathway gets off, it messes up the contractility and messes up the efficiency of the heart muscle. So anytime we run into patients with abnormal heart rhythms, what that really means is the heart is no longer working efficiently and the contraction is also affected. And so I wanna walk you through the normal pathway because again, you'll see this in some of your reports. So the whole kind of think tank or brain of the heart starts with what we call the SA node and it's the sinoatrial node up here in the right atrium. From there, the message goes to the AV node or the atrial ventricular node and that sits right at the bottom of the right atrium and then sends the electricity down into the ventricles. And it goes into the ventricles through something called the bundle of His and then works its way down into these. There's a right bundle and a left bundle and then once it gets to the end of those bundles, it works its way into the Purkinje fibers that then go deep into the heart muscle to then tell those cells to contract. So the contraction follows that electrical stimulation. The challenge is, and actually let me go back to the picture and abnormality can happen anywhere in this pathway. Sometimes the pathway gets blocked, sometimes there's another cell that might throw a beat and that's what's to me is fascinating. So every heart cell or myocardial cell has some interesting properties. So one, there's something called automaticity where each cell can produce electrical activity without outside nerve stimulation. So even though I described that the normal pathway starts up in the SA node and that's really the brain of the heart, a cell outside of the SA node, if it's irritated, can throw a beat and can start the heartbeat and start that electrical pathway. And if it starts in the wrong spot, it messes up the contractility. So number one, every cell can kind of throw things off if it's allowed to do so or if it gets irritated. Second is excitability. So the ability to respond to an electrical stimulus. So every cell, if it gets electrically stimulated can contract. So again, if that pathway comes from the wrong spot and follows the wrong conduction path, it throws off the contractility of the whole thing. Number three, conductivity, or the ability to transmit an electrical stimulus from cell to cell. So again, the whole point here is even though on this picture I show the normal pathway, when we get into patients with abnormal heart rhythms, it's all because that normal pathway is not being followed and there's an excitability or an irritability or there's something going on somewhere else throwing either extra beats or beginning a new pathway that creates a heart rhythm that's not normal. And that then creates an issue with contractility and starts to create symptoms within our patients. So our electrophysiology physicians, and you'll spend some time with them I'm sure, are very busy these days managing those rhythms because it's very important that patients maintain a normal heart rhythm. And the term for a normal heart rhythm is normal sinus rhythm. And the reason it's normal sinus rhythm is because it's supposed to originate in that sinoatrial node. So there you go, normal sinus rhythm because it starts up in the right atrium in that sinoatrial node. So I believe that concludes today. There was a lot of information today. So if you have any questions, please feel, number one, talk to your preceptor. And number two, if you still have questions, feel free to reach out to us at academyatmedaxian.com. And thank you for your time today.

cardiac anatomy

physiology

heart chambers

valves

blood flow

systolic dysfunction