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Okay. Okay. Hi guys, Malayan Push. Um I'm part MediPops International. So today's talk of the doctor's guide is cardiology emergencies and the talk is done by Dr Sunil Nada. Uh He's a senior consultant, cardiologist. So today's talk is sponsored by the MDU and it's one hour CPD approved by the Royal College of Surgeons of Edinburgh. Before I do hand over to Dr Sunil need, uh I just want to mention you'll have feedback form sent to you at 7 p.m. roughly after. And uh if you for the feedback forms in then after that, you'll get certificate for your CPD log. So I'm gonna hand over to doctor. Uh Hi there. Thanks Shannon. Thank you for inviting me to this and asking me to give the stock. Um So today's stock is on cardiac emergencies that you'll be seeing as a junior doctor. Obviously, we can't cover me uh most of the emergencies that we see. Uh next slide, please. But what we'll be doing today, uh next slide. Yeah, it's just to kind of try to identify what the common emergencies are, understand the principles of the management and you know, how do you identify these what do you do and um what can be done to treat these patient's? Uh Next, please. Now, generally, the cardiac emergencies are either ischemic emergencies, arrhythmic arrhythmogenic or heart failure related. And these are the main groups you can say. So we'll talk about the common ones in each of these. Uh Next, please. So the first is the ischemic emergencies. Next, next, please. Yes. So we'll start with the case. So it's a 68 year old diabetic and hypertensive male who presents with sudden onset of central crushing chest pain. Um He came at the pain came on when he was shoveling snow of his drive associated with severe shortness of breath. There's a previous history of chest pain when he walks up an incline and this is what his ECG shows next. Next, please. Yeah. Right. So as you can see, uh this shows ST elevation in the uh anterior leads. Let me just see whether I can put this poll up. Okay. So can you guys see this the poll? We can, we can. All right. OK. So if you'd like to answer. Okay, good. So we've got the thing of anterior stemi and that's what it is next, please. Um So obviously, when you make a diagnosis of a stemi, the first thing you need to do is to confirm the diagnosis and the way we confirm the diagnosis is you need to have ST elevation of two millimeters in the chest leads or one millimeter in the lymph leads um in at least two contiguous leads. Now, what do we mean by two contiguous leads? It means like for example, if it is the anterior wall, you need to have ST elevation and either we one V two or V two, V three or V three V four. And similarly, for the inferior leads, it should be either two and three or 33 and aVF uh next please. And when you make the diagnosis, obviously, you need to think of other things that are involved. For example, if a patient has an inferior lead, as in this case, uh you need to consider whether you need to do right sided leads or posterior leads as well. Now you need to consider put right sided leads. If the patient has ST elevation in lead, we one or if the patient has ST depression and lead we to, you need to think of a posterior in fact and you need to do posterior leads in that case. Next slide, please. And this is where you would consider an RV infarct because if you look at lead, we one, you can see there's ST elevation in you even along with the inferior ST elevations. Next slide. Uh Now what about if a patient has got preexisting left bundle branch block? And you don't know if this is new left bundle or old left bundle because we all know that presence of new left bundle and uh patient's who've got chest pain, you need to think of an acute infarct. So in those patient's where you don't know whether it's an old or new left bundle, you need to do an echocardiogram to confirm whether or not this could be an acute event. If it is an acute event, you will have hypokinesia of that part of the anterior wall. So that part of the left ventricle will not be moving. Then of course, you have this carbos a criteria if the patient has a has pre existing left bundle and you've got further ST elevation on that. I'm not going to go into the details of that, but you can look that up uh because it's not very often that you see it, but it is something to bear in mind. Uh Next slide, please. Now, so what do you do in a patient who has come in with uh ST elevation? Uh As always, you need to assess clinically assess the I have a breathing circulation. So um the airways of the patient is talking to you, you know, the airways patent, the breathing. You need to see whether he's in respiratory distress, uh circulation, check the BP check, make sure that he's um you know, hemodynamically stable measure the vital signs. If the BP is low, you need to institute inotropes, you need to give anti platelet agents and pain relief. Now, we give aspirin 300 mg, stat and a second anti platelet. Now, the paramedics in the UK are usually trained to give aspirin a loading those of aspirin for anyone where they suspect a stemi. So most of the time these patient's would have got the 300 mg of aspirin. So we would give the second anti platelet which depending on which um hospital you are and what the policies are. It could either be clopidogrel or it could be Tiki Accra Law or it could be Prasugrel. Um depending as I said on the protocols at your hospital, these patient's then need to be transferred for primary angioplasty urgently. If the center that you're working and doesn't perform angioplasty, you would need to transfer these patient's urgently. If you think the transfer will take more than 100 and 20 minutes, that's more than two hours, you need to consider thrombolysis, especially if the patient has presented within three hours of chest pain. Because studies have shown that within the first three hours, both thrombolysis and primary PCI have more or less the same outcomes. So it would be worth um you know, thinking, how far is it, how long is it going to take? But up to two hours, it's still probably more beneficial for the patient to have a primary and a plastic. Now, if the pain onset is more than 12 hours and the patient has pain free, uh and then, you know, they present late or whatever and the patient is pain free, primary angioplasty may not be of much benefit. And in fact, the risks involved might be even more. So these patient's would be treated medically, would be treated conservatively and you would transfer them the following day for an angiogram. Now, if the patient has ongoing chest pain for more than 12 hours, you can still consider transfer for primary angioplasty because you can say that um the pain that there is still ongoing, um that there is ongoing ischemia and you can transfer them. But of course, as I said, you need to be aware that this is not pericarditis pain. And this is the question that's just popped up on the chat that how do we know that this is not dress lis or a post infarct pericarditis? So the way you do this is you ask the patient about um the pain. Now, does the pain get worse when they breathe? Does it get worse when they lie down? Is it relieved when they lean forward? And if there are signs or anything to suggest that this could be pericarditis like, then you would still, and it is more than 12 hours, you would not transfer them for an urgent primary angioplasty. You would then just read them medically and keep them there. Um And again, dress Lis syndrome itself is something that presents late. Now, when you use the term Dress Lis syndrome, this is post pericarditis like sorry, post, in fact, pericarditis, it's a syndrome that um presents usually a few weeks later. Um But what we talked, so that is slightly different from the immediate post infarct pericarditis. So these are two different things that we just need to be uh aware of. Next word, please. Now, against certain things that you need to bear in mind. Uh When we talk about the management of patient's with them, I in the past it was common that anybody who came in with an M I, they were given aspirin, they were given morphine, they were given oxygen. Now, surprisingly, studies have shown that when we give oxygen to patients' who present with an M I, it actually causes more harm that these patient's ended up doing worse than patient's who were not given oxygen. And there are many mechanisms that have been described and one of it is that giving more oxygen releases free radicals. So it causes more myocardial damage, more myocardial necrosis. So the current recommendation is that we don't give oxygen unless the oxygen saturations uh below 94%. So if it's above 94% we wouldn't give them any supplemental oxygen. Now, uh if the patient is hypertensive, you need to consider fluids, you need to consider giving inotropes. Again, you need to make sure that the patient is not in failure before we give them uh the fluids because you don't want to rush in fluids in someone in cardiogenic shock and in failure. Now, so how do you know if the patient is in failure or not? And that is whether they've got race JVP, they've got crackles. However, there is one case where the one situation where you can get fluids in hypertension with the race JVP. And that is if the patient had an inferior, in fact, with RV extension, in this case, the JVP will be elevated because there is right heart failure, but the lungs are clear because the LV is okay. So that is probably the only condition where with the race JVP, you can give more fluids, right? But because the patient is not in failure, now again, when you've got uh patient's like this, you need to make sure that this ST elevation is new and not somebody who's had a previous, in fact, and these are old changes. Some patient's with Hokum, for example, also can have ECGS that look a bit like um an acute stemi. The other thing to remember is that if the patient is in cardiogenic shock, the mortality rate is very high. Uh So patient's with cardiogenic shock. If you don't treat them, the mortality rate is more than 90%. And even if these patient's undergo primary angioplasty, the mortality rate is still about 50 to 60%. So patient should be counseled, rather the family should also be informed about the prognosis in these patient's. Uh Next please. Next slide please. Right. So while we make um you know, while we try to uh diagnosed Emmy. We should also be careful about these other, what we call the so called mimics of stemming. Uh If we can, we just go back because this is actually like a second. Okay. So it's not working, the animation is not working because if we can go forward again and if we go to the next slide, right, we'll go to the next poll. Oops, sorry, this is the wrong one. Absolute. Uh No, it's okay. I think that's not that. Um okay. So what do people think this is if you can just maybe put it in your uh in the chat? Okay, I think that pool, sorry, I do apologize that both not working but this is something that you need to remember that this is acute pericarditis. This is not a stemi and the way we diagnosis is because you have ST elevation in leads that are not um contiguous with, you know, in the same in the locations that you would find with. Uh stemi. It's not in the same, it doesn't pertain to one particular category, one particular location because you have ST elevation laterally, you have best elevation inferior early and you do not have reciprocity changes. So if you get to the next slide, next slide, please. Yes. So this is how you find out the difference between early re polarization and pericarditis. So in early repolarization, you have that rise in the point. You do not have Q waves, there are no reciprocity changes. If you do repeat, ECGS every 5 to 10 minutes, they look exactly the same. There is no progression and this ST elevation is usually seen only in the lateral leads and you can have some convex elevation as opposed to the concave elevation that you would get with the stemi in pericarditis. On the other hand, you would get widespread ST elevation that does not pertain to any territory. There are no Q waves, there's no progression with time, know reciprocal changes and you also get pr depression or elevation depending on the position of the leads. So these are conditions that you need to be aware of when the patient comes in with chest pain and you think they've got a stemi. Um uh This is something that you need to be aware of, right? Okay. Next slide, please. So when I talk about, remember one of the things I've just mentioned that how you distinguish pericarditis and early repolarization from a stemi in that there are no changes with time. This is what happens in a patient with STEMI when you're not sure and you repeat after 5, 10 minutes. So the first thing that you would notice in a patient who comes in with the stemi is hyperacute T waves. In this image. It doesn't show as well as it should, but the T wave would be fairly tall. So you'll get tall T waves um in the acute stemi as the first manifestation. And then the second thing that happens would be the ST elevation as you get in slide be in pictures. See you find that the R wave starts to become smaller and the Q wave starts to develop uh panel D, you then find that that ST elevation starts to come down and the T wave starts to get deeper. Again, the Q wave becomes deeper, the R wave becomes shorter. And finally, what happens is that your are wave almost completely disappears. The T wave normalizes, but then you end up having a deep T wave, deep Q wave. Um So there's a question here. Can past history, Muga scan for malignancies cause my cardio fi process. And can the breast cancer pathogenic process itself give rise to America? Um Okay, I'll answer that question a little later. Uh So these are the changes that you would see with time in patient's who've got ST elevation M I as opposed to patient's with pericarditis or with the or with the uh what we say uh with the early repolarization which you do not get where it remains static. The ECG does not change with time. Whereas in a stemi as you can see, it keeps changing. Uh next slide, please. Um So when we talk about reciprocal changes, this is something else that you need to remember. Just remember the uh Pneumonic A Il, right? So this will help you to look for the reciprocal changes. So in an anterior stemi, you get inferior depression in an inferior stemi, you get lateral depression and then the lateral stemi you get anterior depression. So I'll show you some um examples. So, next slide please. So this is an anterior stemi. As you can see, there is anterior ST elevation and look at the inferior leads, you have inferior depression. So this is an anterior stemi with the inferior reciprocal changes. So you have the A and the eye uh next slide, please, next slide, okay. And so here, now you have an inferior stemi with lateral ST depression. So if you look at 23 aVF you have the inferior ST elevation and you have the reciprocal changes in the lateral leads, which is one in aVL. Now you, this patient also has got a posterior, in fact, because you can see the ST depressions and we one V two V three. But that's a different matter. But main thing is when we look for the reciprocal changes, this is the uh what you would see the anterior ST elevation with the lateral ST depression and next slide place. And obviously when it's a lateral ST elevation, you have anterior ST depression. So again, ST elevation in one and aVL with ST depressions in V one V two and V three. So this is just something to remember when you're seeing a patient's with ST elevation and you're not sure is this pericarditis is this ST elevation is this uh early repolarization. Look for these reciprocal changes, look for those changes that happen with time and make sure that they fit within one vascular territory. Uh Next slide, please. So this is something that we rarely see but it can happen. And this is an isolated posterior stemi. So an isolated posterior stemi, you have only ST depression in leeds, we one V two and V three and that's it. You don't have ST elevation anywhere else. You don't have anything else. So this is not a lateral stemi because there's no ST elevation and we want inlayed one or a bl you just purely have this ST elevation, sorry ST depressions in V one, V two and V three. So if somebody comes like this with chest pain and they also have a tall are wave in V one and V two, you need to think very strongly of a posterior stemi. In which case, you need to do posteriorly DCG to have a look for ST elevations there. Uh Next slide, please. Some of the other mimics of stemi is hyperkalemia. If you can see the tall peaked T waves, this is the kind of thing that you would get in uh in the first stage of a stemi. What I talked about the hyperacute T waves, this is what you would get, right? And this is the same kind of tall peaked T waves that you get in hyperkalemia as well. And uh obviously, so this is a mimic. And again, how do you know this is hypokalemia and not acute stemi. You need to keep repeating the, uh you need to keep repeating the ecgs every 5 to 10 minutes in order to see whether it's changing, whether there's any progress or not. Obviously, you need to check the bloods. And so somebody who's got chronic kidney disease, um if they come in just randomly and you get the CCG, you wouldn't be bothered. But somebody who comes in with chest pain, yes, you would be buttered. Uh Next slide, please. Uh The other thing that I said also is that we need to make sure that the patient has not had that the changes that you find on the ECG are not old changes. So in a patient who has had an old anterior stemi with an LV aneurysm, you can see that there is pre existing ST elevations in we one V two and V three, which are fixed. So usually what we do is for these patient's, we give them a copy of the ECG and we tell them to keep the CCG so that the next time they go into a hospital, people can compare against the old ECG. So you know that this is not a new event, right? So this is against something that you need to be aware of. But of course, you need to keep, which is why it's important if in doubt you keep repeating the ECG every 5 to 10 minutes to see if there's any progression. Next slide, please regard to again is uh something similar, which is again a mimic of STEMI where you have a right bundle branch block pattern with ST elevation. Uh Here again, is, is said you need to keep checking to make sure that there is no progression of the ST changes. Again, it's very important to know what the presenting complaints are because if the patient does not have chest pain and you find the CCG, you're not worried, but if they come in with chest pain and you find these changes, uh and you're not convinced you need to keep repeating the ECG to see whether it progresses with time or not. Um The other thing that you can do in patient's who come in uh with chest pain and they have this is an echocardiogram because again, if you do an echo and there is some regional wall motion abnormality again, that would also tell you that probably this is an acute ischemic event next slide, please. Um Okay. So as I said, the other things that we need to consider in patient's who come in with a stemi is cardiogenic shock because if the patient is in cardiogenic shock, uh they have a very high mortality rate and you know, the prognosis is guarded uh auscultate for a systolic murmur because that could uh that could signify whether they've got a ruptured cord a like an acute Mr or a BSD because these are patient's who would then need to be transferred to a surgical center. Anyway, for urgent cardiac surgery, you could also while waiting uh consider hemodynamic support. If it's available into your hospital, things like an intra aortic balloon, perm and impella device, ECMO, these are all just cardiovascular support systems that help you or help the patient uh to tide over this um to tide over the event and to tide over the acute phase while you can get them into um uh while you can get them into a place where they can be monitored more intensely. Next slide, please. Okay. So that is about are ischemic um emergencies which is mainly stem ease. You have non stemi knees and you have unstable angina is, but those are not really uh emergencies, which is why I've just stopped with that. Right. Okay, if you can go to the next slide. So the next case. So it's a 46 year old female who presents with one our history of palpitations. Uh Now, this palpitations have been going off and not have been, she's been having these palpitations for many years, usually subside on their own know, aggravating or relieving factors, not on any regular medications. Um uh and this is the longest that any of the episodes has ever lasted. And on examination, the patient has got um a BP of 110/70 with a heart rate of 1 70 BPM and the lungs are clear. So she's not in failure. And the next slide, please. Right. So this is the ECG and if we can go to the poll and if people can answer, right. Ok. So this is indeed an s sweetie. Go to the next port. How will you treat this patient? Okay. I can see that uh, people have, okay. It's still coming in, just give him a couple of minutes and then she'll be okay. All right. Okay. Okay. I think uh that's enough. So it's a fairly split with 42% saying IV adenosine. Um and there are some who would cardio word. Now, if you remember, I said that the patient has got a BP of 100 and 20/80. So the patient is not hemodynamically compromise. The patient is hemodynamically stable. So really for an SVT, the thing that you would do would be IV adenosine. So if you can go to the next slide, please, so really the first thing you need to do in these cases is to assess the patient. And um you know, so if there are any signs of decompensation, so if the patient is hypertensive, if there are signs of heart failure or the patient has chest pain has got angina as a result of the heart beating at 100 and 80 BPM, you need to consider DC cardioversion, right? But if the patient is stable, there's no need for that. And you can give any of the IV drugs that reduce the heart rate. The communist one that we use for uh SVTS is um uh IV adenosine because what Ivy adenosine does is it blocks the conduction across the IV node, it blocks um the impulses from the atrial going on into the ventricle and it breaks the reentrant cycle. right? I'm not going to go into the pathophysiology of SVTS because that would take another hour on its own. Uh But generally, adenosine is the drug of choice. Now, adenosine has a very, very short life. Um Now looking at the uh sorry, so adenosine has got a very short life of about 10 to 15 seconds. So it's in the system, it blocks the ab node and it's out of the system again, right? And so therefore what you can uh and because of that, whatever ill effects, so you don't have like a permanent complete heart block. You don't patient, don't go into complete heart block as a result of this because it's very transient. Whereas if we were to give things like metoprolol or esmolol, what can happen is that the, the effect of the A B blockage lasts much longer? The question is, is adenosine safe in asthmatics? Yes, it is safe in asthmatics though. You have to warn the patient's that because we just give a single bowlers, you need to warn them that it can precipitate an episode of their bronchospasm and they need to take a puff of g of, um, you know, we need to give them, uh nebulizers or something else. Um Ideally, yes, it is not completely safe, but you do need to warn them that uh, it can precipitate there. Uh asthma, we try to avoid it. But, you know, if you have got nothing else, you can, uh if you can just go back one slide, please. Because the question is, how do we distinguish um broad complex SVT from SVT with a barren conduction? Now, s we t with a barren conduction. Uh and VT, there are many, many algorithms and uh so on and people will spend hours going over an ecg know if you take it to an um electrophysiologist or you get to electrophysiologists, both of them would completely disagree because there's no way you can really distinguish them unless you do some electrophysiological test. So the answer to that question is if and out treat a SVT, right? For a general cardiologist, for a general physician or for a non cardiologist, any broad complex tachycardia is VT unless otherwise uh proven you treat all broad complex tachycardia xas VT. Unless you know that the patient has pre existing left bundle branch block or you know that the patient has pre existing right bundle branch block. In which case, they then come in with a broad complex tachycardia and the QRS complex is look exactly the same as the resting ECG, then you know that this is uh sweetie with broad complex tachycardia, right? Um Otherwise you can go about debating forever and ever you can go about debating about is this s we tea with aberrancy or is this uh VT? So the short answer is if in doubt tree does VT. Okay. Uh Next slide, please. Uh Next, yeah. So next is the atrial fibrillation with a fast ventricular response. Uh because this is again, something that happens quite often, patient's come in with this palpitations. They come in with um they come in with palpitations, they come in with heart failure and uh sorry. Yeah, they come in with palpitations or they come in with heart failure and sometimes the ventricular response is so fast that you can't make out whether it's an SVT or it's an atrial fibrillation. The only way that you can distinguish between the two is um by looking at the QRS complex is now, if in this case, as you can see, the QRS complex is are not regular, it is irregular. So when it is irregular, it is a um a atrial fibrillation with fast regular response. If it is regular, it is an SPT as I said, sometimes the af can be so fast that it appears regular. But what you would need to do is to take a strip of paper and to map it out and keep moving it from one QRS to the next and just see whether it is regular or not. And as I said, if it is not regular, you would have to uh consider it as atrial fibrillation. And because the treatment is slightly different here, uh Next slide, please. Next line. Yeah, because again, uh as with the SPTS, if the patient is in shock, you need to consider DC cardioversion, we always give a bolus of anti coagulant just to make sure that uh you know that if there is any preexisting thrombus, um where you don't dislodge it or uh it actually wouldn't really make a difference, but we just give it to make ourselves feel better. Now, if the patient is not in shock or in heart failure, uh the things that we can do to slow down the heart, basically, we want to block the AB node is to give IV Digoxin IV beta blockers or IV Verapamil. Uh Now, why don't we give IV adenosine here because we're trying to block the A V node. Now, in this case, we want a slightly longer duration of Axion in the S we t we wanted a very short uh onset of Axion and very quick disappearance, right? Because we just wanted to break that reentrant cycle that the patient's have with the svtsvts. So we give the adenosine um and we try to avoid the beta blockers, we try to avoid the verapamil and digoxin excuse me. But in atrial fibrillation, we want that longer duration of Axion. So we give drugs that are slightly longer acting such as the jocks in beta blockers or verapamil. Now, the beta blockers that we can use, uh as I said, are either metoprolol or Esmolol that can be given uh some of the other drugs that we hold, use our IV um your drone. But um your drone takes time to act. Um When people say that we've given IV um your drone, it helped cardio, but that's very, very unlikely because um your drone typically takes hours to act. But that is something that we can give when we wait for the beta blockers and the digoxin to act. It's also very important that we treat the underlying cause and or the underlying precipitating cause. Now, this could be things like hyperthyroidism, my truth, stenosis, any concurrent infection, myocardial ischemia, etcetera. We need to treat all that. Um So sorry, coming back to that uh is adenosine safe in asthmatics. The other thing to remember is that you do not give adenosine infusions or you don't give uh you don't give adenosine infusions in asthmatics because yes, it can precipitate asthmatic attacks. What we give in SVTS is just a single bolus and the adenosine is out of the system in seconds in less than a minute. That's out of the system. So for S VTS, it is safe but you wouldn't use an adenosine infusion. Uh in patient's were asthmatic. Uh next slide, please. Okay. So the next case, we have a 77 year old male who's diabetic, previous history of M I history of lightheadedness and dizziness for a month. Um comes in with an episode of syncope on examination who's got a BP of 100 and 20/80 heart rate of 30 BPM and the lungs are clear. Next slide. Next slide, please. Yep. So have a look at that and we can just okay. So what does this show? Okay. So we've got a few responses still coming in, right? Ok. It's even split between all the three, between complete heart block, between Wenckebach and af it's slow ventricular response. Um The correct answer is actually complete heart block and the reason why it is not a efforts, slow ventricular response is because if it were af it's slow ventricular response, you would get an irregular QRS complex. Uh Okay. But now, so when you look at the atrial fibrillation, um you know, the QRS complex is would be irregular. Whereas here, if you were to map it out, the QRS complex is, are absolutely regular, right? So this is not a drug fibrillation. You can have atrial fibrillation with complete heart block. But in that case, you would not find proper P waves. If you look at the CCG here, you will find that the P waves are regular, that they come with regular intensity and the QRS complex is, are also regular and there is no relation between the QRSS and the P waves. And so therefore, this is a complete heart block. Next slide, please. Okay. So how do we treat these patient's? Now again, if they're hemodynamically compromised, you would try to put in a temporary pacing. Why? Or you would use external pacing or isoprenaline infusions. Um Otherwise, if the patient is hemodynamically compromised as in uh sorry, hemodynamically stable as in this patient, you would just observe them and you would just keep them in hospital and pop in a permanent pacemaker the next day. Uh It's also important to check their electrolytes to make sure that there's no hyperkalemia because that is a reversible uh cause of the complete heart block. So, hyperkalemia, hypothyroidism, these are things that we need to look out for hypothermia as well. Next slide, please. All right. And next one is heart failure. So, have a look at this um X ray and this is the last poll. So what do you think is the diagnosis here? Okay. I'll give you a bit of context to the history. So this is a 42 year old um female patient comes in with acute onset of breathlessness. Heart rate is 100 and 20. That's an A f with fast ventricular response. And so it's just breathlessness. There is no uh chest pain. I know it's not fair to just give an X ray without any clinical context because that makes a difference. So the patient has just come in with shortness of breath over the last day or so. And no history of chest pain patient is an A F with fast ventricular response. The reason I put this is this up is because this is something we don't see very often. If you look at the left cardiac border, it looks like a straight line all the way from the trachea to the apex, right, the whole left side of the heart is a straight line. So is that a clue to anybody? And again, on the right side, you can almost see like there's a double right hot border. So this patient actually has mitral stenosis. All right. So this is mitral stenosis with pulmonary congestion um because there's a classic sign of the straightening of the left heart border over here. Uh As I said, so, I it's always important to get a bit of the clinical context. Next slide, please. So for how do you manage somebody with heart failure? So the first thing you need to do obviously is to confirm the diagnosis, you need to examine the patient, um get their vital signs the usual A BCD. You look at the Airbase breathing the uh cardiovascular system, what what are they like? And examination wise, you will find that the JVP is elevated, they have bilateral crackles. Uh you can hear, look for any cardiac murmurs, they'll be pedal edema and the chest X ray will confirm the findings of heart failure. Now we need to treat them with, you know, you need to give immediate relief of symptoms. Investigate the underlying cause, check for precipitating factors, treat the underlying cause and the precipitating factors and then think about chronic management. So this is generally how you would treat someone with acute boundary edema. These are the steps that you need to go through Next slide, please. So uh confirmed the diagnosis. I just explained about how we confirmed the diagnosis. And then next is the investigating the cause and precipitating factors. So for that, you need to do a full blood count for anemia infection, check the thyroid function test, check the troponin ts to make sure that patient hasn't had. Am I? The BNP helps to confirm the diagnosis, the chest X ray to confirm heart failure rule out infection because that's the communist differential diagnosis. And a person who is presenting with breathlessness, ecg again to rule out ischemia echocardiogram to look for uh LV function and the septic screen. So while all this is happening while you investigate, you also treat the patient. So next slide, next slide please. Yeah. So how do we treat? So these go on side by side. So while you're treating their symptoms, you also do those investigations. So you need to give them intravenous diuretics. Usually we give them frusemide 40 or 80 mg IV as a stat and then you can start an infusion of about 5 to 10 mg per hour. Oxygen as opposed to patient's with M I where we don't give them oxygen. For somebody with acute boundary edema, you would give them oxygen intravenous nitrate infusion can be started, especially if the BP is high or if they are an intractable boundary edema where uh the diabetics are not working, you will start in nitrate infusion depending again on how well they respond. You would consider starting them on an IV or CPAP. And of course, if it's really bad and you think that they're tiring, you would probably even have to intubate a small dose of sedatives such as morphine can be given. But again, you've got to be careful for somebody who's got say COPD and heart failure. You've got to be very careful if you're trying to sedate them because they can go into respiratory arrest or respiratory depression. Some of the other things that can be done if the patient is still not responding is to consider dialysis or ultra filtration to get rid of that extra fluid. Next slide, please. And then of course, while you're doing that, you also treat the precipitating factor. As I said, you need to um while you're treating them for the acute exacerbation, you also need to find out why they, what precipitated it. And so if it's an M I, you need to consider angiography or PCI, if there's an infection that precipitated it. You need to give them antibiotics. If the patient missed medications, you need to restart. If they miss their dialysis. Um, patient's with CKD who have missed a episode of dialysis. Excuse me. Uh, we need to restart that. If they've got arrhythmias, we need to consider cardioversion or antiarrhythmics. Um, if they've got uncontrolled hypertension, we need to try to bring down the BP. Um, and then if there is title toxic osis again, Peter blockers, sorry about that. Uh If they've got thyrotoxicosis, we need to consider beta blockers. Sorry to apologize. And uh yes, so just treat the precipitating factor. Next slide, please. Next slide please. And while they're on the ward, of course, we control the diuretic dose and monitor the renal functions. Okay. Next slide. Okay. This is um the next case. Sorry, I apologize. A 45 year old meal known to have see a lung who presents with breathlessness over a few weeks, um sudden deterioration over a few hours and an examination was extremely breathless at a feeble pulse, low BP and high heart rate, the JVP up into the jaw and clear lungs. Next slide, please. Okay. So this is the ECG um Sorry, I don't think I put up a bowl for this, but as you can see here, excuse me, you can see what we call electrical all Terance where you have QRS complex is that are tall and short, tall and short, right? So this is what we call electrical alternates. Next slide, please. And when you look at the heart, it's a globular heart. Sorry to apologize. You can see it's a globular heart. Uh next slide. Okay. So this is basically cardiac Tampa node. And when do we suspect it? So it's suspected and somebody with acute onset of breathlessness, especially if there's a history of malignancy or trauma to the chest. No, these patient's, when you examine them, they've got soft heart zones, they've got a race JVP, they've got low BP. Uh They've got good small sign. I wanted to put a poll up for waters cause small sign. Um No, basically cause small sign is when the patient takes a deep breath in the JVP goes up. Normally when people who take a deep breath, the JVP on inspiration, generally, the JVP tends to come down, right? But um Tampa, not the JVP actually goes up with inspiration and that's a small sign. They also have something called pulses paradoxes, which is basically with inspiration, the volume of the pulse decreases, right? And when they take the, when they breathe out, the volume of the pulse goes back to normal. So these are signs of uh cardiac tamponade. Now, well, we go to the next slide, next slide, please. Yeah. So this is basically what the echo of the heart looks like. Now, you can see that the heart itself is surrounded by this bag of fluid and with each heartbeat, the heart basically swings inside this ball of fluid and that is why um if you go back, can we go back to that ECG with the electrical alternates? Yeah. So that is why because the heart is swinging inside this ball, you find that the impulses as well. You have a normal impulse followed by the small impulse when it moves to the other side. Right? Sorry forward again, please. Mm Yeah. Yeah. And next, now the diagnosis is obviously made by urgent echocardiography. The management is um sorry diagnosis by cardiogram. Fi the management is pericardial enthesis. You need to put a needle in uh you need to drain it and for loculated effusions, we need to get the surgeons to come in next slide, please. So in conclusion, prompt recognition and in initiation of management of cardiac emergencies is essential. We need to follow the A BCD principles and assessing and often early initiation of treatment can save lives. Next slide, please. Okay. Thank you. And if there are any questions. Mhm. Yes. I think you've just got one question from Dr Addy. Yeah. Just trying to read that in light of deliver. Yes. Basically all patient's with heart failure should get SGLT two. Yes. Firstly, thank you, Doctor Needle for this talk. Um Today's talk was sponsored by the MD you guys and it's one hour CPD approved by the Royal College of Surgeons of Edinburgh. So the next lecture from the doctor's guide is an ethicist any physics emergencies by Dr Noor Elahi. And that's on the fifth of July at 6 p.m. The feedback. So the feedback forms for this cardiology image will be via your email. So you have to fill in your feedback forms and then the certificate will follow guys. Thank you very much. And I want to say thank you for you to Doctor Nadal. Once again, thank you for inviting. Thank you.