Heart Failure Pre-Clinical Lecture
Summary
This instructional session will cover chronic heart failure, a condition that affects 200,000 people every year in the UK. You'll gain an understanding of the function of the heart and the pathophysiology behind chronic heart failure, including causes, symptoms, and diagnosis information. The session will also cover implementing the best management and drugs aimed at improving the patient's quality of life. Being able to formulate a thorough understanding of this condition through the medical perspective by the end of the session will provide medical professionals with the knowledge to give their patients the best available care.
Learning objectives
Learning Objectives
- Understand the basic anatomy and physiological function of the heart.
- Describe the two main types of chronic heart failure and their causes.
- Explain the difference between symptoms and signs of heart failure.
- Discuss how heart failure is diagnosed, including common tests and their respective results.
- Understand how heart failure is managed, including drugs, lifestyle changes, and other treatment methods.
Similar communities
Similar events and on demand videos
Computer generated transcript
Warning!
The following transcript was generated automatically from the content and has not been checked or corrected manually.
wonderful eso days about cortical failure. We've got Annabelle here who's 1/4 year. You're going to talk about heart. Fear should so should be helpful for home. A little bit of motor for some of the drugs that we use as well. Or it also if your DPN so the physiological aspects of it. So I think I'll pass over to animal. Thank you dot okie Um, thank you for coming. I'm san a bell. I'm 1/4 year from need. Um, on welcome to this lecture about chronic heart failure on by Pick this topic for two reasons. Really. First of all, it's common. Apparently 200,000 people every year in the UK get diagnosed with heart. Failure on diet is quite common to see on the ward's. So I've just been on a geriatric ward on so many patients had called a car failure written in the notes on. But they're saying, among the the Geodon is in like the older medical students, commonest common meaning he should focus learning the conditions that you're most likely to see so chronic heart failure. It's a really good one to know about. On the other reason I chose this topic is just because I think it's really interesting on dope. Fully you do too. That's why you're here. Or maybe by the end of it, you will find it interesting if I've done my job properly. So it first fall. I just wanted to gauge how much you know about heart failure. So if you want, you could go to this website slide, oh dot com on deal. Ask you for a code. Um, and it could just put in med bridge. It will let you just type in any think you already know about heart failure. On if no one does it, I'll just pretend people have not read out some things and then only born. So I just give you, like, a couple of minutes for that. Yeah. Oh, someone says something. That's exciting. Yes. You can get a demon. Amazing. We'll talk about that when we talk about science and symptoms. Perfect. Sodium. A is swelling. I don't know why medicine makes you learn extra words. Everything but the demon. His sons. Okay, cool. I will me from So yes, In this talk, I'm going to cover six main points. So first of all, I'll just briefly recap the function of the heart on. But I just think that's kind of important to do so that you understand exactly what the heart's doing so that you can understand the consequences of the heart failing. Um, and then I just go into a different causes off heart failure. So the pathophysiology on then, if the bits that I think the most interesting just because they're most relevant to the clinical context on but what will be thinking about when we're eventually doctors? Eso I'll describe the symptoms on explain a bit about why they happen on. We'll also talk about the signs. So just to explain from the difference between science and symptoms, generally symptoms are things that the patient complains to you about, like a headache or a sore throat, or like a change in bowel habit. On, besides of things that you is the doctor notice kind of when you're examining the patient. So that might be they've got a fast heart rate or their BP is really low. Um, yeah, and then next I'll just go into how we investigate a chronic heart failure on how the test that we do and their results hope you officially diagnosed the patient, and I finally I will take you through how we manage heart failure, which is the best. But it really because it's the management and all the drugs and everything that will help the patient live a better quality of life on. It's kind of the most rewarding bit as a doctor. So first of all, let's just recap the function off the heart. What is it actually doing? So this is my basic diagram of the heart. I personally think you can't draw anything on paint that looks complicated. So if you just use painful of your diagrams, lectures and essays or just be a breeze, so I'll just describe the path that the blood takes through the half. So, as you know, the systemic veins have the D option ated venous blood on that flows into the superior or inferior, be in a cave er on enters the right side of the heart, and then it moves up into the pulmonary artery. On it goes to the lungs where the blood gets option ated, and then it comes back through the pulmonary vein into the left heart on, then out into the aorta and then the systemic arteries and all the organs in the body that the blood doesn't just flow passively on its own. The heart muscle or the myocardium. It has to contract social, sort of like push that blood into the arteries on it, stimulated to contract, fly away off electrical conduction. And that starts in a sign of a chore node, which is in the right, a gym. And then it spreads across both Atria on the A check and then contract to push the blood into the ventricles on. Then the Atrioventricular node receives this electrical wave on it, sends it down through the bundle of kiss on, go up into the beginning of fibers on the ventricular muscle on that allows the ventricles to contract, and that allows the heart to push the blood out into the arteries. So, yeah, I have simplified my diagram even more because I just want to look at the heart as a pump. So, to be very, very simple, the heart is pumping blood from the veins into the arteries, just taking away the fact that there are two sides of the heart. You got eight year and you could venture cools, you've got valves. You've got this wave of electrical conduction. Just forget all of that. This is the basic function of the heart to pump blood from the veins into the arteries to supply the body and meet its metabolic needs. So in Diastole, the heart is relaxed, the pump is off on the heart, fills with blood from the veins and then in Systole, the heart is contracting. So the pump is on on the heart pushes blood into the arteries on the volume of blood that the heart is pushing into the arteries. Every minute is the cardiac output on just to put that sentence into a nice equation, cardiac output equals stroke volume, times heart rate. So if we want more blood pushed into the arteries to a bigger capacity output, we either need a bigger stroke for news or a faster heart rate. So let's just talk about straight for a minute. It'll bit more a stroke. Volume is simply the volume of blood being pushed out of the left ventricle. Each time the heart contracts, a largest bottle of blood will be in the left ventricle after it's finished filling in the left atrium on. That will be just before the heart contracts so that Valium is the end diastolic from you. And then when the heart contracts, it pushes that blood out of the left ventricle. Therefore, the smallest volume of blood is in the left ventricle after it's venous contracting, and that's the end systolic volume. So the volume of blood that's pushed out of the left ventricle each time the heart contracts is the end. Diastolic volumes minus the end system for you on stroke volume is affected by three things we've got preload contractility on after load. So pre load is how stretched the ventricles are a tienda diastole on. But that's just before the ventricles contract. So what makes the ventricle stretched is when they fill with blood. So pre load is essentially how fill up the ventricles are on DCAA interactivity that describes how good the heart is at contracting. So how much force come in? Myocardium produce and after load is the load that the heart has to push the blood against to push it out into the arteries. So a change in pre load contractility or after load will affect strikeful, um, under change in strength volume or in heart rate will affect cardiac output under changing harder. Out is what happens in heart failure so amazing. We've looked at the function of the heart. Now you know exactly what the heart's doing, so we can understand why the heart fails on the mechanism behind chronic heart failure or any condition is called the Pathophysiology. So let's explore what's going wrong in chronic heart failure. What is it that the heart's failing to do? Eso. You can define chronic heart failure as a clinical syndrome where the heart is unable to pump enough blood to meet the matter. Bolic needs of the body just to break that definition down. There's either a problem with the pumping function of the heart or the body needs the heart to pump harder to meet a metabolic demand. Yeah, so let's talk about the first situation in this table. The pumping function of the heart is normal. The massive bolic needs of the body have increased, and that situation is called high output heart failure. And that happens because of conditions that increased metabolic demand, meaning that the organs need more blood flow into the healthy heart has to work much harder. Um, to meet those two months on here, three important courses. You got pregnancy because the heart task to supply blood to the mom on the presenter to support the baby hyperthyroidism because thyroid hormones increase cell metabolism on did hyperthyroidism. You've got too many of them on then anemia because the red blood cells aren't carrying much oxygen. So each bit of blood is carrying less oxygen than normal. So you need more blood to get enough oxygen. So high output failure is one type of chronic heart failure on let's talk about the other type. And this is what most people mean when they say chronic heart failure. This is when the function of the heart itself is impaired. So if the heart can't fill with blood properly, that means that the diastolic function is in pad on. If the heart can't push that blood out into the arteries, that means that the systolic function is impaired. So let's talk about the first case. Diastolic dysfunction. The heart can't feel properly with blood on here. Three reasons for that s o. The walls of the heart might be thick. They might be stiff and so they can't relax properly or the heart might be compressed from the outside on death. Equalisers can be caused by, well, it's called ventricular hypertrophy, and that can be genetic, Um, or it can be in response to, like, high BP. For example, Onda stiff falls there caused by restrictive cardio myopathy. He's so cardiomyopathy just means path E like disease off the heart muscles on in restrictive cardiomyopathy. These you've got deposits off protein or iron or invasion of cells into the heart. Tissue on that disrupts the heart tissue on, so it prevents the muscle from relaxing properly, then finally in external compression. And that's when the heart is compressed from the outside. So that could be fluid or air in the pericardial space between the myocardium, the heart muscle on the pericardial sac that surrounds the heart on, and that's called cardiac tamponade. But I always get confused with tapping are, but that's something different. Or if the pericardial sac is stiff and inflamed, so in pericarditis that will stop the myocardium relaxing properly. So those are all causes of diastolic failure. They make it harder for the heart to fill with blood, but What about Systolics failure, where the heart isn't able to pump the blood out into the arteries? Well, again, several reasons for poor pumping function, and I'll just talk about three. So if the walls they're really thin and floppy, then the Myocardium just can't generate enough force to push the blood out of the ventricles into the arteries on Death in for people's can be caused by another cardiomyopathy dilated cardiomyopathy on. I think that's mostly just idiopathic, so we don't really know, because so we just call it idiopathic. And then Secondly, we've got poor blood supply, so that can also cause systolic failure. Ondra member. The heart is a muscle, so it also needs blood for the cells to function on. But if the blood flow to the heart in the coronary arteries is compromised, then the cardiomyocyte they don't get enough oxygen, they don't get enough nutrients, and they can't contract properly on blood flow will be disrupted. If you've got fatty plaques. Eso, atherosclerosis, um, or if you've got clots in the coronary arteries on that is a schematic artisans. And then thirdly, if there's a problem with the electrical pathway that stimulates contraction, then the myocardium can't contract in a nice, coordinated way so the heart can't pump blood effectively on 40 electrical conduction. That's what happens in arrhythmia. So we talked about diastolic failure. We've done system failure on. We talked about the causes of those two on my previous he told you about the pathophysiology of high up heart failure. So we've done it. We've covered everything on this slide. Amazing. The next part of the talk is the more clinical side. So we'll start off just by discussing the signs and symptoms off. Chronic heart failure on Day one. You're thinking about the science and symptoms is quite useful to divide the heart into the right side on the left side. So let's just start off with the left side. Um, if this diastolic failure, then the left ventricle can't feel properly with blood from the left atrium and coronary vein Baines on. If there's systolic failure, then the left ventricle can't push blood into the aorta and beyond into the systemic arteries. So I just want you to think about the following questions. So what would be the effect off? Poor blood flow through the aorta into the systemic arteries That's number one on, then. Secondly, in left heart failure, there's a backlog of blood that can't move from the pulmonary circulation into the systemic circulation. So what sort of symptoms do you think would be caused by a backlog of blood in the pulmonary circulation? And again, I've got a slide. Oh, if you want to do it, I'll just launch it. And if people don't do it, Then again, I just pretend this is also great cause I can take a drink of water. That's why I did. The slider is just to give me a break. Oh, yeah, we've got Yeah, pulmonary edema s. So that's definitely one of the things that we're gonna talk about. Um, all fainting. Yes. Amazing. Perfect. That is definitely a symptom off left heart failure. Okay, so, um, all breathlessness? Yes. You guys are great. So I'll just start with this implant in this festival, and then I'll explain the signs. So remember, symptoms of things the patient complains to you about and signs of things that you tend to notice when you're examining them s so we'll just start off by thinking about the consequences off the left ventricle. Not pushing enough blood into the aorta on systemic circulation. Um, and as someone very cuddly said, if there's not enough blood going to your brain, then you'll get syncope on. That's just the medical term for fainting, Um, but equally, if there's not enough blood going to the muscles in your arms and legs, then you'll feel weak. So those are two symptoms off know enough blood going into the arteries and then moving backwards from the arteries to the heart itself on what's the effect of left heart failure on the heart? So, if you remember from earlier, a cardiac output equals stroke volume times heart rates on D in left heart failure that stroke volume is reduced. So in an attempt to increase your helper, the heart rate will increase. And so people can sometimes complain of erasing half. They won't come to you and say, I've got turkey cardio. They'll say, Oh, my heart was like It's really racing on Ben, moving even further back from the heart into the pulmonary circulation. If the blood can't flow from the pulmonary veins into the left atrium, you get venous congestion, so that means there's a higher hydrostatic pressure in the pulmonary capillaries. And so you get more fluid for south into the alveoli, the air sacs on into the pleural space, and so you'll get pulmonary a dealer if someone said, um, pleural effusion on because fluid in the lungs in past US exchange your patient will feel breathless, which is once every said is off on. Breathlessness is often worse when lying flat. And that's because when you're lying like this, it's easier for the venous blood to flow from the systemic veins into the right side of the heart because the blood isn't flowing against gravity on. If you've got more flow into the pulmonary circulation and computerese, they're not hard to static. Pressure is going to be even higher, and so that worsen the pulmonary edema on the pleural effusion on both aqua. That's the fancy name for breathlessness. When you're lying flat on DPaT exists more nocturnal. Dyspnea is the fancy name for when people wake up a night and they're like gasping for air. And that's because when you're asleep, you're most often lying down, and so the pulmonary edema will be worse on. Do you get this sort of like urge to get on down fluid in the alveoli. That would also trigger a cough to try and expel the fluid on, Since it's more fluid at night because you're lying down and that cough is often nocturnal on Gwen, you talk to patients. And one, the question just supposed to ask is, How many pillows do you use that night? Because patients with heart failure will often use three. Because when you're propped up that pulmonary edema isn't bad on, they'll be able to sleep without sort of coughing and feeling reference. And you can classify it how bad the breathlessness is, using the New York Association classifications. So, for example, if you got a patient on their getting out of breath when they walk to there gardening back on provided it's not a very big garden, that's not very far. So that would be less than ordinary physical activity. So they'd have Class three. Heart failure on Doctors do actually use this owned classifications to estimate prognosis. So Class one patients and they'll have a much better outlook than class for patients who have a much higher risk of mortality. So those are the symptoms a graft, heart failure, moving onto the signs that things you notice when you examine the patient. So, first of all, cardiomegaly, that's when the heart is enlarged on that can be caused by left ventricular hypertrophy. So remember, that's the course of diastolic failure. Or cardiomegaly can be caused by dilated cardiomyopathy, which is a cause off systolic heart failure. On Did you can see cardiomegaly on a chest X ray on. I will show you that later, but you can also identify it just by feeling the patient's chest for something called the apex feet. So the apex of the heart is kind of like the bottom point of it on that's located at the fifth intercostal space in the Midclavicular line. It's one of those things you learn, in fact, that you're like it's not useful, and then it it actually is. So remember that one on. But it's just what these red hair is pointing to you here on usually. I mean, you can feel it on yourself. It's sort of like down here it's the apex of the heart, tapping against the chest wall that's the apex be on in Cardiomegaly. The apex is displaced because the heart's bigger so you'll feel that tapping a bit more laterally. So when you're examining a patient, you have to make a big point of counting out the ribs. So you can say to your consultant are the apex speech is displaced Ondas. Well, it's feeling that apex. But you can also listen to the heart with your staff a script on but allows you to hear the heart sounds on the important one that you hear in heart failure. In left, heart failure is called the S three Gallop on day, normally, when he listened to the heart, you'll hear those nice to those two nice, clear sounds. So you'll have the love in the tub on the love is the sound off the atrioventricular bowels closing at the beginning of systole On the double is the sound off the pulmonary and aortic bowels closing at beginning of vastly. Uh, but in left heart failure, you'll have this Third sound s three Onda. You're hearing that because of a vibration caused by blood flow suddenly stopping on in heart failure, you get to a point where the left ventricle can't stretch anymore to accommodate any more blood on, So the passive flow from the atria into the ventricles during Diastole suddenly stops on. That course is the vibration, and you'll hear that is a kind of dull thud in the middle of diastole, and that's the asleep on. We've already talked about how pulmonary edema on pleural effusion make you breathless, but you can also identify that the patient has these by listening to or tapping on the chest so you can listen to the basis of the lungs. Which of these yellow dots on the patient's back on? But the patient breathes in the fluid build alveoli pop open on it's that popping sound that you hear is sort of crackles through your stethoscope on the medical fancy term for crackles is crepitations on. You can also identify pleural effusion by tapping or percuss in the basis of the lung so normally the longest filled with air on. There's not a lot of fluid in the pleural space, so when you talk, the sound that you get will be quite resonant, like if you're hitting muscle hollow drum that if there's fluid in the pleural space and that will mask that nice sound so you won't get a resident sound, it will sound a bit dull on the textbooks. Describe it is stone Edo. I've No, I don't know what that means, but it doesn't sound. Resident, basically. And so, if you hear crackles at the bases of the lungs or a dull sound when you're tapping on the back, then the patient probably has pulmonary edema and pleural effusion on Since the alveoli of filled with fluid, the patient will also have a decreased vital capacity so their lungs can't hold it much air on. Do you can assess vital capacity by asking patients take a deep breath in and then breathe all the way out on gee can measure how much they breathe out. Okay, great. So that is thesis. I intend symptoms off left heart failure moving onto right heart failure. The heart isn't able to pump blood from the systemic veins into the pulmonary circulation. So you get that back log of blood in the systemic veins on again. I'm gonna ask you a question. What do you think the symptoms of right heart failure might be And I've got the slider are just trying to launch it. Uh huh. Yeah. What is gonna be caused by this backlog of blood in the systemic circulation are someone's very fast. Yes. Peripheral edema. A demon in the legs. Amazing. Yes. Okay, so, I mean, that's kind of the main thing, really s. Oh, yes. In right heart failure. The venous blood is calling in the systemic veins s. So you get that increase in hydrostatic pressure. More fluid is getting forced out into the interstitial space. And so you get Duma, so patients might complain to you off swollen legs. Um, well, that that's you start for anymore on ball. So just because there's so much excess fluid, they might describe unexplained weight gain. And the edema will usually start distally like someone said in the legs and the ankles, but it can creep up into the sacred. So, like the back of your back on it's called pitting edema. Because if you press on the tissue, the indent, or like, the pit that your finger makes will remain and you can see that really clearly here is kind of bizarre. On importantly, the swelling will be on both sides of the body, so it will be bilateral edema on, but that distinguishes heart failure from something like deep brain from basis, where you've got clots in one leg, and so the swelling would only affect one leg on. Also because there's a backlog of blood in the veins that drain thie abdominal organs, you'll have increased hydrostatic pressure in the paratracheal capillaries on day, so you'll get fluid forced out of those capillaries into the peritoneal cavity on. That leads to this horrible like swollen abdomen on gas called ascites. So I'm moving on to the signs of right heart failure. One cause of right heart failure is right ventricular hypertrophy, and you can actually feel that if you put your hand on the patient's chest to the left of the stone in and and you'll feel your heart being lifted off, know you for your hand being lifted off the chest on each time the heart contracts. And that's called the Parasternal heave. So power of meaning like next to sternal sternum and then, like he on venous congestion in the veins, draining from the head that would lead to neck vein distension. And this lady's got it really bad. I think that's the external jugular on then. Another sign of venous congestion is a positive hepatojugular reflux test. So that's a test where you press on the liver and then you look at the patient's neck to see if the veins get more distended with blood. On the specific vein you're looking at is the internal jugular, and that is this blue rectangle in the picture on the right. So what you do is you push down on the right upper quadrant of the abdomen. Weather liver ease on that pushes the blood out of the liver into the inferior vena cava Onda in heart failure. The right atrium. It can't accommodate that extra blood that you've just pushed out of the liver, so it just sort of sits there on that makes it harder for the blood to drain from the head and arms into the sea, period in a cave on the right atrium, so you'll get more blood in the internal jugular vein. And so when you press down on the liver, you'll see the vein bulge. But they don't. I don't if they actually do this in hospitals. It's one of the things they teach you about, but it's really uncomfortable for the patient to have breast quite hard. Um, but Yeah, it's just one of those things they actually on. Then another test that you can do for a sign of heart failure is looking for her pattern megaly. So if the blood can't drain from a liver into the inferior vena Cavor, the liver will just get bigger. And I engorged with blood and to look for a big liver, you can press down on the right lower quadrant of the abdomen on us, the patient to breathe in on if the liver is bigger than your feel. It's like tap against your hand when you pressed in your hand into the abdomen on Do you can also percussed again see Kentucky on the abdomen. And if you start at the right lower quadrant and sort of like work your way up, the sound will change from resident to dull on. But the reason it sounds dull is because the liver is quite dense as an organ. On day one, you tap on densely things. It sounds dull, so if the area dullness is bigger than you'd expect, then that suggests that the liver is bigger. And then finally, if you treat the patient and we'll talk about treatments in a bit on they lose weight, then that's a sign that they had peripheral edema, secondary to right heart failure. So that's another sign in Connecticut. Okay, so that's the science and the symptoms. Off left and right. Heart failure on dust. A disclaimer, although, is useful to think of the heart. A Zoloft heart in the right heart. When you're remembering these signs and symptoms in reality, patients will probably have a mixture of both. Um, you don't usually get one side of the heart failing on its own. So moving onto investigations, it's really important to take a good history to find out with symptoms on. Also to be very thorough in your examination so you can find out the signs, and that's because those two things are really important in diagnosis. But there is more you can do. There are different tests and things, and that's what we'll talk about. And so I've got another slide. I I think this one's a quiz. Um, yeah, so if you just what's the question? Think it's how do we how to reinvestigate heart failure and you've got lots of different options and there's more than one right answer so I haven't started it yet. Yeah, okay. Had quite a lot of fun is well, coming up with the wrong answers. But most of them all right? So he just, like, pick any of them? Yes. So you could do blood tests. Um, you conduce and the c G. You could do an echo. Oh, yes. Perfect. Blood test. Chest X ray. Are you got a more well exercise stress test? That was one of the ones I had fun coming up with. I don't think you do that in heart failure. Um, no. Well, I know you're doing. There's a pathway that I'll show you later. How you diagnose. I'm not sure what they do that for. Maybe a scheme. A cart disease? Um, yes, we see GI. You don't do, um, a CT angiography. I think just because CT scans have a lot of X rays on you don't want to expose the patient unnecessarily on do you conduce investigations which don't pose as much risk like the blood tests on the east G and the echo. So they're a lot less invasive, but a CT would be really good for a P S O upon very embolism if you've got a clot on the lung, if you do a CT to look about, you can see the clock. Yet the most important investigations chronic heart failure, heart blood tests in the C, G and echo on a chest X ray can also be useful. So you're starting off with blood tests the most important one, the kind of when you do multiple choice questions in clinical school. The one they want you to say is for anti or enter Minnis Pro BMP. So when the ventricles are stretched, the cardio my sights on release Probi MP and that gets cut up into NT probation pee on BNP. BNP is the active hormones that just goes off and doesn't it stuff? But the ones that we measure is an anti program. Be, um, I remember in heart failure. The ventricles will be overloaded so they won't be able to pump the blood out on bail. Be stretched even more on Do the levels of all of these three chemicals here will be higher than they would be in a healthy person on. You can measure BNP, but it's better to measure NT Probi MP because it's got a long half life, so it remains in the blood for longer. So that means if there is an increase in ventricle stretch, you're more likely to detect it. If you look at NT programs. The So, in other words, it's just more sensitive as a test. It's really important to know these levels because it effects diagnosis a prognosis on demonetisation it Treatment's working so normally the levels were quite low, less than 400 nanograms a liter. But if they're raised above 400 then you should start to suspect heart failure on def levels are moderately raised. It's not as much of an emergency, so you can send the patient for echo in six weeks, although it's probably longer now. The coated so disrupted everything. But if it's if the levels are higher, if they're over 2000, then it's more urgent. So the patient needs an echo in two weeks. Just a warning about anti Probi MP. The test might be sensitive, but it's not that specific. So, in other words, lots of things can increase or decrease the levels, and I'll just highlight a few. So, first of all, annoyingly if the patient is over 70. Then they might have higher levels anyway on. But it's confusing because most heart failure happens in patients who are over 65. So it kind of raises the question. Do they have raised levels because of their age or because they have heart failure? Or is it a bit of both on then? Secondly, chronic kidney disease, so CKD that can also increase levels. And that's just because the kidneys can't excrete antibody Probi MP as well. So the leg was will build up in the blood and then on the flipside. The levels might be deceptively lower in patients who are off Afro Caribbean descent. I'm not sure why or if you're a B, so you got to be a my grace than 35 or heart failure drugs. So again, very good using on. Because of all this ambiguity, it's really important to a find out what the patient's baseline level is of anti program pee and also you to interpret whatever the result is in the context of the rest of the signs and symptoms. So the next investigation that would do is an E. C G. So the electro cardiogram to look at the electrical activity in the myocardium and and that would reveal the cause of heart failure like arrhythmia or ischemia on Remember from earlier both arrhythmia. Onda, ischemia, Cardizem. He's they call systolic heart failure. So it was very quickly recap what we see GI is. So this image is the electrical activity from one heartbeat. On the P wave is atrial depolarizations, which allows the atria to contract and then the flat line between the pee on the Q. That's the P R. Interval, and that's when the electrical wave is being transmitted from the atria to the ventricles via be atrioventricular node and the bundle of Pearson Kinji fibers on. And then this upward spike. That's the QRS complex, and that represents a ventricular depolarizations. So when the ventricles contract, um, on atrial repolarization, when the h feel relaxed, you can actually see that on an E. C. G because it's hidden by just how big this QRS complex is. But you can see ventricular repolarization, and that's this T wave. So when the ventricles relax, Okay, so one type of arrhythmia is atrial fibrilation, or F on. This is when the Atria contract really fast so they quiver they don't pump in that nice coordinated way on on an E C g f looks like this. So the classic findings are number one. You don't have P waves. A number two, you've got a new, regularly irregular rhythm. So if you compare the top image on the bottom one, you've got the cure is complex in the top image, and you've got the T waves. But there's just no p waves. Um on. That's because to get a P wave, you need organized electrical activity in the atria on be in atrial fibrilation. The electrical activity is really disorganized, so no P waves and you can also see that the heart rate is very irregular and that becomes more obvious if you mark out all the QRS complex is, um because in f there's no pattern whatsoever. The rhythm is irregularly irregular on, then the other cause off systolic heart failure that you can see on an E. C. G is poor blood supply to the heart muscle. So the E C G can tell you whether myocardial ischemia or myocardial infarctions or heart attack whether those have happened in the past. So if the T wave is upside down that suggests that there has been esquina in the past. On if there are pathological Q waves that suggests there has been infarction. So heart attack on the reason you get these weird key waves is because the electrical wage is trying and failing to pass through scar tissue that you get after a heart attack on. If you just look at the health EEC gi, you've only got a really small little dip where the Q Wave is. But in the pathological Q wave, it's a lot bigger. And then another important sign on an E c G in heart failure is ventricular hypertrophy. Um, remember, ventricular hypertrophy causes diastolic heart failure on but with right ventricular hypertrophy, theoretical wave will be distorted to the right of the heart because there's more tissue there on on an e. C. G. You know this is happening because lead one unleash to the QRS complex is of reaching towards each other. So right up, right ventricular hypertrophy reaching. That's how you remember on def there's left ventricular hypertrophy. Then the electrical way is distorted to the left of the heart because it's more tissue that on on an E C G. That QRS complex is complexes in lead, Woman to they are leaving each other, so left anything perfect. So that's blood tests and e c. Gs, and I'll come back to the chest X ray. But the most important investigation to definitively diagnose heart failure is thie echocardio. Um, And as we said earlier, if you're anti Probi MP, that blood test If that's above 400 then that means you'll be referred for an echo andan echo is ultrasound imaging. So what happens is thist transducer that the person is holding that's emitting sound. Waves on different tissues reflect those back onto the transducer differently on that allows you to see a different tissues as separate structures on the monitor on. There are two reasons why the echo is really important in half you. Firstly, you can identify a ventricular dysfunction because she can physically see how much blood the venture cool is able to push out on. You could also see whether the heart walls are really thick, or if they're really like thin and floppy on that will tell you whether the heart failure is systolic or diastolic on bats really important when you're managing the patient, and I'll talk about that later. But you can also look at the cause of the heart failure. So, for example, valve disease on Do This gift here is showing mitral valve regurgitation in. So when the left ventricle contracts on the mitral valve should be closed so that the blood doesn't flow back into the atrium. But if there's something wrong with the mitral valve and it's not able to close, probably you get back flow of blood. Onda In this gift, it's the sort of blue blood flowing to the bottom of the screen that the little blue our is pointing out A. Finally, I will talk about the X ray findings in heart failure, So just have a little think to yourself. I couldn't do a slide. Oh, because they only let you do four for free. But just have a little think yourselves about which one of these is normal on which one of these X rays is from a patient in heart failure. No, asked my parents this nice of them a medical, and they both got it right. So I'm assuming it's pretty obvious it's the one on the left that's the heart failure. One on the one on the right is the healthy one. On on a chest X ray, there are six Keesee eines of heart failure on DCA NVIDIA Plea. You can remember them as a B C D E f. So the alphabet is very important in that school on Do A. It's for alveola shadowing on bats caused by pulmonary edema. So the fluid in the alveolar I that shows up is white on an X ray because fluid is dense of an area and so there will be black and anything that's denser that there will be more white on D alveola. Shadowing is sort of like a bat wind shape. You can see a lot better here on it spreads out from the highlight of the lungs on Deacon. See, this? Just a lot of like white stuff is not supposed to be there and then moving on to be that stands for curly K e R L y. The lines on what those are is thin horizontal lines of the edges of the lung on they're not very obvious unless you see me. So I assumed in It's not the same X ray. I had to go on Google for a different one. But you can see these very subtle, thin like horizontal lines that the lung edges on what those are is thickened interlobular aceptar. So the divide between different Bunches of alveoli, those divides those SEPTA get thickened because of the pulmonary edema. So I'll be really shadowing on curly be lines. Those are two ways that you can see pulmonary Dema on an X ray. Um, so a be the next to see. So that's cardiomegaly on be discussed earlier about how, when you examine the patient, you'll feel that the apex beat is displaced to the heart or like tack bit further into the armpit. But you can also see cardiomegaly very clearly on a chest X ray on DTaP, formerly determine if the heart is enlarged. What you do is you could measure the lower border of the heart, so that's the top blue line on. Compare it with the distance across the diaphragm or the thoracic diameter, which is the bottom blue line on def. The heart is greater than 50% off the thoracic diameter. Then that means the patient has called, you reckon on diffuse just compare the images on the left and right. You can clearly see that the heart failure heart is a lot bigger. Uh, next is D on that stands. Boards dilated up a load vessels. So in heart failure because there's a higher pressure in the left atrium because the heart can't pump the blood from the pulmonary veins into the systemic arteries, you'll get that back log of blood in the pulmonary circulation, and that means that the pulmonary veins will be dilated on Deacon. Sort of. See that this is like white, streaky things that I've been in circles that you can't really see in the healthy heart. Healthy young um, And then he stands sport pleural effusion. So usually patients have their X rays taken when they're standing up on, but means that the fluid in the pleural space will accumulate at the bottom of lungs at the bottom of the lungs. In place is called the cost a phrenic angles. So that's the sharp angle between the diaphragm and the lateral chest wall, and you can see that really nicely on the healthy chest X ray. They really lovely and Chris these ankles. But if you look in the heart failure image there blunted. You can't see into that group of just it's not there. And that's because of the fluid from the pleural effusion that's getting in the way. And then finally f so f stands for fluid in the fishes. Owns a lot of s in that one on. You can see the horizontal fish actually quite nicely in this chest X ray on that's again just because of the fluid, the pleural effusions. So a chest X ray will show you all of these signs of heart failure. Eso It is useful, but it's not enough to diagnose heart failure on its own on. That's because these signs could be caused by other diseases. And just remember that you might suspect heart failure in a patient that's breathless. But there's other things that could cause that rough listening so the patient could have lung cancer. They could have a pneumothorax. They could have like another lung disease that's causing them to be short of breath on. But chest X ray would be really good to show whether those diseases were present. So it is important just not for definitively diagnosing heart failure so that was all of the investigations. We've taken our history with Donna Exam. We've ordered all of our tests. So we have all of the information that we need to either diagnose or exclude heart failure on Nice thing. What is it? National Institute for Health and Care Excellence. They have this lovely flow chart that you can use to diagnose eso. The first point that they talk about is finding out the signs and symptoms. Onda, all of the ones that I talked about earlier those apart off the Framingham criteria on disses what you're supposed to look for to see if a patient likely has heart failure or doesn't have heart failure on to diagnose. You need either two major criteria, so I don't know the patient's waking up gasping for air on been, you listen to the basis of the lungs. You can hear those crackles eso the either need to major or one major on day two minor criteria so they might have. They might have the lung crackles, say, but they also have soil and ankles and the fast heart rate on go. In that case, you could you could be pretty confident that it was heart failure on, then the next step is using the NT programs. Pee A Z talked about earlier to see how allergic he an echo is needed and then to do that echo. So just to recap, if the level is above 400 years Necco on If it's below 400 it's probably no heart failure. So amazing. We've diagnosed heart failure. Great. But how we actually going to help the patient? How we're gonna manage thumb on improve their quality of life? Because A said breathlessness is quite a common symptom, and that could be reading militating to just be short of breath all the time. So nice. Have another lovely flow chart telling you exactly what to do. I'll just go through it step by step. So firstly, you've got to help the patient with their symptoms. So help him breathe easy. The swelling in their feet in my legs help them sort of get about. Mobilize more. Um, all of those symptoms are caused by fluid overload on DTI. Eat that. You need to get rid of fluid, so that's done. By offering diarrhetics. This is where motor comes in on day. Shinsei like to call diarrhetics water tablets because they make you well off. And they do that because they act on the kidney just very briefly recap kidney function So large gets spilt it at this renal corpuscle. On that filtrates just moves through the kidney through the proximal convoluted tubule for the loop of Henle E up into the distal, convoluted TVO on Ben down into the collecting ducts on as the filtrate moves along the ions and the glucose will be re absorbed. But waste products like urea that will stay on and so they get excreted out in the urine on got transporters in the thick, ascending limb of the loop of Henle e like the N K C C to transporter, which is here on the left, right on. That's really important for creating an osmotic Grady in on the potential for water to be re absorbed a day collecting ducts on Bleek. Diuretics like Brazil, I'd say inhibit this transporter. So that means there's less of an osmotic Grady int so less water can be re absorbed from the collecting duct Onda, so more will end up in the urine. Um, on the basic principle is just that the patient will be out the excess fluid, and that will reduce the limb swelling and reduce the pulmonary edema. But if you're not careful with the dose that you give of furosemide, you can actually cause hypovolemia on. Reduce the blood flow to the kidney on. That will cause an acute kidney injury because the kidney needs blood, too, and then also because this transporter is helping reabsorb potassium when you inhibit it, then you'll lose potassium in your urine and you'll have low potassium in your blood. So hypokalemia on. That's not great, because that disrupts the electrical activity of the heart on that can cause arrhythmia, which wouldn't help the heart failure. So you gotta be careful when you're prescribing on Ben. What you do after giving it's symptomatic relief with these diuretics on do that depends on whether the heart failure has preserved or reduced ejection fraction. So, basically, is it diastolic or systolic heart failure on the echo scan that we did earlier well talked about earlier that will give you the information so it action fraction. All it is is the difference between the end diastolic volume on end systolic volume divided by the end diastolic following. So it's the stroke volume Ascensia li divided by the end diastolic volume on in a normal heart, thie end diastolic value should be big, right, because the heart is able to feel properly, but the end systolic volume should be small because the heart can pump all of that blood out into the arteries. So your ejection fraction is about 50 to 70%. But in diastolic failure, the heart might be hypertrophied or stiff or compressed from the outside so it can't feel properly. Eso this end. Diastolic volume is small, but because the heart is high, perch it bleed or stiff or compressed from the outside thie end systolic volume is also small, so the fraction is it actually reduced. It's the same. So about 50 to 70%. But in systolic failure, the heart confu absolutely fine. So the end diastolic volume is nice and big, but it can't push the blood out into the arteries. So the end systolic volume is too big, and so your ejection fraction will be smaller. It will be less than 40% so that's preserved versus reduced ejection fraction on if you've got heart failure with preserved ejection fraction. So diastolic failure. Nice guidelines recommend that you just manage the other illnesses. The patient. How's that? Could worsen or be causing the heart failure on. Just don't worry about the specifics. And I was a lot of information here, but just to give you a general idea about the treatment that the patient might need s O in hypertension, high BP, you can recommend that they eat less salt, that they lose a bit of weight on Deacon. Maybe start on some drugs, depending on how bad the BP is on Ben. For atrial fibrilation, that type of arrhythmia. You can slow the heart rate and make the rhythm or regular so that the heart can contract in that nice, coordinated way on. You should also consider anti curricula a shin on blood thinners. Because the turbulent flow in the atria, when they're quivering, that can actually increase the risk of clots. And if they go to your brain, that can cause a stroke. And you're not obviously on Ben for ischemia. Cardizem. These you can recommend lifestyle. Things like eating less fat, not smoking, losing weight on deacon also prescribe some drugs that will help us out and then for the other type of heart failure. Systolic heart failure, where the ejection fraction is reduced on top of the loop diuretics that you've already given to manage symptoms, you can adult these other drugs. Onda, unlike the diuretics, which studies have shown that they help symptoms, but they don't actually reduce mortality? A. Send him. It is beta blockers. All the ones here. They do reduce mortality. Eso fast, for he give a sin hip it is on. These are drugs that end in Prilosec, like ramipril or lysine approved again. Motor eso. What they do is they inhibit angiotensin converting enzyme on that catalyze is that production off and you're tense in two. And that's just part of this hormone system called the Run in Andrew Tense in August. Your own system on all that does is it causes base oh, constriction, and it makes the body hold on to fluid. So if you inhibit this system, then you'll dilate the blood vessels and you'll reduce peripheral vascular resistance. And that makes it easier for the heart to pump blood into the arteries and and also the, uh, drugs that you give because they're inhibiting water re absorption of the kidney. They are reducing the volume of blood that the heart has to deal with. But some people on a sin. Hib it is. They get horrible dry cough on, but they're not tolerating the drugs very well. So instead you can give them on Joe tents in receptor blockers on both of those drugs and in certain so like roles, a town. Another interesting thing is that patients off Africa Robien descent don't actually respond as well. Teo a sin hip eaters. So instead you give them these angiotensin receptor blockers and that again just acting on the same pathway at a different point. Uh, yeah, And if the patient doesn't respond well to either a sin hip bitters or andre attention receptor blockers, then you can give them, um, vasodilators like hydralazine or nitrates, and they also reduce the peripheral vascular resistance and make it easier for the heart to pump blood into the arteries. Uh, and you can also give basic blockers on. They all end in law her, which is quite fun, and Andi. The reason you give those is because in heart failure, the body's response is to activate the sympathetic nervous system on DCruz. Sick, sympathetic stimulation is really bad for the heart. You get down regulation of the beta, one receptors on back can cause cell death and the cardio my sights. And so the beta blockers will actually prevent. That's That's good on then. If the patient is on both of these drugs, a Z well assay that diuretic. But they're still breakfast, you know, they've still got that swollen limbs. Then you can start them on and spironolactone, which is the MRSA, that the flow chart mentions S. O. M. R A stands for mineralocorticoid receptor antagonist. So basically, spironolactone blocks the effective aldosterone on, so it also acts as a diuretic to get rid of that extra fluid. But unlike loop diuretics, like for Rossa myd, it's a potassium sparing one so it doesn't cause that problem off hope Ocaliva on Brittania and then just moving on to the next step. Don't worry. We're always at the end thought both types of heart failure a song is the patient is stable. You can offer cardiac rehabilitation on, but it's basically a bunch of exercises that help the heart to work harder. Um, in a sort Safeway's the patient could exercise safely. Basically on also, a cardiac rehab involves teaching the patient about eating healthfully, exercising safely and reducing stress. So basically managing the lifestyle risk factors for heart disease heart failure on If you've done all of that you've done over the floats up on the patient, for whatever reason is still worthless. They're still got that swelling. Then you do the classic Ask for advice. Always ask for help. S O hear you ask the specialists on about they'll discuss with the patient. Is these five options? But I'll only talk about the ones I've highlighted in blue eso, starting with the one on the far right digoxin that is, sit from some like Foxgloves or something. It's got a cold history. It's also a poison, but anyway, it's an I know tropic drug. So it helps the heart to beat harder on with more force. And that's useful in systolic failure because it helps the ventricles to push that blood out in cr trees. Um, it doesn't actually reduce mortality, but it does improve symptoms. On day studies found that it's really good if the patient has atrial fibrilation on day Finally, the box on the left Cardiac resynchronization therapy on the implantable cardioverter defibrillators. Lots of long words. But basically what that means is you're trying to restore the regular heart rhythm. Eso that the heart can contract in the nice, coordinated way on effectively pump the blood from the veins into the arteries and do its job. So that's it. That's all six. Um, that brings us to the end of the lecture. We've covered everything. Thank you very much for listening. Does anybody have any questions?