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Hello, everyone. Welcome to mind the Bleeps, second part of our cardiology final series on heart failure. I'm just gonna give e everyone a couple of more minutes to join. But in the meanwhile, to make sure everything is set up, can anyone confirm on the chart if they can see my slides? Fantastic. And I'm assuming everyone's heard me because they've replied. Yes. Fantastic. I'll give everyone a couple more minutes and then we can get going. Cool. Let's crack on. So my name is Nel and I'm an F one currently working at Barnett and along with ALA another f one with two of the cardiology leads for mind the bleeps cardiology final series, the previous session focused on valvular insufficiencies. And today we're going to focus instead on, on heart failure. And throughout we're gonna do quite a comprehensive overview of heart failure, but we'll pay key attention to points that may come up in the A KT or the CPS A and we hope everyone enjoys it. I'll try and make the part specific to the CPS A interactive on the chat. So we would love it if you interact whenever any questions are asked and I can see the chart. So everything will be read as quickly as possible. So let's start. So firstly, what is heart failure? So, heart failure is a complex clinical syndrome characterized by dyspnea or exertion or limitation due to the heart not functioning properly. Now, this is either due to a structural or a functional impairment of the heart that results in either or both of the ejection of blood or ventricular filling. Now, epidemiological data suggest that the prevalence of heart failure is increasing in England steadily, but the largest changes are seen in the oldest age brackets. Now, it's a very hot topic of cardiovascular research and because of that survival rates are improving because of wonderful clinical trials. But the prognosis generally still remains poor at one year, the mortality after diagnosis is 20% and at five years, it's 53%. So heart common heart failure is very common cause of morbidity and mortality and you'll come across it in clinical practice all the time, especially on acute medical take. So let's focus on the causes of heart failure. Now, on the chat, could anyone put down what they think is the most common cause of heart failure? Ok. For example, in the A KT, if it was asked, what is the single most common cause of heart failure? Yes, I've someone has put coronary artery disease and that is 100% correct. So by far the most common is ischemic heart disease from coronary artery disease. So, this causes heart failure through a vicious cycle of ischemia, myocardial cell death and then the resulting maladaptive remodeling that happens and this vicious cycle ultimately leads to heart failure. So, what are some other common causes of heart failure in the chart? Someone's correctly said hypertension. That is another very common cause well done. Anything else that anyone can think of arrhythmia is fantastic. Excellent. Yes, valvular disease and cardiomyopathy are the two other very common causes well done. So here is a table of the common causes. Everyone's correctly identified coronary artery disease, hypertension, valvular disease, cardiomyopathies, arrhythmias and these cause heart failure through a variety of etiologies including pressure and volume overload that ultimately will lead to decompensation. There are some other causes to be aware of in your A KT. So infective is one. So Chagas disease is a rogue link to heart failure infiltrative which includes these depositing diseases such as amyloidosis and sarcoidosis of particular interest where they can test you in the A KT is drug induced courses. So, DOXOrubicin, which is a type of anthracycline has is a chemotherapy agent which very commonly results in heart failure as does trastuzumab, which is the anti her two receptor antagonist, which is used in the treatment of breast cancer. Clinically, immunotherapy is becoming more important because as research develops, we are finding more immunotherapy agents which target specific cancers. And it's this these immune checkpoint inhibitors that people are noticing heart failure as a more and more common side effect. So that's something definitely to be aware of. So now focusing on CPS A presentations, how might, how might you expect to see a patient with heart failure present? Let first let's focus on symptoms. So if anyone could put symptoms you expect to see on the chart. Shortness of breath. Fantastic, fatigue. Yes, orthopnea. Brilliant, pitting edema. Fantastic. And I'll say there's just one more. I'm looking for P ND. Fantastic. So let's talk about symptoms before we talk about signs. So, exertional breathlessness is the most common presenting symptom in heart failure and is a result of when cardiac output is not enough to maintain oxygen demand on exertion. Another symptom is orthopnea. So this is when patients can't lie flat because of their breathlessness. Now, orthopnea is c caused by gravity induced, worsening of pulmonary congestion. But interestingly enough, it's not got as good a sensitivity to diagnose heart failure as PMD, which is paroxysmal nocturnal dyspnea. So this is when patients wake up at night, gasping for breath and have to sit up to be able to breathe properly. This is more predictive than orthopnea for heart failure. And the reason you get the symptom of P and D is because at night, there's increased ventricular filling pressures. And this is because at night, your kidneys res uh resorb more water and salt and the fluid redistribution at night changes so that your increased your ventricles have increased filling pressures and in people with heart failure, who can't compensate, they start to become symptomatic. And people have correctly said also lower limb swelling, fatigue, lethargy, and you might also notice a chronic cough in these patients due to their chronic pulmonary congestion. So well done on the symptoms. Now, let's focus on what you might notice on examination, the signs feel free to put any signs you might notice in the chat. Yep. So acutely, they might have an increased work of breathing to meet the oxygen demand. Tachycardia. Fantastic by basal crackles. Brilliant. So if someone said cardiac asthma, if you don't mind in the chat, could you expand what you mean by that? RJ BP. Third heart sound brilliant. People have given fantastic suggestions. So let's start to talk through that. So when you examine, so someone let's start with the obs you might already have in front of you before you start examining them. Someone's correctly said tachypnea more common than that would be tachycardia. And that's because in heart failure, you'll have reduced stroke volume naturally. And so your body to compensate for that reduced stroke volume, in order to maintain cardiac output would have, would increase the heart rate. So you'd notice they might have a resting tachycardia. That's what that's higher on exertion. So moving on to auscultation of the first the lungs before the heart in the lungs, you might notice bibasal crackles and in particular, it will be coarse crackles, signifying pulmonary edema. When you listen to the heart, you might hear a third heart sound. This is called a gallop rhythm. So the third heart sound will come after the second heart sound and it'll happen during ventricular diastole, which follows the second heart sound. So the reason you hear this heart, heart sound is because when you have a volume overload in the ventricle, such as the case in heart failure, and when there is ventricular diastole, that's when the blood from the atria rapidly fill into the ventricles. So if blood from the atria is filling into the ventricles, but the ventricles already volume overloaded, that creates turbulence against the ventricular walls. And this creates turbulence against the ventricular walls. And you hear this as a third heart sound or a gallop rhythm because of the impaired feeling. Thanks for letting me know in the chat. So that explains what you hear in auscultation of the heart. So now let's move on to symptoms when looking at the r the signs when looking at the rest of the body. And these are particularly related to signs of chronic venous congestion. This happens because you get ultimately in heart failure, you get right sided failure as a result of the pulmonary congestion caused by the left heart failure. So when you have this right heart failure, you'll get this backflow of blood into the venous system. You'll see this as jugular venous distension f further down the venous system. You'll see this as Hepatomegaly and you'll notice hepatojugular reflux. So that's when you press against the right upper quadrant, you'll notice blood backflow in the venous system. And the most, probably the most common sign of the chronic venous congestion caused by heart failure will be the peripheral pitting edema that will start in the ankles and the worse it gets, the more it will move up towards the knees and even to the hips and the sacrum. So that's because of the increased hydrostatic pressures that will be present in the venous system causing fluid to move into the interstitium. So that's a good overview of the symptoms and signs you get in heart failure. So let's now move on to investigations. What are some investigations you want to do to diagnose heart failure? And as always, it's in a bed in a CCPS, a setting, it'll be a bedside bloods and then further investigations. So what's, what's the first bedside investigation you'd want to do when suspecting heart failure if they present to the emergency department? So BNP is a brilliant answer, but unfortunately, that will fall under the bloods category and in your C PSA, they really want you to be systematic. So before you get this, the blood test of the B MP, what can you do at the bedside that you'll do for many, let's say many cardiology presentations. Great. So ECG is the correct answer. ECG and observations. We've already talked through the observations ec G. What might that show? Well, it will show it could show sinus tachycardia, it could show arrhythmias, which we identified as a common cause of heart failure. It can also show signs of previous ischemia such as T wave inversions or Q waves. So it can actually give you a lot of information on the background of this heart failure, but also s signs leading towards our diagnosis. Then we move on to bloods and a lot of people have correctly said B MP B MP is a very important blood test as it's, it's a hormone essentially released by the ventricles in response to increased wall stress, volume, overload and pressure overload in the primary care setting in the context of chronic heart failure can be actually a very important tool to stratify. What happens next. For example, in the GP setting, if ABM P level comes back as 2000 or above, then that warrants an urgent referral for specialist assessment and an echo in two weeks. If it comes back, intermediate between 400 to 2000, then it's a routine referral for the same within six weeks. But actually, if the levels on 400 heart failure is unlikely overall. So this table is mostly for the primary care setting, but B MP is very, very useful even in the emergency setting to quantify the extent of heart failure that the patients presenting with. Now let's move on to further investigations and that's imaging. I've already seen fantastic suggestions in the chat talking about chest X ray. Absolutely. If a patient comes in with exertional limitation, dyspnea, a chest X ray would be done to help with heart failure diagnosis, but also exclude other respiratory diagnoses. And ultimately, the goal standard that someone set in the chart is echocardiography. Now, nowadays, a lot of people can perform bedside echoes, but formal echocardiography will be the best way to show systolic or diastolic dysfunction and diagnose heart failure. Excellent. So let's now move on to the chest X ray. So when presenting a chest X ray, as you'll commonly find in your CPS, A, there are certain signs we look out for that might reveal heart failure as the cause. And there's an ABCD E system. A refers to alveolar edema and this is often caused called batwing opacification. So that's not actually present in the chest X ray here. But what it, what it might look like is batwing spreading from the middle. And that signifies edema in the alveoli, you might notice curly bee lines, they're probably gonna be hard to appreciate in this, but they're very faint lines that show interstitial edema. Something you can see here is cardiomegaly. So you can see this informally in this chest X ray to formally say someone has cardiomegaly, it needs to be APA film and the ratio of the cardio cardiac ratio to the whole film ratio needs to be more than 0.5. And that would suggest cardiomegaly. You might also notice dilated pulmonary arteries like we discussed. And you'll notice that just around where the hilum is projecting upwards and outwards and lastly, you might notice effusions. So these can be, these are very commonly bilateral and you'll notice blunting of the costophrenic angles, but just because they're bilateral, they may be asymmetrical. So it might be left more than right and right, more than left. But commonly, it will be both that, that will be affected. If you notice a unilateral pleural effusion, that's rarer that might suggest more of a pneumonia, a malignancy or a connective tissue dis disease disorder. Great. So let's move on to classification. Having gone through the investigations. How can we diagnose it? There are two systems that are commonly used. The first one actually focuses on more functional classification and it's called the New York Heart Association class. So this describes this stratifies heart failure patients based on the effect that has on their day to day life. So for example, class one patients may have no symptoms during ordinary physical activity. And that's actually described as walking for class two, they might have a small amount of difficulty while walking, but not enough that it disturbs their day to day activity, moving on to class three, it gets more severe here. This is when walking leads to significant symptoms which impairs their ability to carry out that function class 45 is the most severe and that's when they can't do any activity without symptoms. And as a result, they'll be bedbound and not be able to move because they're limited by dyspnea. The European Society of Cardiology however, focuses on a classification system that's based by ejection fraction. Noted in echocardiography. If the ejection fraction bearing in mind, the normal ejection fraction is above around 52% bearing that in mind. If someone has an ejection fraction of 40% or less, they're, they're called HEF ref which is heart failure with reduced ejection fraction. If they have a ha a ejection fraction of above 50% roughly normal, they're called HEF pef. So heart failure with preserved ejection fraction. And there's another term which is called he MRE, which refers to the people in that intermediate zone with the ejection fraction of 41 to 50%. And that's heart failure with mildly reduced ejection fraction. Great. So we've talked about the causes. We've talked about the history and examination. We've talked about some classification sys systems based on investigations. Now, before we move on to the treatment of these types of heart failure, the next slide will talk about some of the mechanisms of actions of the common drugs we use. But before we do that, would people kindly put in the chat, some of the common drugs they know are used in heart failure. And the general drug classes would be all right. Great. We've got beta blockers. Ace inhibitors, two fantastic examples anymore loop diuretics. Fantastic SGLT two inhibitors. Very good aldosterone antagonist. Fantastic. That was the last one I was waiting for. Brilliant, well done everyone. So now let's quickly go over the mechanism of action of these common agents. That's one of the most common ones to use, which are the ace inhibitors and the ARB S. So ace inhibitors and Arbs target the R system. The renin angiotensin aldosterone system. This is a very important system to be aware of because a lot of medication target this system to try and improve the heart failure. So let's go over the physiology of what happens normally. So normally, when there's reduced renal perfusion such as in a state like heart failure, the renin is released by the kidneys which converts, which converts an angiotensinogen to angiotensin one, the ace enzyme. So the angiotensin converting enzyme commonly found in the lungs converts angiotensin one to angiotensin, two, angiotensin two will then act on the adrenal gland to release aldosterone, which then acts on the collecting duct of the renal tubules to cause sodium and water reabsorption. What do ace inhibitors and AB S do is they target this R system. Ace inhibitors target the angiotensin converting enzyme A S block the receptors of angiotensin two. Ultimately, what this all does is it reduces the amount of angiotensin two available. And why is that useful angiotensin two causes peripheral vasoconstriction and blocking that will allow peripheral vasodilation. And secondly, blocking angio angiotensin two prevents further aldosterone release, which reduces salt and water reabsorption. The reason this is all beneficial is that by reducing the salt and water reabsorption and by preventing this v vasoconstriction. By angio angiotensin two, you reduce the cardiac preload, you reduce the cardiac afterload and the cardiac, the ventricular wall stress. So all of this will improve heart failure. There's a new class called ARNI. So these are angiotensin receptor blockers coupled with Neprilysin inhibitors. Now, the addition of this nephrosin inhibitor is key. What the nepro lysin enzyme normally does is that it breaks down the natural peptides produced by the heart when it's struggling in such as BNP. So the NAT peptides are produced because the heart is struggling. So therefore, it will act to prevent salt and water reabsorption by the kidneys to try and reduce the strain on the heart. If Neprilysin blocks this, it's counteracting the measures the heart is trying to do to improve its own function. Therefore, neprilysin inhibitor will block neprolyzin and allow the natural peptides to oppose naturally the R system. So when you combine a Neprolyzin and a ARB, you get double blockage of the R system which improves the heart function. We've got beta blockers and these are normally beta one receptor antagonists. They have both negative chrono and inotropic ef effects on the heart which reduces the myocardial oxygen demand. But interestingly enough beta blockers also have a secondary effect of inhibiting renin release. So this also inhibits the RS system. We have MRA S which are the aldosterone antagonists. These prevent intravascular fluid retention B by the same mechanism. We've disco we've described for the other drugs. In this case, they'll block aldosterone acting and prevent salt and water reabsorption. But interestingly, Mra S also can directly prevent myocardial fibrosis. But the mechanism of this is not really known yet. The new kid on the block is this SGL D2 inhibitors such as Agli Flosin and empagliflozin. How this works is really unclear. WW. They're meant to be a diabetic drug. So by inhibiting the SGL T two channels in the kidney, they can prevent glucose reabsorption in increase increase glucose excretion. This might have a secondary effect in that you prevent fluid reabsorption and e er reduce the effect of the on the heart. But for them to be as effective as they are, they clearly have other cardioprotective features related to fibrosis. But it's really unclear and it's a hot topic of research in the community at the moment. But what we do know is they are effective to finish off. We also have ivabradine, which is a funny channel current inhibitor that works at the SA node. It works through a negative chronotropic effect through the essay node. So can reduce the heart rate and lastly, nitrates, nitrates work for releasing nitric oxide. Nitric oxide predominantly in the heart causes veno dilation so will reduce preload. But nitrates can also cause peripheral vasodilation through the arterioles altogether. This can reduce preload, afterload and increase the oxygen supply to the myocardium. So I thought it would be just important to go over the mechanisms of action just so you can put the following treatments into context. Let's start with HEF ref. So to diagnose HEF ref you need to have the clinical signs and symptoms we've described earlier, but you must also have an ejection fraction of 40% or less the pathophysiology of he normally there's an initial injury. This can be, this initial injury can be ischemic damage, for example, which causes either impaired ventricular contrail or increased volume overload such as in the chemo case of aortic regurgitation when the blood flows back from the aorta into the left ventricle, but regardless the most common cause of Heff is coronary artery disease. Now, how do we manage this? Luckily, for us, the European soy cardiology has very thorough guidelines to treat he FF and they managed to get this by having numerous and numerous randomized controlled trials which are of very high quality. But what are the key points you need to know for exams? He ref if someone's diagnosed with he fre there's a bunch of drugs which are have been shown to improve hospitalization and or death and they should be started. This includes ace inhibitors, beta blockers, aldosterone antagonists such as aldosterone or Epler Lerone and new to the 2023 recommendations. SGL T two inhibitors, loop diuretics. This is a very common exam questions. Loop diuretics do not provide a mortality benefit in heart failure. But what they do provide is symptomatic benefit from the fluid retention caused from the heart failure. So if you want to offload someone offload the fluid in the lungs or in their peripheries, you give loop diuretics such as furosemide but does that prolong their life? And no, it doesn't. It's of key note that R NS can actually be started instead of ace inhibitors and RNI S or those angiotensin receptor blockers coupled with Nepro inhibitors. The common one you'll hear of is entresto that can actually be started instead of ace inhibitors as they've both been, they've both been shown to have beneficial effects in terms of hospitalizations and or deaths. So here are some secondary recommendations. So A BS are not as preferred as ace inhibitors or ARNI S, but they can be used in people that can't tolerate ace inhibitors or ani S ivabradine. The one I talked about it does have a role, it has a role when patients despite optical medi medical management are still struggling from heart failure. In the case of those that have an injection fraction of less than 35% and have a heart rate of above 70 in sinus rhythm. You can give ivabradine. Why do you want the heart rate to be above 70? This is because it's a funny channel current inhibitor at the SA node. So it there's a risk, a natural risk of bradycardia. So if someone has a heart rate of above 70 they might still become bradycardic, but it will be much safer than those are that are already bradycardic. And there are some other drugs that patients can be started on for those that have failed optical medical management. This includes hydrALAZINE and nitrates shown to be particularly beneficial in the black population sGC so soluble guanylate cyclase, I think stimulators. So these actually work. These is a these are a new group of drugs that target the nitric oxide pathway which ultimately causes the venodilation, peripheral vasodilation that we talked about and they're still under investigation, but they have been shown to have some benefit. Although the data is not as strong as the rest before your exams to summarize ace inhibitors, beta blockers, Mra S and SGL T two inhibitors. They're the mainstay of pharmacological treatment in he ref now if the UK MLA is feeling mean, they may ask questions further to the pharmacological treatment. So a we know that a high proportion of patients with heart failure can die from sudden death. And there are some recommendations regarding the management of cardiac rhythm in this population. For those that have a reduced ejection fraction below 35% and a normal QR S length. So technically normal QR S length is 100 and 20 milliseconds or less. But here they decide 100 and 30 has the limit. You can give an ICD so implantable card, cardiovert cardioversion, defibrillator to these patients. It's particularly indicated in those that have had ischemic etiologies of heart failure, but can also be considered in those of non ischemic. It's unlikely they'll ask you a question on this side. But what they may ask you a question in their A KT might be for patients that have a reduced ejection fraction and a prolonged QR S duration in sinus rhythm. And that's where there could be a role for cardiac resynchronization therapy. So this is where they try to get the two ventricles of the heart to contract in similar time frames to improve overall effi er efficiency of the heart. Sometimes these CRT devices are coupled with ICD S when they're implanted. So it can serve both functions together. These CRT S are thought to be particularly useful in patients that have had a left bundle branch block in the future in the, in the past. Sorry. But it's unlikely you'll get question on this. But it's a good fact to know. All right, let's move now on to half, half. So how can we diagnose half paf? Well, patients must have the symptoms and signs of heart failure. Like we talked about, they must have an ejection fraction of at least 50% or higher. And in addition to this, they must have structural or functional evidence that there is diastolic dysfunction or increased LV, filling pressures. Now, in the past, the theory of the pathophysiology of FP was that the progressive pressure overload would cause concentric ventricular hypertrophy in the heart over time. This would stiffen the ventricles and this maladaptive remodeling would ultimately cause a diastolic dysfunction. So the inability of the heart to relax appropriately. But what they found out is that not all patients with Heppe F have hypertension, which is a cause of pressure overload in the left ventricle. So because of this, people are really unsure how Hef Pef happens, but there seems to be a big link with, with other comorbidities in particular obesity and diabetes in addition to hypertension. So this can be thought of as a multisystem in inflammatory disorder that's still being investigated. But the problem is when a consi a condition is as heterogenous and as multisystem as Hef Pef is thought to be management can be very challenging and that's always been the case of Hef Pef. The evidence has been very weak for the treatment and a few years ago before 2023 there was actually no recommendations in terms of pharmacological treatment that improved hospitalizations from heart failure or mortality. But in 2023 ba based on some good randomized controlled trials, live being one of them, they found that SE LT two inhibitors, the dags reduced a joint composite measure of hospitalizations and death. And as a result, it's now reached class one recommendation in the treatment of HEP. So the single drug that can improve this in HEF PF is SGL T two inhibitors. Again, diuretic loop diuretics are the same. If a patient is symptomatic with the fluid retention, you give stuff like furosemide to help with that, but it does not improve mortality. And as always, you have to consider the comorbidities in heart failure, the diabetes, the obesity treating that will help treat the HEP pef. So a quick slide on the other one he FM. So it's a funny sounding name, but it's actually quite a new construct because it represents the patients that were commonly thought of as he pef patients. But they're not really he PF patients because these pa the the patients that have the heart, the ejection fraction between 41 and 50 you do find some of them respond to the drugs that work in the HEF ref population, the ones with their ejection fraction below 40. So this is quite an underrepresented underresearched class. And because of this limited amount of evidence, not much is known definitively about how to treat this because the ejection fraction of 41 to 50 were used in the same randomized controlled trials as the ones above 50. We know that SGL T two inhibitors are effective and are recommended in this patient group. There may also be a role for the classical drugs. We talked about the ace inhibitors, the ARNI, the ARB S, the MRA S, the beta blockers, but they are only class two recommendations as of now because there's not enough evidence, but a lot of the patients do respond to those drugs and it is something to keep in mind. So I've spoken a lot. Let's move on to some before we move on to acute heart failure. There's two SBA S that we've constructed for you. So, question one, I'll give people around a minute to answer this and we've got a poll ready. Wait for about 15 responses. Cool uh very close to 15. So we'll just move forward. So let's talk through this question. So this 63 year old patient presents to a clinic with four months history of worsening, shortness of breath on exertion and ankle swelling. Now symptomatically, this sounds just like the heart failure we've described. But do the investigation suggest anything different? Well, the chest X ray shows mil mildly blunted costophrenic angles that's in keeping with heart failure. So we do think this is a heart failure picture going on. And now the echo which is the gold standard for diagnosis shows ejection fractions of 55 to 60. Now, that seems pretty normal, but there is a grade one diastolic dysfunction and raised LV, filling pressures. So what this sounds like is a heart failure with preserved ejection fraction. So we've diagnosed that part. So let's think about the treatment. So a as we've discussed, there's only really one class of drugs which have been shown to be effective in the heart failure to preserve the ejection fraction population. And that's SGL T two inhibitors which makes C the correct answer. Dapagliflozin. The other ones mentioned in here are all drugs which are used in heart failure but have not been shown to be effective in preserved ejection fraction. So C is the correct answer here. Let's move on to question two again. I'll give everyone about a minute to answer this. Just give her a few more seconds for some final responses. Brilliant. Let's talk through it. So what this question is essentially asking is which heart failure medication causes hyperkalemia. Now, the first way to go through this A KT question is which of these medications are even heart failure medications to begin with. And you'd notice that you can rule out e omeprazole straight away because it's not used in heart failure. Now, D is a ra rogue drug name and it's actually one related to the sGC S class, the soluble Guanylate Cyclase Stimulators. Now, this is far too advanced for them to question in your A KT. So it's very rare that will be the answer. So you can almost definitively exclude that, which leaves you with the three common drugs you should know about A B and C. Now, which one of these causes hyperkalemia. The answer to this is actually B spironolactone which is known as a mineralocorticoid receptor antagonist. An aldosterone antagonist, also known as a potassium sparing diuretic. How does spironolactone retain the potassium? Well, normally it functions to block aldosterone effect on the collecting duct. So that means n normally, aldosterone will try to encourage sodium retention and potassium excretion through the enac and ROM K channels. If you block that, you encourage potassium retention and sodium excretion and a common side effect of spironolactone as a result is this hyperkalemia, furosemide actually causes hypokalemia and bisoprolol doesn't really have any effects on potassium. So the correct answer here is b great. So let's move on now to acute heart failure and we're on the home straight now, just a few more slides on acute heart failure. But before we move on, does anyone have any questions in the chat that I can help to answer? I'll just give anyone a couple of couple of seconds to type any questions otherwise, feel free to put your questions in the chat. My colleague will be a my colleague allo will be able to answer them if possible. Otherwise I'll just crack on of acute heart failure and this will just be a couple of slides with two more SBA S right at the end. So acute heart failure is quite important to think about because it can definitely come up in your CPS A and your A KT S both in terms of diagnosis management. A two E is something to be very much aware of and what is it is when there's a rapid onset of the symptoms and signs you've described of heart failure, but this time, they're severe enough to warrant a trip to the hospital. And it's one of the leading causes of hospital admissions in those aged 65 or over. People can either be presenting with new heart failure or more commonly an acute decompensation of chronic heart failure. So, when the heart can't pump blood effectively in the queue setting, you get pulmonary congestion and if this worsens you get systemic hypoperfusion due to the heart dysfunction. If left untreated, this progresses to cardiogenic shock, which has a high mortality. So the most common presentation to acute medical take will actually be acute decompensations of chronic heart failure most commonly caused by in concurrent infection. But you you might also have to think about patients that are not adhering to medication, a new ischemic event or just worsening valvular disease. Why might someone have a new heart failure? Now, most commonly, this is will be because of an acute myocardial infarction, acute valvular insufficiency. So whether there's acute mitral regurgitation, for example, tachy or brady arrhythmias that will cause heart decompensation and also a less common one to be aware of is a hypertensive emergency which can present as acute heart failure. So what might the op show patients may be hypoxic? They may be tachypneic and tachycardic if they progress to being hypotensive, that might suggest onset of cardiogenic shock, e CG will give a lot of clues. It might show elevation ST elevation or ST depression to signify acute ischemia. It might also show brady or tachy arrhythmias which shows acute arrhythmias. What bloods do you want to do? Well, you want to do a BNP. This is still very useful in the acute setting. Must say troponin to to investigate the ischemia that might be driving this. But remember, the troponin might be raised anyway, with this acute heart failure. So what you really have to think about is the dynamic element of the troponin changes and the dynamic element of the E CG changes, you'll order a chest x-ray, you'll notice the ABCD signs we talked about and you really want an urgent echo which will show the heart failure. And so how do we manage this? The management is really different if they're unstable or stable in hemodynamically unstable patients shown by the signs of cardiogenic shock, they might have weak pulses, they might be cool peripherally. They'll be tachycardic to try and compensate, they'll have rapid breathing and they might be hypotensive. If they, if they are hemodynamically unstable, first, you have to really quickly find the precipitating cause. If, if this is ischemia, an A CS event, they must be treated for that with PCI, for example, itu are involved really early in this setting. And that's because they may need vasoactive substances inotropes, vasopressors, which are commonly given in itu if the patient is hypoxic ie their saturations are less than 90 you can give them respiratory support in the form of oxygen. But you don't. There, there used to be an acronym that used to go around which suggested oxygen was a mainstay of acute heart failure treatment. It is not. And the reason for that is oxy over oxygenation of patients can cause vasoconstriction and this will just result in a reduction in cardiac output. So it will be counterintuitive. You must only give oxygen when they're hypoxic and the hypoxia will kill before anything else. If the Respi if the respiratory support they need is more than just oxygen, you might consider N IV in the form of CPAP or if they're even worse than that, if they have, if their CO2 is too high, if their oxygen is too low, if they're acidotic from the sh cardiogenic shock they're experiencing and nothing you do is helping. You might consider invasive ventilation. Beyond the scope of probably finals, there may be surgical support devices that can be used in specialist cardiothoracic centers. But that's beyond the scope of this lecture. How do you manage hemodynamically stable patients? Now, probably this will be more of the patients that have had a acute decompensation on the background of chronic heart failure. Again, you still have to try and look for a course because ultimately treating the course will be the best way to improve the heart failure. But normally what you first wanna start with is addressing this aggress, addressing this fluid overload. And we just do this with normally IV loop diuretics such as furosemide that can be done with stat doses of IV furosemide. But you might also wanna consider furosemide infusions. Again. The acronym that used to go around moat in the past used to suggest nitrates were a mainstay of treatment. Intravenous nitrate infusions can be given in acute heart failure. But that's only if you're suspecting uh myocardial ischemia at the same time or vascular insufficiency such as aortic or mitral regurg, they're not really used. If you think that an infection is driving the acute heart failure. If these loop diuretics are not working, you can try the mineral corticoid receptor antagonists, the potassium sparing diuretics, they may help and you still would do the same respiratory support as you did previously. When you stabilize the patient, when you've sufficiently offloaded them and got control of their heart failure, you really need to look at the medications they're on to try and optimize them. And that can include the ace inhibitors, the RNI S, the MRA S, the beta blockers and the SGLT two inhibitors. But remember in patients that are presenting with an acute heart failure on the background of chronic heart failure due to an infection, you would not give SGL T two inhibitors acutely because there's a risk of euglycemic ketoacidosis. So normally SGLT two inhibitors are always held in the acute infection period because you don't want to risk that side effect. They can be started in the community afterwards though. Great. So the two more questions before we finish, let's start the poll for this. Great. We've got 12 responses. So let's go through this question. So this 82 year old woman has had a subacute onset of worsening symptoms. When you examine them, they have quite bad peripheral edema up to the knees and has also got creps at the lungs. Their obs are somewhat stable. What do you wanna do for this patient initially? So they're presenting with um acute heart failure on the background of most likely chronic heart failure, the obs are stable. So there's no real suggestion that itu level steps need to be taken such as the vasopressors, the inotropes, the nitrate infusion. But what this story does suggest is that they need aggressive fluid, resuscitate, uh fluid um offloading. First, how do we do that? As we discussed? We do that through IV loop diuretics. So, e is indeed the answer in this case, after you've sufficiently offloaded them improved this terrible peripheral edema. You can consider steps such as A and D which is optimizing chronic long term medical management. Now, the last SBA I'm gonna give a bit more time to read this one. Fantastic. We've got more than 10 responses. So let's talk through this question. This middle aged man is presenting with symptoms of chest pain and shortness of breath Now, that doesn't quite sound like the normal picture we get for heart failure and the very acute onset suggests it may be a different cardiac pathology. But let's explore this further on presentation. He's hypoxic to keep tachycardic. So there's definitely an acute event going on which is causing decompensation concl to the diagnosis comes when his ECG shows an ST depression in V one to V three with dominant airwaves. Now, this could sound like an NSTEMI but actually when you see se depression, if you want to be free of dominant airwaves, it could indicate that these are reciprocal changes coming from the posterior heart. So what this actually is is a posterior stemi and that is causing these acute symptoms. His chest X ray shows severe interstitial edema. Now, that's suggests in the posterior stemi is causing an acute heart failure. And so he's needing oxygen diuretics. The Q question here is what is the definitive management for this patient? Now, this might be uh my fault in the slides. But the answer is e it should say percutaneous coronary intervention, PCI. The reason is, as we said in the treatment of heart failure. For hemodynamically unstable patients, you first try and find the precipitating cause. In this case, it is an A CS event causing the heart failure. So what you want to do definitively to, to treat this heart failure would be PCI stent, the stenosed part of the arteries and you'd notice an improvement in the subsequent heart failure. So the answer is indeed e alright. Everyone that brings us to the end of the session. I hope you found it informative and useful. I hope I've explained everything clearly. But if you have any questions, please drop it in the chat, we'd really appreciate it. If you managed to fill out the feedback form for myself and ala who created our this session today, we really want to learn from your feedback and make it better for next time. So the next session, next session I believe is on the 10th of February and my colleague Allo will be delivering it on A CS. We hope to see you there. But before that to make it as good as possible, please fill out the feedback forms and do ask any questions you might have on the chat. Thank you um Zher for the, for the um for the lecture. Um And yeah, just as you said, um please fill in the feedback forms and um we hope that er you enjoyed the session. Um As much as I did, actually, I learned quite a lot. Thank you for your comments. Everyone. We'll stick around for a couple more minutes to answer any questions that might pop up. But otherwise, it was lovely having you all. Thanks for engaging so well in the chat and I hope you have a good evening. Mind. The bleep is packed full of great lectures, preparing you for your UK MLA. So please keep in touch. Thank you ever. Yep. Once you fill out the feedback form medal automatically gives you access to the slide deck. Ok. We're gonna end the session there. Have a good evening, everyone. Oh.