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Yu. All right. Um Good morning everyone, short introductions. Um I am George. I am an F one in Oxford. I'm on orthopedics, which I don't love, but it's ok. Um uh You might have met me if you came to our second session, but otherwise I was helping out last year quite a lot with this teaching. Um So that's me. So you guys want to introduce sales as well? Yeah. Hi guys, I'm Nas. Um I'm 1/4 year at MRI. Um And it's my first time teaching scrib up today and I'm also for and I beautiful. Well, I'm sure this session will go fine. And so, um overall we'd like everyone to be as inactive as possible through the chats. OK. That's how it's gonna make it um as interesting as possible cos I know it's a bit hard to keep it as interactive as face to face. So be chatty. OK? But don't on mute. Um Hopefully you'll know what's couple of this. Um Now this is obviously created by med students um for med students. It's not intended to replace the original um uni teaching. OK. Um But we think it's pretty good quality but now that you decide that um ignore this. So um as I said, contribute as much as possible, ask questions um if you don't know something that absolutely fine, just ask away. Um and enjoy. Right. So today we are covering heart failure, infected endocarditis and aortic stenosis um quite detailed, but it's not too much. So um just stay as focused as possible and we'll get through this. So starting with heart failure, um this all based on GL from 2022 what is heart failure? So, it's important to have a definition for ourselves and then define it for patients as well. So, as far as ourselves, um heart failure is defined as inability to generate enough cardiac output to meet the demands of the body without increasing diastolic pressure. So that's pressure when the heart is fully dilated just before it contracts, it can result from many, many diseases. Um So it can be ventricular systolic ventricular diastolic function or both. And we'll go through the categories a bit more in a bit. We also refer to congestive heart failure sometimes. So that's when you have heart failure, which is symptomatic and decompensating essentially. So, it's patients with heart failure that are very symptomatic. So they're gonna be breathless, they're gonna have pulmonary edema, they're gonna be fluid overloaded. Um So they can have water retention, um edema everywhere they can have ascites and that can also affect their sodium. So that's normally abnormal, probably a bit low. Um We'll go into that in a bit more detail. A bit later on. Um As far as the classifications, there are loads and loads of ways of actually, um categorizing it. Um So the main way we do it is through the ejection fraction and the timeline of it, the symptoms, the severity of them if it's left sided or right sided, although that's a bit old fashioned now and then if it's systolic or diastolic heart failure. Ok. Now, for patients, um this is a bit more acu um and it's quite a common conversation explaining what heart failure is. They've been diagnosed with this, tell them what's happening. Um Hopefully you should still be comfortable doing this. So it's when the heart can't pump around enough blood around the body to meet its demands. And overall as a disease, it can't be cured, but we can try and manage it as best as possible. Ok. Um Is that ok? So far? No questions. All good. Cool. So loads and loads and loads of causes. Ok. So we've tried to split it into a few categories. So starting off, we've got vascular causes. So you can have coronary artery disease. So that's ischemic heart disease. You have a heart attack, uh you have stenosis, it means the myocardium is stretched. Um And you that can result in diastolic heart failure. Ok. High BP as well. Then as far as muscular causes, you have dilated cardiomyopathy where the ventricles are institutionally dilated. So that can be a familial cause, it could be a genetic cause. Um but it can also be caused by many other diseases. Infections. Again, high potential coronary artery disease, et cetera. You can have hypertrophic cardiomyopathy, uh which again is genetic. So that's where the muscle is too bulky um to be built up and again, it results in heart failure. Um you can have congenital heart disease, you can have cardiomyopathies as well. So, familial um so again, inherited you can have infective causes. So, myocarditis, endocarditis as well. Um you can have immune mediated ones. So, autoimmune um heart failure, that's a bit more rare. Um toxins can also cause symptoms of heart failure. So alcohol, cocaine, certain venoms as well, pregnancy as well. Um I don't have an idea why pregnancy might cause heart failure. How would that uh what's the explanation behind that? All I want this chat to be buzzing. Ok. Just any any ideas? Why? Why would pregnancy potentially cause heart failure? Oh, there we go. Higher oxygen demand. Definitely increased blood month. So you have an an an extra little human in there. They've got extra volume on board through your placenta. You can have extra volume that can stretch out a bit more and then a heart failure picture good. Ok. Happy days. Um and then we can also have infiltrative causes. What does that mean? So, diseases such as psychoid dosis amyloidosis hemochromatosis, connective tissue disorders, um can result in build up of certain proteins or amyloid or granulomas or iron. And that can cause extra tension within the muscle itself. So that cyst or a affected and again, you can into heart failure. Is there any questions or not? Just fire away? Ok. We can have valvular causes as well. So, aortic stenosis, aortic regurgitation, mitral stenosis mitral regurgitation, those are the main valvular disease that can cause heart failure. And again, the cause is relatively straightforward. If you think about it, you're gonna have volume mismatch. So if you have aortic stenosis, you're gonna have a big volume overload in the left ventricle. So then the ventricle dilates to compensate and that can slowly develop into heart failure and similar stories with the rest of the valvular diseases. Ok. And they can have electrical causes. What do you mean about that with the arrhythmias? So, if you have af or tachyarrhythmias, that means again, there's a misbalance between the volumes of blood in the atria and the ventricles. Ok. So some chambers will have more blood, some will have less. But overall, there's a imbalance which can cause abnormal stretching, stretching and then um worse systolic or diastolic function. Ok. And another cause can be heart block. So that is when we have a complete mismatch. Well, it depends on heart block, but you can have a complete mismatch between the atria contracting and the ventricles contra contracting. So again, you have um a loss of balance between the volumes which can result in abnormal fluid status within the heart. Hopefully, that makes sense. I hope I'm not going too fast if I am. Let me know. Um So we have more courses. So we have high output heart failure. What does that mean that in causes where it's not necessarily a structural issue with the heart, but there's an increased oxygen demand, for example, in anemia, you have less blood going less hemoglobin going around. So what do you need? How, how's the body gonna compensate to get more oxygen around? It's the heart is gonna pump faster. Ok. And stronger. And that can result chronically in heart failure, thyrotoxicosis is the same. You're gonna have high t four, high t three, a high thyroid state, which is gonna have increased sympathetic response and an increased output as well. And again, chronically, that can result in heart failure, pheochromocytoma a bit more niche. But the main problem with that would be hypertension. Ok. And, and again, chronically can result in heart failure, sepsis, liver failure. V shunts is in on. What's the most common, how would you describe AV shunts? What's the more common term we use? If you don't reply quickly, I'll give you a hint as well. Let's think about kidneys, renal stuff. Um Not really thinking fistula. Yeah, perfect fistula. So what does that mean? So you're gonna have a lot of blood that's leaving the arterial system entering the venous system again, is causing a bit of a fluid imbalance between the compartments and can cause ventricular overload. And again, um disrupted systolic or diastolic function. Ok. Paget's disease. Um a bit more again, but that's essentially um a bone remodeling issue. So you have abnormal formation of bone, abnormal blood supply there. Again, imbalance and thymine is a similar cause. We have ba dilation, which can really be compensated. Sorry, that's quite a lot of detail there. So as far as drugs that can cause heart failure, we have alcohol, we have cocaine, chronic NSAID, use chemotherapies, especially um radiotherapy in the mediastinum beta blockers, calcium channel blockers. Those two, not as much. That's why we've not got them in red, they're not that common. Um But it's something to keep in mind and we have other causes. So pulmonary causes. Um We've not massively gone into this yet in our sessions, but you have CO PD, you can develop pulmonary hypertension. So high BP in the pulmonary vessels that can cause right sided heart failure and then you go into the complete heart failure. As I said before, overall, if your volume overloaded, you can increase the diastolic pressure. So if you have end stage kidney disease or nephrotic syndrome or are very obese, that can again, chronically result in heart failure is everything. Ok? I hope everyone has understood all that. Any questions just fire away. Ok. So moving on this is a bit more of a pathophysiology approach to um heart failure. So, the overall issue would be that if you have decreased cardiac output, you're gonna get an increased sympathetic response, you're gonna get vasoconstriction and you're gonna get stronger contractions by the ventricles. So an increased afterload. Ok? Another thing if you have low cardiac output, you're gonna have low BP. So you're gonna get a rash response which we have spoken about. OK. Um At that point, you're gonna have more fluid retention and you're gonna increase the blood volume. Ok? Um So overall that's gonna increase the cardiac output, but chronically, that will result in cardiac strain. Ok? And that chronic cardiac strain will result in heart failure. Ok. So it's a normal sympathetic response. But if it's chronic and long term due to underlying conditions, then that can result in heart failure. Ok. This is just a, this is a Frank Starling curve. OK. So again, it's a bit more of a representation of if you have a sympathetic, um the, the top curve would basically be the normal response if it's an acute phase of um sympathetic stimulation. So what we described before, but not in a chronic element and more in acute phase, then you have the normal phase and then we have um heart failure. Ok. So, decreased stroke volume and decreased diastolic volume. So what does diastolic volume mean is the amount of blood that's left in the heart just before systole starts diastole, relaxation, systole contraction. Ok. S now your input, um, how is someone going to present with heart failure? What symptoms are they going to have? There are quite a few things. So just at least one thing in the chat and, uh, shortness of breath or apnea. Perfect. And can someone actually tell me what Ortho apnea actually? Is edema correct? Um, anything else raise J BP? Perfect. Ok. So again, it's all the symptoms that are associated with fluid overload. So you can get ting edema. So that's edema, close to the ankles, you can get ascites. Um You can get um raised JVP. You can get pulmonary edema, pink, frothy sputum. Perfect. Yes. So again, that's coughing up pulmonary edema. Ok. Oral is shortness of breath when lying flat. That is correct. Perfect. Um And one more thing which has been mentioned. So it's yeah, paroxysmal nocturnal dyspnea. So we'll talk through that. So firstly, it's quite complex. Ok. Um So, so symptoms, you said breathlessness, so shortness of breath on exertion. Um General classifications um system of defining shortness of breath on exertion. It's used quite a lot in heart failure. Mm N yh A Perfect. That's New York or deal. Where is it New York? Um Don't remember what it sounds for because I can't heart association. That makes sense, doesn't it? Great? Thanks. Cool. Um Then breaths a rest and it's the same system. Ok. So off apnea. Um did someone define off apnea for me. I think someone did. But yeah, shortness of breath when lying flat. Does anyone know why that happens? Ok. Never mind. The venous return increases. Perfect. So you lie down, you suddenly get an increased venous return and fluid overload within the lungs, fluid overload within the heart. Ok. So that's why suddenly they get short of breath when lying down. Ok. Nocturnal cough starts coughing at night. Um, paroxysmal nocturnal dyspnea. So it's a similar pathophysiology process as or apnea. You lie down, it's just through the night. There is a bit of a change between the extravascular fluid distribution that causes build up of fluid again, which can suddenly mean that a few hours in of their sleep, they can suddenly wake up be quite acutely short of breath, coughing, pink frothy sputum. Um And that can happen quite a few times through the night, through the night and then I'll be sleepy all day. Ok. So we mentioned fluid retention as well. So, ankle swelling is the most common one. abdominal swelling. So, ascites um you have excess um you have a lot of fatigue as well. Um You can also get syncope. So whats syncope? Very quick definition? Mhm Painting, perfect loss of. So we have a question confused by a difference between par and alternatives, you know, or so, orthopnea is the acute symptom when you, so you're sitting upright, you suddenly lie down and you acutely feel short of breath. Ok. And that is because of the sudden increased venous return, paroxysmal nocturnal dyspnea is, you lie down fine. You might get apnea, you might not. But through the night you are asleep, um, because there is, um, fluid distribution as you're sleeping, as you're lying down a few hours in, you might suddenly wake up and have symptoms of shortness of breath, coughing and pink coughy sputum. Ok. Does that make sense? So it, it's a bit more of a not, not chronic, but it's a bit further down the line as you're sleeping after you've, you've laid down for a few hours. Ok. Cool. So, um a few other symptoms, you can have acute pulmonary edema, cardiomegaly. We'll talk about that in a bit hepatojugular reflux. So that's when you pressure on someone's tummy, you can see a raised a VP um neck vein distension. Um We said P ND or apnea or rales. That's uh crackles. Basically, you can hear a third heart sound. Um And you can also get weight loss as well. Ok. And that's because of treatments. So you're treating a further overload and that's gonna cause weight loss. Um, edema dys exertion, we've mentioned all of these. Ok? Is the pink sputum specifically also associated with P and D. No. So pink sputum is more referring to pulmonary edema. It's, it's not P and D. Ok. That's more just a hemoptysis situation. It's hems, sorry, that's blood. Um It's just coughing up pulmonary edema basically. So it's not infected. So it's just you're coughing up fluid. Ok. Uh So that can be, that's not specific to heart failure. That's just a bit more of a pulmonary edema, specific symptom. Ok. Any more questions? Just fire away. Ok. So moving on, what risk factors can we have for heart failure? We've already mentioned a few as far as the causes. Um, but you're taking a history, what, what should you make sure you're asking about quite a few again. Uh We'll answer that in a bit. Um So far away risk factors, we should know quite a few here. And this is, yeah, hypertension. Perfect. Yep. Rheumatic disease. Ok. Yes. Why is that? Um, fire away continue. You've got quite a few diabetes. Yes. What are the lifestyle factors as well? My cholesterol. Perfect. Yes. Um, so I'll just run through the smoking as well. Yeah. So most important one is probably gonna be ischemic heart disease. Ok. So you're gonna have disrupted coronary arteries. Um, you're gonna have ischemic parts of the myocardium. They can't contract as well as they could. So you're gonna have a volume imbalance. You can't have normal diastolic and systolic function. Ok. So that's really important to ask about diabetes, old male. Um, that's just epidemiological, probably because of risk factors. Um, hypertension. You mentioned high cholesterol. We mentioned obesity. I think we mentioned smoking, physical inactivity as well and many, many, many more. Um, let me just go back to a question. I've got raised J BP, raised in right sided failure only or left two. I mean, raised JPP would be a symptom because you definitely have right sided heart failure. But a lot of the left sided heart failure will result in right sided heart failure that will result in a raised J BP. OK. So the rough rule to remember is that if you have left sided heart failure, the blood is building up in the lungs. So you're gonna get pulmonary edema. If that's very bad, it'll move into the right side, get right sided heart failure and that's gonna backtrack. OK. So you get a raise ABP um as um pedal edema, pitting edema, all of that. OK. So that's the referral. So moving on, we've mentioned these. So symptoms, fatigue. OK? Makes sense. You're working much more hard to get your basic oxygen requirements, shortness of breath. You can get wheezy off apnea, weight loss, cachexia, elevated JVP, displaced apex. Can someone tell me why you'll get displaced apex in heart failure? And if it's left sided heart failure, why will it be displaced towards? There's a bit of ecg knowledge we'll go through in a bit uh cardiomegaly hypertrophy. Yes. Yes, perfect. So I perch feet towards axilla, perfect, more lateral. What does that mean you have left axis deviation? OK. I don't know what your ECG knowledge is currently. I appreciate it's a very difficult content we're not gonna massively overanalyze that, but we'll mention it a bit later on again. All right, peripheral edema, um, crackles, additional heart sounds, you can get an S3. So, again, that's because you have a much bigger ventricle which is contracting, it can generate a third sound. I've never heard one. I'm sure they exist. I'm not cardiologists but, um, it's something to definitely mention in exams. Ok. So we have the New York Heart Association symptoms, severity. I'm just gonna talk through this cos it might take ages to get through this chat. So, class one, we have no limitation of physical activity. Um, then class two, you have slight limitations. So you can still do your ordinary activities, but you're a bit more tired than normal. Um, class three have limitation of your physical activity. Um, you'll be comfortable but uh, any, any ordinary activity has fatigue and then plus four, you're basically, um, you can't do anything, um, any, any extra movement, any sort of exertion causes you symptoms. Ok. Um, so quite an easy system of classification. Really? Ok. No. How are we going to diagnose heart failure? Um What blood tests can we do? And it's not called British National Party BNP, correct. What does, what does BNP stand for? And wires are produced? Oh, silence. No, I want someone to at least give it a go. I don't care. Yeah. Brain natural peptide. Yes. Excellent. And it is produced in the Myocardium beautiful. You think it's in the brain? It's not? Ok. No. So we have the signs we have the symptoms and I want to investigate. So we'll start off with PRO B MP. Ok. Uh 01 sec. Um perfect. And it is released when you have excess ventricular, well, not excess ventricular stretch. Ok. So it makes sense that when you have a response where your ventricular, where, where your ventricles are stretched, there's gonna be some sort of mechanism to bring you back to a bit more of a balance. So normally a stretch. So it gets um reduced systemic vascular resistance. Ok. So you have smooth muscle relaxation, your vessels dilate a bit. Um It has a diuretic effect on kidney. So you offload some fluid. Um So overall, it will offload the heart. Why? Because cardiac output is systemic vascular resistance times um BP. Ok. BP is gonna go down through the loss of blood for you and from vasodilation and peripheral vascular resistance is also going down by the relaxation. So overall reduced cardiac heart but reduced cardiac strain. What's the difference between B MP and anti B MP? That's a great question. Um I don't know, to be honest, I think it's the same thing, but um I will look into it after I'm done with my slides and I'll come back at the end. Good question. Um So if you have a high result that shows that you have heart, um heart stretch, you know, ventricular stretch stretching. Ok. Um And a chronic effect again, that means that you're probably gonna be in heart failure. All right. So, overloaded, not pumping effectively as we said before and show the graph. That's according the Frank Starling lot. OK. Uh Sorry, checking the chat again. Um I'll check, sorry, I will check the B MP versus probably B MP in a bit. Uh on a bit of a side note, um overall this can be treated with so a bit more niche but angiotensin receptor, neprilysin inhibitors can help produce um pro B and P levels. Ok. Um So medications such as Valsartan and secure. Ok. That's a bit more new stuff. Cool. Now, how do we interpret pro B MP? So if it's very high, more than 2000 urgently cardiology clinic, we normally have heart failure specialists and they need to get an echo and they need to be seen within two weeks. If it's raised, you'll refer routinely for an echo. So, within six weeks and if it's normal, then you'll look into other diagnoses. Ok. Now, it can be falsely low or falsely high depending on the situation. So sometimes you can have heart failure where um there is not necessarily increased stretching, but there's just um a high proliferation of the myocardium itself. So you just have impaired systolic function, but it doesn't necessarily mean that it's stretched. Ok. So it's something to cons, so, you know, you always think is PRO B MP gonna be enough to make a clinical decision. Probably not. Ok. Um So moving on, say we have done the B MP, it's come back raised and we are going to send them for an echo. Now, what do we look for in an echo? What is an echo of the, an ultrasound of the chest? Which is here? I I'm gonna speed through this a bit. Uh What's the chest hang thickness of walls? Yes, that's definitely one thing. So overall, you want to assess systolic and diastolic function of both ventricles, but you get many view. So you're gonna see the valves and you're gonna see the pericardium, you're gonna see the thickness of the walls. So it's a very, very useful investigation and it's one of the main things, one of the basic cardiology investigations that is done for most cardiology patients. Ok. Now, it can also show coronary disease. Um How would this show on an echo? How are you gonna identify if there's any coronary disease? We've kind of made a few, a few suggestions earlier on about how this can be demonstrated. Uh Anyone in the chart? No, just fire away any ideas how you can assess. So obviously, each coronary artery is gonna supply specific territory of the myocardium. How are you gonna assess if one is affected or, or not? Mhm. Ejection fraction. Yes. Yes. That's not gonna be very specific to a coronary artery though. Is it when the walls are thinner than usual, you're closer. Uh You are closer. I will give it away. I think. Um you will see regional wall motion abnormalities. OK. So you're gonna assess the myocardium, see specific regions of the myocardium that are not as mobile as before, not moving much, not contracting, not relaxing either. So that shows a bit of ischemic heart disease. Um Yeah, perfect. So will certain parts of the walls work less? Exactly. That's exactly what happens. Um They're not supplied with as much blood as they need. So they're slowly not gonna move as much. Ok? And if you have a heart attack, if you have a big one, then you can have many areas of dismotility or complete immobility, which won't move at all. Ok? So what can we see if they have heart failure? You will see depressed and dilated ventricles, hypertrophic ventricles. So that's why there's a lot of muscle bulk. You will see the ventricles not filling normally. So, impaired ventricular diastolic filling. So during diastole, um and then as far as um ejection fraction, it is the amount of blood ejected out of the ventricle compared to the initial amount in the ventricle. Ok. So it's basically a percentage. So, so you have 80 ML S eight ML s of blood, it's gonna be more than that in the ventricle and then 40 of it is released during systole. Um then that's an ejection fraction of 50%. OK. Quite simple. Really. Yeah. So a formula of basically what I just said is stroke volume. So that's the amount of blood um that is leaving the ventricle joint contraction divided by left ventricular end diastolic volume. OK. So that's the total before systole. OK. I hope that makes sense. No, the definition that we use for classification a bit more commonly nowadays is heart failure with reserved ejection fraction with sorry with reduced ejection fraction. So that's an ejection fraction of under 40%. And that's normally a systolic problem. But you can also have heart failure with preserved ejection fraction. So that's more than 50%. No. How can someone have heart failure but have preserved ejection fraction? And I'll ask her this one of the chat questions in diastolic. She definitely and the actually diastolic issue covers most of the things really cos it means that you can have if you have a very reduced enddiastolic volume in the left ventricle. Sure, maybe all of it goes out. You have an ejection fraction of 100% but it's not much at all. Is it? So you can still have heart failure because you're not getting enough blood um to perfuse all the distal organs. OK. Um So yeah, it might be all of it but it's not enough. Perfect, cool. I hope that's all making sense. Um I wanted to ask that of mind, what if an echo is inconclusive, then we move on to a much more specialized tests. So you can have a cardiac MRI. Ok. So this is gonna be much more accurate. It's much more expensive and you can also do debut stress testing. What this involves is having someone on a treadmill um and getting some exercise and assessing symptoms and then assessing severity of heart failure and having a look at the chambers in a live view. Ok. Could you briefly explain, reduced, best preserved? Yes. So I'll go over it again if we have um reduced ejection fraction. That means that um so what we're aiming for normally is an ejection fraction of 55 to 65%. Ok. So that means the 55 to 65% of the blood that was in the ventricle before systole is sent off. Ok? And that means that roughly 40% remains in the heart. Ok? Now, if you have a reduced ejection fraction, it means that out of the blood that's collecting in the left ventricle before contraction, not much of it is actually going away. So a lot of it is just staying in the heart. So more than 60% is staying within the heart, ok? And that could be for many reasons, but mainly because um systole is impaired. Um and you don't have enough energy to send off all that blood off, ok? If it's preserved, it means that enough blood is exiting the ventricles. Ok? So more than 50% which is normal, but that's not enough blood still. Ok. So if you're in heart failure, preserved ejection fraction, yes, your heart is pumping out whatever it can, but that's blood isn't enough. Does that make sense? If anyone still doesn't understand that? Let me know and I can explain it again. There's no issue. Um Another question is echo first or chest X ray, chest X ray is a bit more useful in ruling out other things. Um And it's more for acute acute heart failure, although you will get chronic issues as well. Um I'm sorry, we'll just say here again. So if we preserved, is there less blood entering the actual ventricle? But all of it does leave, correct. So you have reduced blood volume in the ventricle. OK. But enough of it goes. So when you have a reduced fraction, could you please explain it again? Yes, I will. Um Let me just wait for theo one you have reduced. Yeah. Mhm Is it the preserved bit? That's uh is it the reduced bit? That's co that's more confusing or the preserved bit? Just so I can focus my explanation a bit better than preserved? OK. So preserved, right? If you have preserved ejection fraction, it means that more than 50% of the blood that was in the ventricle before contraction has left. OK. Has gone through the aorta and gone to the rest of the body. OK. So more than 50% has gone. But it means if you're still symptomatic with heart failure, ok. It means that not enough blood, the, the, you know, the walls are so thick that you're not getting enough blood in the heart. Um, to actually send off enough blood to the brain to the kidneys, et cetera. What would be the difference in presentation? Um, presentation would be the same cos the issue is that you're getting, you're not getting enough blood to the end organs. OK. So preserved versus reduced is gonna be more of an echo finding rather than a presentation aspect. Now, what I'm gonna do, I'm going to move on to the next bit. However, at the end of this, if he is still confused, we can have a better chat about it. OK? With the difference between a hypertrophy. Yes. So if, if it's hypertrophy, then there's not enough space for enough blood to come in to the ventricle. OK. So you're not gonna have enough, a big enough end dilic end diastolic volume to send off enough blood to get a good enough cardiac output. OK. Right. OK. We're gonna move on now, we can chat about this again at the end. All right. Sec next step of the diagnosis, you will get an ECG. Now what findings on an ECG can suggest heart failure or prior ischemia because that's been more helpful. Would that could be done for chest X, chest X ray and E CG probably not just because of a practicality, uh element of it, but it could be um so ecg findings deep Q waves. Yes, thank you. What about the QR S arrhythmias? Sure. What's the QR S gonna look like? So, the QR S is what QR S is ventricular contraction. So, if you have a bad ventricle, how's that gonna present longer, QR S so broad QR s, correct? Deep Q waves, correct? Ok. I'm gonna speed up a bit just because we have still, we have a lot to go through so broad QR S that can be again, previous, it can have a hypertrophic ventricle, left axis deviation. So as we said, as we explained before, that's going to be the because of hypertrophy, your heart is gonna be contracting a bit more towards the left side because you have a big left ventricle. OK. So left axis deviation, you get QT elongation. QT is what it's the sum of ventricular contraction and ventricular relaxation, repolarisation. OK. You can have a bigger ventricle, you can have a prolonged QT, deep waves, large R waves, T wave inversion, all the same principle, larger ventricles and potentially abnormal rhythms, which can result in these changes. OK. This is an E CG. So uh if you can see my cursor, um this would be the S waves. Uh you can, you have a slightly broad cures, I'll be honest, it's not great quality and I can't really measure the small boxes either. Um There's some inverse T waves. Uh Not really. Anyway, this is just an example of what we said before. Ok. Uh Cool. So back to the basics of it again. Uh One sec, please go back on with our ECG in screen for sure. Uh What's that called? One sec? There we go. So UR left a deviation bong t deepest waves, large R wave, I would suggest going life in the fast lane is a very good ECG website. You will find all of this there. Ok. Right. Moving on back to basics. Where are we? We've taken our history, we've got signs, we've got symptoms. We've done an E CG, we've got a PRO B MP. Um We have done an echo and hopefully at this point we have a diagnosis. Ok. So as we said, we can have reduced EF to under 40%. You can have moderate, moderately reduced. EF don't pay too much attention to that. So that's 40 to 50% and then you can have preserved ef so that's above 50%. So after that, you want to assess the risk factors and then start the treatment? Ok. Good. So can anyone see anything on this chest x-ray that could be just in far for you? I can't see much here. Oh Batwing. Ok. Ok. We're gonna move on a bit of a trap. There's nothing. Ok. This is an absolutely normal chest X ray. All right. Cool. So moving on, um, this is more what you will see in an abnormal chest x ray of heart failure. So we have mentioned one thing back wings that wings are gonna be here and here if you can see my cursor, I'm not sure you can. Ok. And that's overall congestion in the pulmonary vessels. Any other signs that we can see on a chest X ray that you're aware of? Hopefully you should know at least a couple of things. Curly bee line is perfect. So there's a curly beeline here, there's a color B line here, here, here, all of the white lines. OK. What else? Um Co beelines. Yes. OK. So alveolar edema battling sign co be lines, we said cardiomegaly as well. Do you want an AP or APA film to assess for cardiomegaly? And why PA correct? Y I'll get to uni in a second. So why do we want APA you're not on AP correct? Heart is enlarged in AP. So if you think about it, yeah, close proximity. So when you're doing an AP, um you're gonna send the X rays from a larger distance. So whatever happens, you're gonna see the heart in a magnified state. OK? Pa is gonna be much closer to the heart, so it's not magnified. So you'll get a much better sense of the actual size. However, in an AP, if the heart is normal, if it doesn't look enlarged, then you're probably safe to say there's no cardiomegaly, but always say that you want to assess heart failure or cardiomegaly rather from APA film. What are col beelines? So that is collar beelines, a pulmonary edema in the fissures between the lungs. Ok. Um If that makes sense, so we said cardiomegaly dilated upper load vessels. So you normally get them around here. Um Then we have effusions. What's the main thing we look at in effusions? What's the main sign on the chest X ray? It is not very evident here. But what, what would you, what would you be looking at? Costophrenic angles? Perfect. So blunt costophrenic angles. Ok. So that's gonna be these angles here. If it's a big effusion, then you'll get a meniscus sign. Ok. So that's a disc, almost like a disc um shape at the top of the effusion. Ok. Um So fusion is very common in heart failure, right? So moving on, we don't all these investigations, but it's, you know, if you just take it in isolation, they're quite nonspecific symptoms. Really? It's shortness of breath on exertion. It's a bit of pulmonary edema fluid overload. If you just see an acutely one patient like that, it's not, you know, heart failure is obviously gonna be a differential, but you're gonna have to consider other things as well. So CO PD is one asthma coronary embolism, you can have again, shortness of breath, uh obviously, you can have a little bit of chest pain probably in that, but not always, he might be have a have a bit of hemox, but again, it might be a bit difficult to differentiate between hems and pain across his fet, for example. Um I'm not saying, you know, PD obviously is gonna be a slightly different presentation, but it's something you need to consider. Ok. It's not black and white, um anxiety, shortness of breath, um lung cancer, um then I'll just run through the other ones as well. So prolonged inactivity, manage insufficiency, nephrotic syndrome. So that's when you're peeing out too much protein. So again, you have load imbalance some drugs, um low albumin, you can have pelvic tumors. Um you can have so, oh, how can you cause? Uh yeah. So if you have a pelvic tumor, how is that gonna cause pulmonary edema? Peripheral de relatively straightforward? I think if you compress any of those, if it's infiltrating in one of the vena cava or uh one of the lower limb veins, then you can get Perine. Ok. Then obesity, severe anemia, bilateral renal artery stenosis, you can get hypertension. Ok. So it's just a list of things to keep in mind. Just always remember they're broad symptoms. So you need to keep a broad mind to start off with. Ok, cool. And while we stop. Oh dear. Ok. Now, complications you can get arrhythmias. Ok. Depression is very, very, very common. Why it makes sense means, you know, especially if it's a very severe form of heart failure, you can't immobilize much any sort of immobilization is very, very tiring. Um You have a very, you know, you probably have a heavy disease Burton previously as well. Um And you have quite a low. Um, the survival rates aren't great either. We'll have a look into that. So 20% of heart failure patients can present with depression cachexia. Um Again, you have a big fluid overload. Um And you have cardiomegaly, you have a lot of things that can contribute to protein imbalance, et cetera, which can cause cachexia. Ok? You're gonna lose muscle, um chronic kidney disease as well. You have fluid overload. Um sexual dysfunction, that's important as well. Sudden cardiac death, again, very common in 50% of heart failure patients. Ok. Um So it, it, it sounds like it's uh you know, you think heart failure as, as a chronic thing, but it has very severe implications. Ok. And death. Unfortunately, so 50% of people with heart failure will die within five years. Ok. So that's massive. That's absolutely massive. Ok? I think that is my section done. Um Any questions so far? What time is it? Yeah, I think um all right. If you have any questions, private message me. OK. And I will try and answer them either now or at the end, right? I will hand over. Do you wanna share your own screen up front? Sorry, just give me one second. I can see that. Ok. Dokey. Right. So George has just been going through like symptoms, signs, how to investigate it. So now we're gonna go through the management. And so like George said, it does, it can go up as an osculation, which is basically just explaining the management for it for a patient. So the first thing before we go into medical management, lifestyle management is also really important. Um So a few things to remember is for heart failure patients, they get vaccinated annually influenza and they get a once only hemocoel vaccination. So that's in terms of vaccines and then in terms of lifestyle modifications or if you're explaining to a patient, you can tell them like these are the things that we can do at medical and this is something that you can do as well that can help like the prognosis of your condition. They'll like try to reduce smoking if they smoke, try and reduce alcohol. Um advice about traveling, driving that sort of thing. Ask you if you can also like name drop heart failure, specialist nurses as well because they have a lot of influence in like patient information about heart failure. So that's really important as well. Um So that's in terms of lifestyle, then we'll go on to medical management. So this is kind of an overview we love pneumonics and medicine. So the one that we got taught was a a so Aba L like an overview of the medicine of the main drugs that use in heart failure But when you think heart failure management, think of these four drugs. So how, how we're gonna split heart failure management today is preserved ejection fraction and reduced ejection fraction. So if you've got reduced ejection fraction below 40% then you're gonna use a certain set of drugs. And then if you've got preserved ejection fraction, the management is sort of different. So we'll go through first to reduce the ejection fraction. So if you've got below 40% which obviously we'll see on an echo, the main things that you're gonna start with the A and the B of our A bons. So you're gonna start with an ace inhibitor and a beta blocker. Anyone know the mechanism of action of an ace inhibitor? Can I see tough, I can't see this. So it's fine. I'll just talk through it. So ace inhibitor, we know it stops the conversion of 10 to 1 to 10 2. So you're gonna stop the vasoconstriction of the vessels and you're gonna cause vasodilation. And then beta blockers, we know reduces the heart rate by reducing the heart rate. You're trying to reduce the workload on the heart, allow it to pump more blood if that makes sense. So you're reducing the workload in the heart. Those are the main two first line drugs that you're gonna give patients with a reduced ejection fraction. Um Obviously, for both of them, you're gonna manage comorbidities. So for example, if you've got diabetes, if they've got other CO PD other conditions, you're gonna manage them as well. Separately. Seven, then if your symptoms persist and the ace inhibitors and the beta blockers aren't doing what they need to do. Then you go on to A and L which is the second half of the pneumonic. So, A stands for aldosterone receptor antagonists and the L stands for loop diuretics like U furosemide, for example. So for reduced ejection fraction, you can give aldosterone antagonist. Now, what they're gonna do is aldosterone antagonists, try and reduce the fluid overload that you can have in patients. Um And then the loop diuretics, loop diuretics aren't really used in, in like the routine management. But if patients have symptoms or if they have like really puffy legs, for example, or a lot of fluid overload in the chest, for example, you can give lo loop diuretics to reduce fluid overload. And if your symptoms persist, then you're gonna go on to these which are your extra drugs that aren't really first line. So this is, it looks very overwhelming, but this is I believe European Society of cardiology. So these are the guidelines. So if we talk through it, step on, you've established diagnosis of reduced ejection fraction. So someone has a reduced ejection fraction of below 40% you're gonna initiate your medical management. First one is an ace inhibitor and A and I in depending on. So usually they start with an ace or an alb if an ace is obviously under indicated or for example, they have like a dry cough that's persisting. So you change it on to an AL B and you have a beta blocker, which you talked about, then you have the MRA which is stands for aldosterone antagonists. Um and then diuretics as needed if you have symptoms SGLT two I, these are the inhibitors that um flosin things like that. These, these are like the newly added in heart failure management that can be helpful, especially for example, you've got a patient with type like diabetes and you can give this drug um because it kind of manages both. And I think that kind of also reduces the workload on the heart as well. Step two, if they're not helping, then you can just titrate basically the doses, increase the doses, then if these aren't working. So these are kind of like the a a drugs that we talked about. If they're not working, then you can add the extra drugs. Um Let's go back uh these ones. So hydrALAZINE azine, this one and digoxin. Um So if you've got an african-american patient, they usually start on hydro nitrates. Um and then you can add these as well. We don't really need to know much about them. But those are the second line drugs that can be added if symptoms existing. Then after that, then you can start with like interventions like these, these on here, which are kind of like mechanical interventions. So ICD is implantable defibrillator. All that is, is patients with heart failure are, it's, it, it's kind of like a two way street. They're more likely to develop arrhythmias and people with arrhythmias like atrial fibrillation that can sometimes cause heart failure. So if they have because they're more likely to develop arrhythmias, obviously, we don't want them to have arrhythmias. The d it can cause loss of complications like strokes or. So, what an ICD does, it basically monitors the heart rhythm and anytime they see a change in our heart rhythm and then they like it's beating faster or there's, there's uh there's like something not normal, it kind of like zaps an electrical pulse that kind of resets the heart rhythm again. So they can have that implanted or they can have um the CRT which is card fibrillation something and then the defibrillator. So what that is is that basically there are some patients with heart failure can have electrical desynchrony. So what that means is the heart, basically, the ventricles aren't pumping at the same time. So what and if they're not pumping at the same time, that's gonna reduce the ejection fraction even more and cause even more symptoms. So what CRT D is for it basically again, causing electrical holes and trying to and cause the ventricles to contract together. If that makes sense. Then step five, you can reassess symptoms. Look at what's working if it's refractory. Basically, it's, it's not treated, it's untreated, like it's basically not worked with any other medication and you're gonna continue here GD and just basically medical therapy or if that's not worked, then the last line basically is a cardiac transplant. OK. So a heart transplant is the last one I've talked through things. So that's reduced ejection fraction. Now, with preserved ejection fraction, again, try to address any underlying cause. First, if you've got any underlying causes to treat that lifestyle changes. Again, we've talked through and comorbidities, but with preserved ejection fraction, they're not started on a routine medication. It's usually just loop diuretics. If they have symptoms. If they have symptoms like really puffy legs that causing a lot of concern, then you can give them um fewer of mind for that. So then these are the guidelines diuretics as needed. SGLT two, which we talked about and then these ones in orange. So basically this guideline is split into classes. So like one plus one is like there's loads of sufficient evidence. So that's really helpful and efficient QB is where it kind of goes. Like the evidence is a bit conflicting. I don't know if it helps or not, but it can be basically given um bilateral compression. OK. So we've talked about CRT ICD, we talked about how they work. There's more guidelines that we look through here. Um And then we talked about the heart transplant as well. If, for example, they've got valvular disease. They can also have like valve replacement or val, which we'll talk about like stenosis. And again, this is really important. Yeah. So Georgia was talking about there's loads of causes of heart failure. So we always need to address the underlying cause. Like if you've got thyrotoxicosis, put them on anti drugs, you've got valvular disease and try and treat that as well. And 07 shots. That's good. Oh, there's loads of questions, I'll go through them later because so much. Um So CRT, again, this is quite detailed. So I would just know what CRT is, how it works and why it's important. But we can go through it very quickly if you have a left ventricular ejection fraction of below 35%. And it depends on your ification. So it depends on your symptoms. Again, we looked at if it's two B, it basically means I've written it down, but it basically, it's, the usefulness is less well established by the opinion. So we don't know, there's not enough evidence basically um to say if it's really useful and should be given to everyone. But it can be considered if they've got like a left bundle branch block with that with a QR s longer QR s longer than that. So what that means is basically, there's a problem with the electrical conduction system where they go through like the A V node and then it goes down to like the fibers and the, and the bundle of his, and there's this kind of a block in the electrical conduction system. So they kind of the ventricles contract a bit differently. So that can be given that in NIH a class two. So they've got some symptoms and if you've got a left bundle branch block of that, the PR S is longer than that, then they can be given CRT. And we know that there's good evidence for that. Um If they've got between 36 to 50% so it's kind of in the middle and they've got heart, high degree, complete heart block. So there's no electrical conduction going down and they can be given the CRT again with this, this is very detailed. So you can look at it in your own time. Um If you're really interested in it. Um But yeah, I think the main principles we've um talked about are important and this is quite interesting. So basically, this is what we're saying, if anyone has heart failure and have COVID disease, always remember to treat the COVID disease as well. We can't just focus on heart failure. So it's very simple to go through. So if you have hypertension, you're obviously gonna give them treatment according to the hypertension guidelines for anti hypertension hypertension drugs, if you got type two diabetes. So he said that they can be given SGL T two inhibitors. So it kind of works for the hyperglycemia. And we know that it helps with heart failure as well because it reduces the workload in the heart. Um If they've got, if they've got ejection fraction less than that, and they got to a Coronary anatomy. So there was sort of like history of ischemic ischemic disease, then they can be given revascularization. Um And if they have, for example, heart failure and atrial fibrillation. So we said it's quite common for them to either have a AFIB because of heart failure or they can have AFIB with heart failure. And obviously, you need to anticoagulate them, which is really important. Um Again, these are so these are two A. So this is obviously less well established evidence than class one. But again, you can go through this for management and then the last thing is Cor Pulmonale. So I think George to touched on it a bit, but it's basically right sided heart failure. Now how it happens in second year if you remember you have the VQ ratio. So you have the ventilation to perfusion ratio, which we need to stay at about usually not 0.8. Now, in, for example, COPD is caused by loads of pulmonary diseases. But the main one is COPD in COPD because of the pathophysiology, you're gonna have reduced ventilation and basically it can cause hypoxia. So you're gonna, the ventilation is gonna kind of go down and the perfusion needs to go down to match that and keep the ratio of naught 0.8. So to reduce the perfusion, you're gonna like basically vasoconstrict the pulmonary arteries to try and reduce the blood flow going through that. Eventually. If you keep doing that, you're gonna get really high, high pressure in those vessels, you're gonna get pulmonary hypertension. And that can basically cause a back flow. Loads of blood goes back into the right ventricle. And that basically causes right ventricle failure. And because you get hypertrophy to try and push against that high pressure in the pulmonary vessels. And so you get right sided heart failure, initially, they could be asymptomatic, but then you get very similar symptoms to your heart failure. So shortness of breath, um edema, syncope, fainting, um and other signs on examination. So for example, Sinois raised J BP peripheral edema very similar to a heart failure presentation. You can get different heart sounds as well. Now on ECG, if you look at this, on the right, basically, people mo and so people moles, you've got like a really tall peak P wave and that can be indicative of right, right atrial abnormality, which fits into our picture because we know it's rightsided heart failure. Pmi is kind of like indicative of left atrial um abnormality. So if you have that, then you kind of know it's not a Cor Pulmonale picture in terms of management, you, they don't really do much. You obviously try and treat the underlying course, optimize the COPD management and then often they just, um, on oxygen basically to try and manage the symptoms of hypoxia. But it does have quite a poor system. Um, and, yeah, that's it. So, I'll just quickly, sorry, I just go through the chat to make sure, um, can you see the chart in line? I can now? Yeah. Oh, George's reflects them. Yeah. Ok. That's fine. Ok. I just, yeah, go ahead. Ok. Ok. Can you see that? Yes. Ok. So, hi guys. So I'll basically be covering um sort of acute heart failure today and also infective endocarditis. So, um with acute heart failure, um essentially what it is, it's a type of life threatening heart failure caused by a patient who already has chronic heart failure and they kind of decompensate. So they'll present um sort of potentially A&E with sort of shortness of breath. Um and hypoxemia. Um it's very rare to have heart failure as like a first onset. Ok. Most patients do have a history of chronic heart failure. But if they do have a first episode of acute heart failure causes can be things like viral myopathy valve issues or like mitral regurg or some type of toxins as well. Um So pulmonary edema, um George kind of explained it well before the sort of the passive physiology around it, essentially what it is in left side, heart failure, you get a backlog of this blood. Ok. And it goes to the pulmonary veins and causes sort of like sort of hypertension there. And that causes sort of um fluid to leak out into the lung tissue. And that's how you get pulmonary edema. And so patients again will present with shortness of breath and also hypoxemia. So low oxygen. So, um so I can't really see the chart, but at this point, I probably asked for what kind of things could trigger a decompensation with chronic heart failure patients. Um And this is actually really key to remember because in our sys last year, we got like a picture of um like it was like a pa patient presentation who had heart failure and then they had an episode of acute heart failure. And you had to kind of like find out based on ECG and symptoms, what that trigger was for decompensation. So different reasons could be things like an M I. So in a CS, you could have a sty a non ST um you could have a hypertensive crisis, you can have an acute arrhythmia, you could have valve issues, they could be septic and they can even be IIC as well. So if you give really aggressive IV fluids in an elderly patient who has heart failure, that can also be a trigger for decompensation. So with this, it's kind of key in looking at what, what kind of symptoms and would show and sort of like observations. Ecgs try and figure out what, what is the trigger for their decompensation. So when a patient does have acute heart failure. Again, they'll present with this rapid onset shortness of breath and also type one respiratory failure. So type one, we know that type one, it's one gas that's gonna be affected. So it's the oxygen levels um and you'd see it on ABG as well. So tests are kind of run in a patient with acute heart failure. You want to have a chest X ray, you wanna have an E CG, an ABG, obviously take a good past medical history. Um do the full A two assessment and also look for blood. So any infections is there, is there raised drops, a raised BNP, things like that to try and figure out the underlying cause of that decompensation. Um So, yep. Um oh yeah, before we do that. Yeah. So you need to think about what kind of things you'd see. So especially an ECG, if it's an acute arrhythmia, you'd see changes on an ECG to represent that. If it was sep sepsis, you'd do an ABG sort of high lactate things like that if it was an infection R ICR pe sr um and if it was an mir drops, ok. So it was last year, it was an M I they had, so we got given ECG with sort of like the um sty changes. Um So yeah, um and acute differentials, again, the patient could be having an asthma exacerbation, ac O PD exacerbation, they could be having pneumonia. So there's, there's sort of three main differentials, sort of rare ones you can come across are good passer syndrome. That's sort of like a past med one that if you know that you know that, but it's essentially, it's like a autoimmune disorder that affects the lungs and the kidneys. That can be a differential for acute heart failure and also ad S as well. So, a s is acute respiratory distress syndrome which again, you can read a little bit about that if you're interested. Um So, yeah, so key things make sure you remember the triggers, what can cause decompensation. So, in terms of treating patients, um there's a good pneumonic. So I don't know if it'll pop up on the screen somehow. Um but I'll come on later. So how they present is shortness of breath, they'll be very, very unwell, they'll be er very edematous. So again that pedal edema pitting edema that George mentioned before, um and they can have this like frothy wink wink, white, pink sputum being coughed up, ok. And that's essentially the edema from the lungs kind of being mixed in with blood, I guess being coughed up. Um because there's quite a lot of pressure going on up there. Um and different signs. So things that you'd see on sort of examination, they'd have a very um increased respiratory rate. So they're breathing quite a lot because they're very short of breath, they have um low oxygen sets they're tachycardic, they have a Rage J BP which is again, George mentioned before. It's, it's a sign of both right and left sided heart failure over time. Um an S3 gallop which I've again, I've never heard. So it it's it's there. Um they can have bilateral crackles and also there can be hypertension as well, so that can indicate some sort of cardiogenic shock going on there. So again, yeah, these are important signs to remember. Um And again, you want to treat them based on the signs of any underlying causes. So if you have an A CS, treat them for an ACF if it's sepsis, treat them with sepsis, et cetera. So why would a CS cause acute heart failure? So again, I can't read the chart um but I'll give you guys like a bit of a minute to think about it like why would having a heart attack? Why could that be a trigger for decompensation? So just think about it. Mm. But yeah, I'm trying to see if I can read the chart, but I don't think I can. No. Mm. Ok. So um with a CS um obviously if there's ischemia to the heart muscle in the heart tissue, um the heart won't be able to pump properly. Ok. It can't contract properly to then squeeze blood out to the rest of the body. So that can be a cause for the failure um an arrhythmia. So why would an arrhythmia cause acute heart failure. So again, in heart failure, the heart's already finding it difficult to pump and keep up with the demands of the body. If you then put an arrhythmia on top of that sort of AFIB or some sort of S VT, for example, that's gonna make the heart, the heart even harder to contract normally. So, an arrhythmia again can set someone off into heart failure. Um and again, they can also have signs of right heart failure. So again, the hepatomegaly, the ascites or ABP, they can all be signs again, seen in heart failure. Um So yeah, so this is a treatment for it. So there's a good um sort of um little a room in the corner, so poor sod. Um and it's really useful to remember that. So poor being pour away any IV fluids, the patient could already be on because again, you don't want fluid, overload them and make their pulmonary edema worse. Um You wanna sit them up so make sure they're not lying down, you want to sit them up nice and tight in the bed and then sort their oxygen out. So again, if their is below 94 s, that's wise you wanna increase their oxygen with s sort of like um high flow nasal oxygen. Um And again, if you've got a past medical CO PD, you wanna make sure it's within the oxygen range for that as well. Um And again, you wanna get some IV access, you wanna monitor EC GS and treat any arrhythmias they might have currently. Yeah. So carry out chest X ray, ECG use knees drops ABG and echoes and B and P as well. And then what you wanna do is give diuretics. So the one that they tend to give normally is IBU which is either 40 to 80 mg very slowly as well. You don't wanna give it too fast. Um because that can be quite aggressive. And if they've got renal failure, give a higher dose. Ok. Um So, diuretics sort of the mainstay, a bit of a treatment of the edema going on there. And again, diuretics can help the patient start to breathe properly back again as well because they're suffering with the shortness of breath. Um A March doing all this monitor all their fluid intake, their output, their using. Um this is a very standard procedures to carry out. Um And obviously, if the heart failure gets too much to the point where they have to be put in HD U, which is high dependency unit, then things like dimorph can be given. Um dime morphine is really useful for the shortness of breath, helps them breathe it better as well. Um You can give isosorbide dinitrate which basically relaxes the blood vessels and makes the sort of blood, the heart pump a bit more smoothly and softly. Um And you can also give CPAP as well. So if they're, if they're struggling with their breathing as well. CPAP helps keeps the alveoli open and helps them breathe better. Um And ionotrope again. So this obviously this is a bit more difficult things that you don't need to necessarily remember, but it's things that you know, can come up with exams. So past med more and more of the time rather than your ays. Um But yeah, I would recommend just learning the poor. So in in the corner there. Um So yeah, so that's acute heart failure. So very short, about a bit about it. But um the next one we do is ie so infective endocarditis. So with this, it's um it's quite a common sort of um presentation with patients. They're normally quite elderly patients or they're um intravenous drug users and they have a new murmur and they have a fever as well. So the fever is above 38. Um And what's going on with them? It's infective endocarditis until proven otherwise. Ok. So what actually is IE, so IE is essentially it's um sort of an infection of the endocardium. So the endocardium is the inner lining of the heart and also the valves as well. So if there's an infection going on there, that can potentially be ie so risk factor is pretty easy if they've had it before. For example, if they've got rheumatic fever, if they have a recent valve surgery again, postoperatively, um Strep Vidin is the most common cause of ie in patients who have had a recent valve put in, um C HD, um and IV drug users. So which valve do you think would be affected most in IV IVD users? Um If you think about it logically, is it Matra Valve or the Tricuspid? But again, I can't check the chart, so I don't know if there's any answers there. Um, but if they're an intravenous drug user, um, the Tricuspid valve will be factored most, most time because if you think about it, if they're injecting, I don't know, like drugs into their femoral vein or their, you know, vein in their arms. Um It's obviously gonna go back to the venous side of the heart. So your tricuspid valve um can be affected and that's something they commonly ask as well. So, um so yeah, and with intravenous drug users, the most common um bacteria that is staph staph aureus. So it's, it's important to remember the different causes. So, in patients with the recent valves, it's strep Vidin in patients who are intravenous drug users. It's Staph A. Ok. And there's another one here, but it's not on the slide. Um But strep Bovis is, is um the bacteria in patients with potentially colorectal cancer. So patients can present with sort of weight loss, night sweats, fevers change in bowel habits, sort of um blood coming from the rectum and it can be like which, what's the cause? It's bovis and then what you then need to do is give the patient a colonoscopy um to then rule out colorectal cancer as well, but they'll have signs of IE as well. Um So yeah, it's really important to run with three different bacteria there. Um And yeah, if they've got Staph a go floxacillin. Um So yeah, so the modified duke criteria is the criteria used to actually diagnose IE. Um And it's, you have to do you kind of have to remember it. Um Like when you do pass me questions, I'll expect you to know the Duke criteria. So there's major and minor. So a major criteria is something that's very obvious and you know, it's, it's based on good results or um diagnostic results and the minor ones are things that you can see in the patients are things like um you know, like Osler's nodes, j lesions, things like that. So we'll touch on that. Um But yeah, so to get diagnosed, either two majors, OK? One major and three minors or five minors. OK. Um But yeah, once these patients present, um obviously, before you've completely diagnosed them, you can give empirical antibiotics just to make sure you're treating them. Um So sort of broads back. OK. Um And then once you've obviously got the specific bacteria culture back, then you can give the specific antibiotics needed according to the trust guidelines at the hospital. So, so yeah, so on a cardiac exam, this is something they can do in a osk. So, carry out a cardiac exam for ie what could you be looking for? So, these are the sort of four common things you'll see. Um, and a cardiac exam. So Oz's nose, they're basically these like sort of red, um, nodules at the end of the fingers which are quite painful. Ok. You can look for those, um, January lesions are, again, these sort of like purply slash red marks in the palm of your hand, which aren't painful at all, but they're still there. Um, and you've got splinter hemorrhages in your nails. Um, they're basically like sort of a septic emboli that have come from the valve down into, into your nails. So you can potentially see those as well and Roth spots. So you don't see this on cardiac exam because you're not gonna whip out a fundoscope. But if you do funduscopy on a patient, you can see these sort of hemorrhages called Roth spots. So, yeah, they're four sort of things you look for on a cardiac exam. Um Yeah, so the duke criteria. So if I just go through it. So, um definite ie so they have either two major, one major, three minor or five minors there. That's the findings there. Um If it's potential um endocarditis, one major and one minor, um or more than one minor and if it's rejected, it's sort of any other alternate diagnosis or, you know, nothing else. There's no other criteria that can be met. So with the major criteria. So it's, it's two blood cultures for typical organisms, them organisms being staph a Strat vidone or Strat bovis mucosa blood cultures that counts the major criteria, an echo which can either show vegetation or an abscess. Ok. So an echo is also carried out. So essentially what happens in ie is that because the valves have no sort of blood supply to carry out an immune response, The bacteria kind of latch onto the valves and they start growing and forming a vegetation. So if you can see that on an echo and that's a major criteria for them. Um And again, the new murmur that can be her, so it can be ma regurg most time. Um So yeah, that's major criteria. Now, this one here says Coxiella boneti infection. If someone has a, a blood culture positive for Coxiella, that automatic diagnosis of IE. Ok. So this one here counts as just two majors anyways. OK. So in other patients, there'll be two of these major criterias. But if they just have Coxiella, that's instant two. OK. So that uh they've got diagnosed. So Coxiella is um associated with patients with QQ fever if you've heard of that. So patients who don't like work on a farm, work sort of animals like that can be um caught in them, I guess. Ok. So any of those are major. Um So minor criteria, um these are a bit more easy to remember. So these ones are sort of like if they have a predis predisposing heart condition. So for example, if they already suffer with sort of valve issues or they're an IVD user, that's a, that's a minor criteria for them. If they have a fever, anything above 38 is minor, minor criteria um if they have any vascular issues. So again, the rough spots and fundus, fundus, er funduscopy, um or if they have spent hemorrhages in the nails, if they have um rough spots, s nodes, again, these are all minor criteria that can be checked off to give a diagnosis of IE. Um So yeah, um another thing can be this one here. So positive blood cultures that don't meet the specific criteria, there can be loads of other bacteria that causes IE but if it's not the main three, so staph a strep or the other one, then again, it can just be, it can just be a positive blood culture. Um So yeah, that's ie um yeah, that's pretty much it. So what will go now is over aortic stenosis? So do you want me to just flip through the slides for you? Yes, please. OK. Cool. Yeah. OK. So we'll start off with aortic stenosis. Does anyone know any causes of aortic stenosis that they can think of? I can see the chart now. So, I who is it more common in where do you usually if you were to have a patient what, what kind of demographic usually? No. OK. You want the flick for it. So, in patient, yeah, brilliant. All the patients with CAL Yes. So if the patient is like for example, o over the over 65 usually the cause of aortic stenosis is like calcification. It's just after getting older, the valve is like thickening and getting more stenos. If they're under 65 then it could be like a congenital bicuspid valve. So usually the aortic valve is tricuspid. So you have 33 leaflets, whereas congenitally, they can be born with two leaflets or for example, like rheumatic fever. So a lot of valvular diseases have a receptor of if you have like rheumatic fever, then it's a risk factor for developing that condition. So what aortic stenosis is obviously, the aortic valve is from the left ventricle to the rest of the body, taking blood to the rest of the body. So, if that's thickened and calcified, and what happens is the left ventricle ends up the muscles kind of starts developing more. So you get left ventricle hypertrophy and the whole point of that is, is basically what the, what the heart tries to do is it tries to build the muscle to have more force to try to push the blood out because it's pushing the blood, it gets very hard thick valve. So left ventricle hypertrophy um starts occurring. Now how it presents, it presents with this sad triad. So, syncope you said that's basically loss of consciousness or fainting. So there can be cardiogenic causes and a cardiogenic cause. For example, optic stenosis, a angina. So just like chest pain and dyspnea. So shortness of breath and around like 40 50% of patients have these symptoms. Now they kind of make sense. So if you have aortic stenosis there, the the heart is having to push harder against that above, to move blood around the whole body. So sometimes you can get less blood going around the body. So you can get less blood going to the heart muscle. You end up with chest pain, angina, you have less blood going to the brain. So you have syncope and you have less blood going on. So you end up with shortness of breath. So those are the main symptoms of aortic stenosis. Now, on examination, what you can hear is ejection, systolic murmur is a systolic m not diastolic and it's push, push. But what it means is it's the flow is very slow at the start, which makes sense because the heart is trying to really hard to push against that well, and it kind of goes faster in the middle of cyst and then right at the end, it slows down again the flow and and it also important thing is it radiates to the carotids. And then if you listen to the carotids, which is important in your exam, then you can hear like because blood flow is going really quick, turbulently towards the carotid arteries. Um Now, for the disc, specifically with aortic stenosis, it's something called exertional syncope. Um So, not dis for the syncope. So what that means is when they're exercising, they get the symptom of lightheadedness and fainting. And what they say is basically the heart gets used to that stenosed valve. They end up having a very fixed cardiac output because it's gotten really narrow. And when they do exercise and when they exert themselves, the heart isn't used to that. So they still give the same cardiac output as if they were like sat down, for example. So you end up with the symptoms, there's not enough blood flow going and you get less, less, like more less symptoms like and breathing. But these are the main three that you need to know to the next slide. Ok. So in terms of before we go to do this, in terms of managing for aortic stenosis, it's, if they're asymptomatic, usually just kind of watch and wait and monitor. If they're symptomatic, they usually have a valve replacement. So if, for example, they're really old and frail, then you'll give them like a, a tab which is a transcatheter valve replacement. So like go through the femoral artery and then put a catheter through it to get to the heart. Um But if they're like, yes, you're more like more young, like more fit, they can handle like an open valve replacement. So just open them up and replace that valve. I think the slide is, do you mind if I can't see it anymore? Yeah. Perfect. Oh, if you just go back. So I don't know if you'll go through this in more detail in other sessions, but I'll just quickly go through it. And so with murmurs, they are quite hard to get your head around. So it's important. It's good, I think to just sit down and go, go through it. But um we got taught in place in arms and I'll just write it in the chart and I'll just talk through it. It might be helpful, it might not be, but this is the way that we got it. So A MS arms always remember that it is for diastole. So A R stands for um aortic regurg and stands for mitral stenosis. So, you know, that arms are two diastolic murs and then automatically the other two are if that makes sense, which in a stenosis and mitral reg, which are the systolic MS. Um Can you, I don't know. Yeah, perfect. So, aortic stenosis who said it's an injection systolic and said that it radiates towards the carotid, then we have a MS. So we're gonna go to an early diastolic which makes sense because the blood is just leaving from the left ventricle. So it's an early diastolic, it's right at the beginning and then the middiastolic stenosis, it can be best had at apex, but there's no radiation that you need to go for. And the last systolic murmur is a mitral reed gauge murmur as pansystolic and not as best heard of the apex. And it can radiate to the axilla sometimes as well. So you want to listen to the axilla and you will do all these maneuvers when you get told about the card, um, cardiac examination. Um Yeah, that's it for now. That's most of what you need to know for aortic stenosis. But if anyone has any questions, I don't want it to either. I think George is going through progress questions now. Yeah. Yes. Um I've just had a question if we can go through the ask Mr Arms stuff again if that's OK. Do you mind talking? Yeah. Is that OK? Yeah. Yeah, that's fine. So, um I can't know, I don't know that, ask Mister Arms when you want it cause I've been put the other one. So I'll talk through the one that I was talking about. So, a MS Arms always remember that that's the diastolic murmur. So it's a murmur that's heard. So for example, when you listen to the murmurs, you can put your heart, you can go for the pulse at the same time and it's a diastolic murmur, meaning the murmur can be heard when the heart is relaxing with a systolic murmur as you can hear it when the heart is just doing its contraction. So, arms is vastly. So aortic regurg and the mitral stenosis murmurs or diastolic murmurs, they happen when the heart is relaxing. You can hear the sound when the heart is relaxing and they're both diastolic and I just remember them as they both don't radiate. Whereas the other two, the systolic murmurs are aortic stenosis and mitral aortic stenosis is an ejection systolic and it makes sense because that's when it's aortic stenosis. So the, the heart muscle, the left ventricle is just squeezing to try and eject all the blood out of the out of the heart. That's an ejection systolic murmur and that can radiate to the cartage just because the blood flow is going up and it's quite turbulent. So you can hear it to the car as well. A good man is a pansystolic. So it basically happens throughout this rather than like a start at the end and that can radiate towards the axilla. So when you're, if you, when you're doing the maneuvers in a cardiac exam, make sure to listen to the axilla and the cortex as well, just so you can hear where the sound is going and that can tell you where the murmur is and all the memories is literally just the blood flow going against that valve creates a sound that you can hear through, through your stethoscope. Basically. No, it that makes sense. All right, could you please explain microorganisms, risk factors. Uh Let me see that one Yeah, go for it. Yeah. So um it's only three that I run from the top of my head, which is the most common. So, Staph aureus. So, Staph A is for IBD users. Strep Viridans is if you've had a recent valve surgery, a prosthetic valve put in, that's the most common one that can affect them. And strep bovis again can cause ie in patients who potentially have colorectal cancer and who present with symptoms. So they're the three that I would remember. Cool. Should we move on? We have 67 questions, I think. Um, so we'll just go through them. Are you? Ok. Uh Yeah, just if you, if you, if you're happy just to continue sharing and we'll just do it that way. Right? Yeah. So what I suggest, read through the question and then just type in the chat and then we'll discuss through the question. Ok. So we'll give it a 3rd 2nd or so. Just give it a go. It really doesn't matter if it's wrong or right. Ok. It's just a, a good discussion to have. Ok. A few CS happy days. Do you have any other, um, stuff CC CCC? Good. All right. Um C is the correct answer. So it makes sense. We have a bit of a heart failure, picture, paroxysmal nocturnal dyspnea. She needs pillows, sleep at night. That's a really important question to ask for us. Um, short of breath immobilizing. And as we said, pulmonary edema is gonna be one of the main things associated with heart failure. You have cardiomegaly upper load diversion. You mentioned those pulmonary fibrosis not linked to pulmonary embolus. You wouldn't really expect pulmonary edema correct pneumonia potentially. But it's again, more of a heart failure picture. CO PD doesn't really fit in again. Cool. Next question. Sorry, not a great format but give it a go. Do you have any replies? Nothing yet. So we have phrased GWP. Yes. E we have one E do we have anything else? We've got one E so far we are 56 people in here. So let's get a few more. Couple of es more es anything else, right? Let's talk through it. So we have raise JVP. Pitting E map. Uh A your heart rate is a bit high type two diabetes, long term oxygen. What's more consistent with the underlying? Right? So again, we probably think this is heart failure related. So chest X ray show consolidation probably not. So that's more of a pneumonia picture, x-ray, enlarged left atrium and all right atrium. Uh potentially. But again, that's not really gonna present with heart failure symptoms so much. Um And especially so the the important point to take from here is it's a normal right atrium. Um So if you have pitting edema, you'd expect right sided heart failure as well. Ok. E CG with left a deviation, to be honest, that could be. Um But again, you're seeing more of a right sided heart failure picture rather than a pulmonary edema picture. Um Low hemoglobin doesn't really make sense. E CG is showing evidence of P Pulmonale. So what did we say before? What is P Pulmonale? Is it right sided or left sided heart failure or rather a l enlargement? Oh, it's right sided. Yes, perfect right sided. Therefore, people, but people on fits in with right sided heart failure, which is the clinical picture we have good. All right. Next question. Uh Cool. Here we go. I have also just sent an email with the feedback request. So once you're done with this, please fill that in and they can get the slides. Uh Right. We have some answers here. Mhm This is a bit more of a slightly random question. Um but we'll give a bit of a background to this. So this just needs a bit of understanding of how each medication works by su be blocker. What happens if you have heart failure? It's like it reduces the contractility a bit. So what we'll do it'll slow down the decay of the heart. So that's good. That will probably increase mortality. Ramipril. It's an ace inhibitor. It's protective for the kidneys, especially in this situation. So it's probably gonna increase mortality. What kind of drug is digoxin? Mm. Right. No reply. So what is digoxin? It's important to appreciate what it is positive trope. Mm Not really. It's so it's antiarrhythmic. Ok. So that might, it, it is mostly given in an acute scenario of atrial fibrillation to bring a bit more of rate control. Ok. Um So is that gonna help in chronic heart failure? Not really. So, mortality wise, it doesn't necessarily provide much help. Ok. Eplerenone is an, I think it's aldosterone receptor antagonist. So again, um renally protective. Ok. So again, it'll have mortality benefit. There's a bit more of niche knowledge of. Ok, To remember which drugs are symptomatic and um which actually improve mortality. Is it general knowledge saying that digoxin and loop diuretics don't help with mortality benefit. I'd say it's general knowledge. Yeah, it's not that uh I mean, if, if you can apply a bit of physiology to it, it's a bit more of a symptomatic management with digoxin and loop diuretics rather than actually significantly helping the heart failure. Sure is a positive iron trip. You might be right. I'll be honest. Um I haven't come across the drugs in a while. Uh positive. Let me have a look. We will be uh hm So a positive inotrope, it means it will increase the heart contractility. Ok. So make stronger contractions. So I am pretty sure digoxin is not a positive. Ipe. Um So yeah, I'll be honest. Um I might look into that again, but um we'll have a look at that right. Next question. Um Sorry, previous one, the correct answer was uh digoxin. It's not, it doesn't increase mortality. Uh morbidity doesn't improve morbidity. Sorry, we have b we have a any of the takers another egg. Um Sorry, correct answer is a. So what's the restaurant behind that? We have started Bisoprolol. So we started our base blocker. We've started our ace inhibitor. So we've started our loop diuretic. And what is missing is our A AB OK. Or potassium sparing diuretic. So that will be spirolactone. OK. Um So again, that's just straightforward chronic heart failure management. OK. So hopefully that makes sense. Cool. Next question. Far away. Any answer to this one, we did mention it on the chest X ray findings. B perfect. OK. So again, pleural effusions are a big finding in heart failure patients and that presents with bilateral blunting of costophrenic angles, not necessarily bilateral, but at least one of them. OK. Cool. Next question we have one day. Anything else? You have A B B all A number B? OK. So um oh yeah, correct answer is a, I'll be completely honest. I have to reread this question a bit to remind myself as to why it's a. But if we look at it, we are on an ace inhibitor, we are on a beta blocker. Eplerenone is an A RB. We are a loop diuretic and oh dear, what is ivabradine? Don't remember what ivabradine is any idea whatsoever. Mhm mhm mhm Chemical funny current inhibitor. Excellent. Um I will be completely honest. I can't remember the protocol when we reached five medications. However, digoxin definitely not increased fursemide. We are already at uh 40 mg twice daily. We can't really go higher on that. Amiodarone, antiarrhythmic cardiac resynchronization again, not really beneficial for heart failure. So, Spirama is gonna be the next sensible step. Ok. Um I'll be honest, I'm not completely confident as to why it's a, it's been a bit of a, it's been a while since I've had to reach the sixth step of management. Um So yeah, sorry, that's not the best explanation. And they are um which is why I'm also slightly confused. They are both aldosterone antagonists. Um That's why I'm also a bit confused. Um I'll be honest, I'm not completely sure. I wouldn't worry too much. We are talking about 5th, 6th level management at this point. Um I will try and get an answer though and I will get back to you by email when I do get an answer. Sorry about that. Right. Final question, right? It should be relatively quick and straightforward. A A AAA. Oh What's this? OK. Um AAA. Cool. Right. Correct answer is a so ove edema and that presents with batwing opacities. OK. Um Wedge shaped density, no Western's golden sign. None of those are related to heart failure. OK. So that should be relatively straightforward. All right. And the next slide, OK. Um Just skip through until we get the whole thing. Yeah. So just a bit um a bit of a recap on how you can apply this knowledge to in a oy scenario. Um As I said, they're quite nonspecific symptoms. And even if you think it's heart failure from the very first minute, you need to keep a very broad approach from the first minute. Ok. So ask about paroxysmal internal dyspnea. That's a big giveaway. Ask how many pillows they need at night to fall asleep. Um Ask about exertion difficulties, ask about hemoptysis, ask about pink frothy sputum and very important. Ask about risk factors. Ok. If you have a CS previously, any mis hypertension smoking, family history, really important. Ok. Um, explain it sensitively as much as you can. Heart failure doesn't sound great. Um, explain medications. Um And then Fortas interpretation and ecg chest xray do it nice and structured. Ok. Obviously, we've picked a few signs for the chest X ray, but you always need to be very systematic. Ok. So take ABCD approach with chest X rays. All right. Um Yes, I'm gonna interrupt very quickly. George. Do you know for that? A question for spinal? Yeah. Um So I've just read it again if you go back to it. We're saying CRS is like 100 and 35 I think. Yeah. So for, for CRT, it needs to be usually it's a cure duration of like more than 100 and 50. So they need a really long CS for them to start doing CRT. So that's why they probably put her on another aldosterone antagonist um for management. Thank you very much. That is very useful. OK? So I'm guessing maybe bone is on the maximum already. So you can't add another one, you can't increase that. So maybe you add spironolactone. OK? That makes more sense. Um I wouldn't worry too much about this. This is very much for 5th, 6th level of management, but it's useful information. Thank you very much. Cool. All right. That is the end of the session. Um I'm just going to put a feedback link for this session. I if a few of you are saying you didn't get it for last week's, I'll be completely honest. I wasn't part of the session last week and I don't really know what happened. Um And we don't always send the automatic one. However, um I will put in this week's in the feedback in the chat. Now give me one second. This is session four, isn't it? Yes, one sec. Same. Please let me know if this works. I don't think that should work. Um So fill in the feedback and then over the next couple of days, we will um put in the slides and we will also upload the recording as well. OK. Do we have any questions left over from this session? Sorry about the end of the questions. I wasn't completely sure about the Spinal Act One. But thankfully, I think we do have an answer now. Um Any questions, feedback anything you want to bring up at this point? No, not in the feedback form. Oh, we have Marie. Marie. Mm. I promise the rest of the session was better than how we handled the, the end of the questions anyway. Right. Um OK. I think we can stop the recording at this point. He's on the recording as a recording again.