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Summary

This on-demand teaching session will cover a comprehensive range of topics in cardiology. This collaborative effort between the 6 p.m. series and a medical education society aims to best prepare attendees for their final medical exams. With this talk, individuals have the opportunity to not only refresh their knowledge but also gain new insights into cardiology. Lead by Dr. Ismael, an internal medicine trainee based in Northwest London, this seminar will explore both acute and chronic cardiology. By utilizing an engaging MCQ-focused approach, the talk will prompt active involvement from participants, enhancing their learning experience. Beneficial for all aspiring or current medical personnel, this cardiology-based teaching session is aided by various healthcare companies, with special offers ensured by the use of unique codes.
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Description

Join us for an immersive learning experience designed to streamline your revision process, boost confidence, and maximise performance in your medical school finals.

Taught by doctors, each episode delves into a different medical specialty, delivering crucial insights, expert tips, and comprehensive knowledge tailored specifically for medical students preparing for their finals. Our Road to Finals series aims to provide a well-rounded understanding of key topics essential for exam success.

Learning objectives

1. Understand the signs and symptoms of heart failure and the various ways to classify the condition 2. Gain knowledge on how to diagnose heart failure using an NT Pro BNP as a first line test 3. Learn about the different treatment options for heart failure, understanding when each should be implemented 4. Familiarize with the causes for both reduced and preserved ejection fraction heart failure 5. Understand the concepts of left-sided, right-sided and congestive heart failure in detail.
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Computer generated transcript

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The following transcript was generated automatically from the content and has not been checked or corrected manually.

Hello. Um Hope everyone can hear me and see me. Ok, but thank you all for coming. Um This is a first in our road to final series and this is gonna be a talk on cardiology. Um So this is a joint partnership with the 6 p.m. series in between us. I hope we can cover all the different specialities and get you best prepared for final, which is just round the corner. Uh We also just wanna say a word for our sponsors who are sponsored by ques Meed and Medics and we have different codes and um, yeah, definitely, if you're planning to use these, uh use our code er, to, er, er, enroll, we also have a partnership with the Medical Protection Society as well. Um So uh all the details for that will be in the chat. Um, before we get into er, cardiology, I just wanna talk a little bit about what NS ES actually is. So what we do is we match mentees with mentors and help them prepare for prior to surgery. Um, and all the links to this er, scheme is gonna be in the chat. So, er, please feel free to join. Uh apart from mentorship, we also do a lot of er, talks like this educational talks and just to be updated on uh all our uh talks coming in the future to make sure you stay in touch with our socials. Um So without further ado I just want to introduce our first speaker. So it's er, his name is uh doctor Ismael, which is who is an incoming er internal med er medicine trainee in the Northwest London. He's completed his foundation year training from er UCL H and the Royal Free Trust and he's currently undertaking clinical research fellowship in uh neurogastroenterology during his f three year at the Blizzard Institute. Um So without further ado um I'm just gonna hand over to do Isma. Great. Thank you so much. Can, can all of you hear me? OK, I'm just going perfect. Just gonna present my slides. Is everyone able to see the slides? Yeah, looks good. Ok, perfect. First of all, I was gonna apologize. Um my camera doesn't seem to be working. Uh So sorry about that. But um uh yeah, thank you so much for the introduction and a big thank you to the National Surgical Educational Mentorship Society as well as the 6 p.m. series for letting me give a talk. Um So essentially today's talk is on cardiology, I think um covering all of cardiology in a one hour talk does seem like a little bit of an impossible task. Um but I will, I will do my best. I think in terms of the contents for today's lecture, the focus will be on both acute cardiology. So some of the emergency emergency presentations, we'd like you to come across as well as chronic cardiology. This session will be M CQ focused. So there'll be a lot of um interaction with the MC Qs. Um And as you see the MC Qs on the screen, um there'll be an interactive poll here on metal. So you should be able to um respond to the polls and put in your answers and we'll, we'll go through the answers um together as well as some of the explanations. If you do have any questions at any point, feel free to put them in the chart and I'll try to answer them as we go along. Um And if you have any questions towards the end, we can cover that as well. So just due to time constraints, there are a few topics I haven't been able to cover um including infective endocarditis, rheumatic fever, and valvulopathy. Um But having said that, um I've tried to cover uh the main um, conditions and presentations um that you'd likely to come across. Um And I think the folks at today's session isn't to introduce you to a lot of new topics, but it's revision on the, the key topics which are likely to come across. And I think the main ones which you will be examined on both in uh MC QS as well as AUS and just remember common things are common. It's all well and good knowing, um you know, rare conditions but um the, the burn butter will be things like a CS heart failure. Af um So I think that's why the focus should be on these. The key topics is that's where we're like you to come across. So, without further ado, let's get started with the first M CQ. So a 67 year old lady with a background of type two diabetes, ischemic heart disease and hypercholesterolemia presents to the GP with a two month history of worsening, ankle swelling, um and shortness of breath on exertion. The GP orders an NT PRO BNP which is 1200 PG per ML. What is the most important? Next step? A start the patient on 40 mg of fursemide and monitor response. B start the patient on a beta blocker ace inhibitor and spironolactone C arrange a transesophageal echo within two weeks. D arrange a transthoracic echo within six weeks or e advice to attend A&E for urgent cardiology assessment. So I wanna see if you guys um just uh a few seconds just to read through yourself and your responses and we'll go through the answer together. OK? I see we have five responses so far. We'll just give her another few seconds and then we can move on, uh see your range of answers. So I see a combination of AD and E so far. Um OK, fine. So you have minor responses. So let's um go ahead with the answer. So, um this is someone who's clearly coming with symptoms in keeping with heart failure. So, ankle swelling, shortness of breath, um and an anti pro B and P is ordered, which is 1200. So actually, the correct answer was arrange a transthoracic echo within six weeks or d. So why is this the answer? So let's just go through that together. Um So very quickly, what is heart failure? So, heart failure is a, a chronic condition characterized by the heart's inability to pump blood efficiently to meet the body's metabolic demands. Um So it's um ineffective pumping action of the blood for a number of different reasons which will come on too. So any patient coming in to GP with signs and symptoms of heart failure, regardless of their previous background, all of the patients should have an NT Pro BNP as a first line blood test. Um Now based on the PRO B and P, um we, we then decide what, what, what's the next best um action. So essentially, if the patient has um a high um BNP or an PRO BNP, um then they should be there, there should be um a specialist assessment including a transthoracic echo within two weeks. So, a high anti Pro BNP is above 2000 and A BNP is above 400 and if it's raised, so an anti probion P between 400 to 2000. So, in our case, the patient's anti probion P was 1200. So it comes under raised. Um then they should be referred for a transthoracic echo within six weeks. Um So again, I think nowadays the BNP isn't ordered as much. It's now the NT PRO BNP um which is more commonly ordered, more sensitive of the two. So I think it's, it's worth memorizing uh the, the threshold for high and raised. And just remember if it's high, then within two weeks um arrange a, an echo, uh transthoracic echo and if it's raised, then within six weeks, arrange a transthoracic echo. Now just going back to the question. Um I think obviously A and B are, are reasonable options and if we're just talking about symptomatic treatment, then obviously A would be important. Um And B um is also um treatment which has prognostic benefit, but in terms of the most important next step, uh in terms of diagnosing the heart failure, um it should be a transthoracic echo within six weeks. So there's a lot of different ways to, to classify heart failure. Um So I'll just go through some of the most um important ones. So, um the first one is to do with the ejection fraction. So how much of the blood um within the left ventricle is the heart able to pump out? So, you have heart failure with reduced ejection fraction and heart failure with preserved ejection fraction. So a reduced ejection fraction is anything below 55%. We really, we're talking about below 35 to 40% is is when um you have reduced ejection fraction and if it's preserved, it's 55% or above the old terms for these. So for reduced ejection fraction, it used to be called systolic dysfunction or systolic heart failure and preserved ejection fraction. Heart failure was known as diastolic heart failure. But now the more common terms are reduced and preserved ejection fraction. So what are the common causes for each? So, if it's reduced ejection fraction or systolic dysfunction, you have conditions such as ischemic heart disease. So, post A CS um dilated cardiomyopathy, myocarditis and arrhythmias and then diastolic dysfunction. So, with diastolic dysfunction, um the heart is still able to pump. Um So the cyst uh ejection fraction is maintained, but it has to do with relaxation. So you have conditions like hypertrophic ob uh ob obstructive cardiomyopathy, restrictive cardiomyopathy, cardiac tamponade and pericarditis where the heart isn't able to properly relax. So that's um where you have heart failure with preserved ejection fraction. Um and then it can be characterized by which part of the heart is affected. So you have left-sided heart failure or right-sided heart failure. And if both the left and right side is affected and you have congestive cardiac failure or congestive heart failure So with the left-sided heart failure, um you have cong congestion within the pulmonary vasculature leading to symptoms of pulmonary edema, which is primarily shortness of breath on exertion orthopnea, um, which is shortness of breath when lying flat. Um, and P and D uh or nocturnal dyspnea when you wake up in the middle of the night, gasping for air. So that's when you have left-sided heart failure. Then with a rightsided heart failure, symptoms are predominantly due to fluid overload in the peripheral circulation. So what symptoms does cause? So that's peripheral edema, whether that's pitting edema in the uh in the legs or the, the sacral edema. And you have a raised JVP and hepatomegaly. Then of course, if you have congestive heart failure, you'll have both the symptoms of left and rightsided heart failure. Now, so far, all of these causes of heart failure are due to low output. Um then there is high output heart failure. So in this case, the heart's um pump. So the pumping action of the heart is unaffected, but the body has increased metabolic demands. Um So in, in certain conditions like anemia, Paget disease of the bone pregnancy, thyrotoxicosis and thiamine deficiency, the body has increased metabolic demands and the heart's um pumping isn't able to meet those demands, which then lead to some of the symptoms of heart failure. Um So again, I think for um SBS, it's important to remember these conditions as as they can commonly come up and the last classification is the New York Heart Association classification. And this is again just due to the symptoms of heart failure. So in NYHA class one, you have no or minimal symptoms and in class four, you have symptoms of shortness of breath at rest and two and three is just somewhere in the middle. So with NHA A class two, ordinary exercise causes symptoms and in class three, less than ordinary um exercise causes symptoms. Again, it's important to know these classifications both for AY and for SBA. S. So let's come on to another SBA now. So an 84 year old gentleman with a known background of N yh A three congestive heart failure presents with a sudden deterioration in his breathing over the past 24 hours and vital signs are 100 and 80 SB BP, 100 and 86/100 and three heart rate. 89 respirate 27 sp O2 of 84% on room air and temperature of 36.4. So which of the following would not form part of the management plan? Hi A high flow oxygen B IV Furosemide C reposition the patient in the left lateral position. D continuous positive airway pressure or e sublingual GTN. So which of these five would not be part of a management plan for this presentation? Ok. So I can see six responses so far we'll give it another couple of seconds, eight responses. OK. Right. OK. So, so let's go ahead with the answer. So this is someone who's presenting with what seems uh seems, seems like uh acute pul edema or flash ply edema secondary to a decompensated heart failure. So essentially the incorrect answer or the correct answer rather was c so reposition, the patient in the left lateral position is incorrect. So um in someone presenting with acute pulmonary edema, what's the management? So the pneumonic is L MN op so loop diuretics. So, obviously, um the pulmonary edema. So you need fluid overload. So you wanna try and offload the patient. So loop diuretic IV, furosemide either through a bolus or a continuous infusion would be part of the management. Um morphine, again, this can help with breathlessness and pain would be part of the management. Um nitrates. So, sublingual or IV is part of the management. And why is that? So the nitrates are essentially vasodilators. So they, they um decrease the preload and the afterload uh which puts less strain or less stress on the heart. Um So, nitrates um vasodilate, um the arterial and the venous system. So, nitrates are part of the management um high flow oxygen. So, in this case, the patient is hypoxic with um so that's 84%. So you would give oxygen and finally position. So you wanna sit the patient upright. So the left lateral position in, in what sort of emergency presentations would someone be put in the left lateral position. Um Just wanna maybe send a message um on the chat. Um As there are some emergency presentations where the left lateral position is the appropriate position for the patient. Um off the top of your head. Does anyone know what, what that would be every block? OK. Any other, any other suggestions? OK. So essentially, um yeah, yeah, maternal collapse. So essentially it's your um obstetric emergencies um in which you put the patient in the left lateral position. So things like um postpartum hemorrhage or, or preeclampsia, um you wanna put the patient in the left lateral position. Um in terms of um airway blocked, obviously, you have things like the head tilt, chin lift and jaw thrust. But um the left lateral position, if you ever see that, that buzzword um in an SBA or in an OS, um it's usually in, in, in the context of um uh obstetric emergency. Um So, in our case with flash pede, you wanna sit the patient upright um and then CPAP. So continuous positive airway pressure um essentially um is a type of ventilatory support in which there's um a continuous um inspiratory pressure, which essentially just happens to uh helps to push the fluid um from uh o opens up the alveoli and pushes the fluid from the alveoli back into the, the vasculature. And it's been found that um early CPAP reduces the need for mechanical intubation and ventilation. So, CPAP, um certainly does have a, a role in um acute pulmonary edema. And lastly, if the above measures um all fail, then um inotropic support. So again, this would be your your inotropes um such as is isoprenaline um dobutamine um to, to provide cardiac support in the case of cardiogenic shock. Um you'd be looking at inotropic support in ICU. I think one thing to remember is um always um in an a sort of situation, mention that you will um discuss treatment escalation plans with patients against an 84 year old patient. Um in terms of things like inotropic support and intubation and ventilation, um you have to consider the the success of these sort of interventions. So always just mention the buzzword of treatment escalation plan and deciding whether the patient is for ICU or not or whether they're for a um a ward based healing affair in terms of why the patient is encouraged to sit upright. Um Again, uh I think primarily it is um to do with um just symptom relief. So, again, in patients who have pulmonary edema, when they lay flat, it causes worsening of of the breathlessness. You can see the patient has a respirator 27. So primarily sitting upright, um just helps with actual sensation of, of breathlessness. Um So it it is primarily uh symptomatic. So, again, this is the management for acute um pulmonary edema in in the context of decompensated heart failure. In terms of the, the chronic management for heart failure. So, in terms of symptomatic treatment for managing fluid overload, you, you would give first line loop diuretics such as furosemide or a stronger version such as Bumetanide. But it's important to remember for S PA S that um loop diuretics don't have any long term reduction in mortality. So they're purely symptomatic. Um and there's three medications which um do have um a, a positive impact on mortality and prognosis. And so first line, you have your ace inhibitors plus beta blockers and with your beta blockers is the cardioselective one. So, Bisoprolol, carvedilol and Nebivolol, these are the three in the UK which are licensed for heart failure. Then, in addition to ace inhibitors and beta blockers, the next line would be to add an aldosterone antagonist such as spironolactone. Um And again, this has been proven to improve mortality in patients with nyha three or four heart failure already taking an ace inhibitor. So, so these three medications um would form the initial management for heart failure. And so, more to mention that these three are for heart failure with reduced ejection fraction. So if they have preserved ejection fractions, so, diastolic dysfunction, then these three medications aren't licensed for reduction in mortality. So this is for reduced ejection fraction, um additional treatment. So you have your SGLT two inhibitors. So this essentially reduces reabsorption of glucose within the kidneys. Um So it's essentially helps to diurese the patient as well. And it has been shown to reduce hospitalization in both reduced and preserved ejection fraction, heart failure. And it's important to remember that is not just for heart failure with type two diabetes. Even without type two diabetes, it can still be used in heart failure. Um You have ivabradine, which is a funny current inhibitor also used for angina. But in this case, it's used for heart failure with a reduced ejection fraction and um a heart rate or, or in sinus rhythm of above 75. So they have a high resting heart rate and reduced ejection fraction. If a branding can be used, um then secure Valsartan. So again, this is used for red, reduced ejection fraction. So, um if the patient is still symptomatic on ace inhibitors, so, Valsartan is an angiotensin receptor blocker. Um So again, it works on the angiotensin receptor. Um and then secure is something called a Neprilysin inhibitor. So, Neprilysin is an enzyme which breaks down your n natriuretic peptide. So your A NP and BNP. Um so a Nepro lysin inhibitor stops the breakdown of A NP and BNP. So why is it good to have A NP? And BNP will essentially, they're, they're natural um diuretics. So they prevent reabsorption of sodium in the kidneys. Um So they promote sodium excretion and fluid um excretion from the kidneys and they also are vasodilators. So that's why in patients with heart failure, you have high BNP because the body naturally is trying to, to offload or, or get rid of this fluid overload. So, so Cuba TRL um prevents the breakdown of molecules like A and P and BNP and lastly very quickly. So, digoxin, it's supposed to be atropic. It's indicated that there's coexistent af and finally, hydrALAZINE in combination with nitrate. So both of them are vasodilators um and they're specifically um beneficial in Afro Carribbean patients. So, again, in an M CQ, by the way, if you have an Afro Carribbean patient, think about hydrALAZINE in combination with nitrate as an appropriate um additional management. So next SBA so a 24 year old male was playing a tennis match when he suddenly felt faint and collapsed. He has no known cardiac background though he has been experiencing palpitations for the past six months. He was managed by paramedics for VT arrest and successfully resuscitated. His ECG is as follows. What is the most likely diagnosis? A Brugada syndrome B hypertrophic obstructive cardiomyopathy, c arrhythmogenic, right ventricular cardiomyopathy D Wolf Parkinson White syndrome or est elevation myocardial infarction. So, this is a trickier question. Um And I think i it depends on, on your med schools, but I mean, these sort of questions um would really be differentiating sort of the upper decile. Um So it's um yeah, definitely on, on the trickier side. So just keep that in mind when you're answering. Um So let's give it a few more seconds, but just while you're answering. So I think for your exams, it's important to know uh some of the common causes for cardiac arrest in young, in younger patients. Um And there's, I think two or three which commonly come up in med school as common causes of, of cardiac arrest in, in young patients. And there's a few different ways in which you can differentiate them. Um So we'll just go over that. So we have five responses, eight responses now. OK, fine. So, so let's go for the answer. So in this case, the answer is C so arrhythmogenic, right ventricular cardiomyopathy. Um So essentially the two main causes of cardiac arrest in young patients. I want you to know is B and C. So hypertrophic obstructive cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy. So, ho is the leading cause of cardiac arrest in young patients below 40 arrhythmogenic right, ventricular cardiomyopathy is the second leading cause in patients under 40. So how do you differentiate the two? So essentially in, in this ecg you can see in V 12 and three, there is T wave inversion. Um and then right, where these arrows are pointing, you can see a notch, something called a terminal notch um right at the end of the QR S complex. So this is called an epsilon wave. So the combination of an epsilon wave plus T wave inversion is pathognomonic of A R VC. So what's the difference between the two? So first of all, broadly speaking, what is a cardiom? So, cardiomyopathy is any disease of the actual heart muscle where the muscle becomes either enlarged, thickened, stiff or weakened. Um And this disease of the cardiac muscle affects the heart's ability to pump blood efficiently. And over time, cardiomyopathies can lead to heart failure. As you said, heart failure is anything which affect, affects the heart's ability to pump. So there are two main cardiomyopathies which I want you to know of just because both are leading causes of cardiac arrest in young patients. So I'd say the first is Hoki. So how does ho present? So it's often asymptomatic and the first presentation is with cardiac arrest. But when it does have symptoms, it can cause exertional dyspnea, um angina syncope and I'll see sudden death, arrhythmias and heart failure and then with a VC, again, very similar. Um although it's more known for causing palpitations as well as syncope and then cardiac death as well. So just for your BS and MC Qs buzzwords, which are suggestive of Hokum. So a jerky pulse and a systolic murmur. So both of these are due to left ventricular outflow tract obstruction. So essentially, when you have um hypertrophy of the left ventricle, it's usually asymmetric and it can affect the flow of blood out of the left ventricle into the aorta. So this can cause a jerky pulse and a systolic murmur and the systolic murmur in Hoki is worse during the valsalva maneuvers if you ask them to exhale through a syringe, that can make the murmur worse. So, these are buzzwords um which suggest ho in an SBA or an osk inheritance. So, they're both autosomal dominant. Um And with, is due to uh genes encoding B myosin heavy chain or myosin binding C, is it worth memorizing? That? Probably not? That's pretty y low yield. But remember it's autosomal dominant. So, if you have a family history, so a father, um a mother, an uncle, aunt and again, for a R VC, it's also autosomal dominant and it's a gene encoding desmosome. Um So, pathophysiology. So again, with ho it's predominantly diastolic dysfunction. So you have left ventricle hypertrophy um which causes decreased compliance or stiffness of the left ventricle and decreased output. So it's predominantly the, the left ventricle which is affected. Whereas in a VC, it's predominantly the right ventricle, the muscle is replaced by fatty or fiber fatty tissue. Um and this fiber, fatty tissue um increases the risk of arrhythmias um such as VT and VF. So, ecg abnormalities, as I said, um with ARVC, the prim, primarily one you're looking for is T wave inversion in B1 to B3 and the epsilon wave which is a terminal notch and the QR S complex in uh Hokum. So, it's predominantly Laar hypertrophy. Does anyone wanna put in the uh in the uh me section? How can you see um left ventricular hypertrophy on an E CG, what would it show up as? And just while someone's messaging, um you can also see nonspecific ST segment changes, ST elevation or depression and T wave abnormalities. Um and occasionally af um yep, so an axis shift. Exactly. So you would see axis shift um in uh left ventricle hypertrophy. And then the other one is so essentially in V one, V two, you'll see very deep S waves. Um And then in V five and six, you'll see very tall R waves. Um So that's another way to see left ventricular hypertrophy uh on an ECG. So either axis deviation or as a deep S waves in V one V two and tall R waves. Um So the management, so for both, it's important to remember that um especially if they've had um cardiac arrest, uh an implantable um defibrillator or an ICD. Um II is the mainstay of um management and that, and that's how you're gonna reduce mortality by an ICD. Um But there are some drugs. So in ABC drugs like sotalol, which is um essentially a potassium channel blocker. And then in so drugs like amiodarone, also potassium channel blocker or beta blockers or verapamil can help with symptoms. But by, by far and away, the main take on point is for both of them and ICD is life saving. Um And again, just for A or BSI want you to remember in ho you always avoid nitrates and ace inhibitors and inotropes. So essentially, you know, the reason why you avoid nitrate ace inhibitors and intros is because it can worsen the left ventricular outflow tract obstruction. So it can, um, worsen essentially the flow of blood out of the heart. So these three medications always avoid in hon. So, um, I think that's a, just a clinical trial to remember for BS. Ok. So next, um M CQ. So a 56 year old lady with endstage renal disease on dialysis, currently awaiting transplant presents with central chest pain. She unfortunately missed her last dialysis appointment. She has no other symptoms. So just the chest pain on auscultation of the chest. A crunching snow sound is heard over the sternum. Her bloods and ECG are as follows. So sodium 140 potassium 5.3 urea 18.1 creatinine 340 white cells, 4.2 C RP eight troponin six. This is her ECG. So what is the likely underlying cause for the most likely diagnosis? Is it a atherosclerotic plaque rupture and thrombus formation? B, uremia C coronary artery spasm, D coronary artery embolism or e viral infection? Ok. We'll just give a few more seconds for you to get your responses in. Um I can see that most of you have gone. Ok, perfect. So all of you have gone for B uremia, which absolutely is correct. So, what is this presentation? So she has um central chest pain and she has a crunching snow sound um which, in other words, is a pericardial rub and um on the ECG, what can you see? So we can see widespread saddle shape or global saddle shaped ST elevation. So all of this together suggest that she has acute pericarditis. Um now going through the answers. So answers, ac and D are all causes of A CS. So, sties and sties, um and answers B and E are causes of pericarditis. So we'll come on to that in the next slide, but essentially um uremia. So, having a very high um urea in, in the serum is a cause for pericarditis and is seen in um endstage renal disease patients, especially if they miss their dialysis. The very high um urea can cause a pericarditis, other causes of viral infection in this case. So she has no other symptoms, her white cells and um C RP are significantly elevated. So it makes infection less likely. Um So u uremia is the most likely cause of her pericarditis in this case. So, what is pericarditis? Essentially, it's inflammation of the pericardial sac. So it's the membrane covering the heart. Uh and usually pericarditis tends to last about 4 to 6 weeks. So, one of the features which you can see um in BA S which tends to cause pleuritic chest pain. So, that's chest pain, which is worse on deep inspiration and is relieved by sitting or leaning forwards and it's worse when, when lying flat. Um and another buzzword is a pericardial rub, um which is a, a grating heart sound or again, it can be described as crunching snow, but essentially, it's due to um, inflammation um of the visceral and parietal pericardium as they rub together. So usually between them, there's a thin layer of pericardial fluid. So it tends to be quite smooth and there isn't any sound, but when they're inflamed, they rub against each other and create this pericardial rub on an ECG. You'll see global or widespread saddle shaped ST elevation as opposed to the territories seen in a CS in a CS, you'll see it, for example, in 23 and A VF or V 123. But in pericarditis, it's more widespread and it's sidal shape. But if it ask in an uh s be the most specific sign, um, then it's, it's pr depression, the most specific sign for pericarditis. All patients with pericarditis should have a transthoracic echo. And that's primarily to look for any pericardial effusion or tamponade, which is um uh a common, not, not common, but it, it it's a known complication of pericarditis. So all patients should have a transthoracic echo and it helps to confirm the diagnosis and troponin may be elevated in 30% of patients. So, in those 30% where it is elevated, it suggested that there could be an underlying myopericarditis where the muscle of the heart can be affected as well. So the vas major of patients can be managed as an outpatient. However, if they're high risk. So for example, if um they're febrile or they have elevated troponin, then consider inpatient management. Um obviously treat the underlying cause. So, in this case, the patient has a very high urea, they needed dialysis essentially to get the urea down. And then a combination of nsaids and colchicine are now generally used first line for idiopathic and viral pericarditis. So, um next question, a 24 year old female who recently tested positive for COVID-19 has presented with a three day history of dyspnea, palpitations and central chest pain radiating to the left arm bloods and ECG are below. What is a likely diagnosis. So the sodium is 143, um potassium is 3.6 urea 5.1 creatinine, 90 white cells are 14 crp 103 troponin is 230. Um ECG is seen there. So, what's the diagnosis? Is it a viral pericarditis? B, semi C and semi D unstable angina or e viral myocarditis? Ok. So we have six responses. So far, we'll give it another few seconds and then OK, nine response is perfect. So, um the vast majority of you have gone for e viral myocarditis, which is correct. So, why is it myocarditis? So, what can we see here? So, it's a young patient presenting with chest pain following a recent COVID infection, you can see they have high inflammatory markers. They have a high troponin, a high BNP. And you can see they have um some t depression, e said, uh especially in uh well, V four V five V 60 we can see some ST depression. So, um I'll come on to the next slide. Why this is viral myocarditis. So what is um acute myocarditis? So essentially, it's inflammation of the heart muscle or the myocardium. Um in any young patient presenting with chest pain, myocarditis should always be a differential. Um in a young patient with chest pain. So that's the buzzword for SBA S. So causes. So again, our patient recently had a COVID infection. So, viral myocarditis is one of the most common causes, but essentially bacteria such as diphtheria and clostridia lyme disease, as well as some protozoa such as Chagas disease or um can all cause myocarditis, autoimmune. Uh So it can be autoimmune and some drugs like chemotherapy drug DOXOrubicin um can cause myocarditis. So, again, in, in this case, we have a young patient with acute history of chest pain, dyspnea and arrhythmia. So again, she's coming in through the history of dyspnea, palpitations and chest pain. So, it's a classic history. Um She's recently had COVID um and COVID has been known to cause myocarditis. You might have seen it um during the pandemic in the news because the Pfizer vaccine was associated with uh myocarditis in young males in their twenties and thirties. Um So some people were scared of the vaccine, but actually, subsequent um study showed that the risk of myocarditis is higher with actual COVID infection compared to the vaccine. Um So that should have dispelled some people's fears of, of having the, the vaccine. Um um So in terms of blood, you'll tend to see very raised inflammatory markers which usually is inflammatory in nature or infective in nature. You'll see raised troponin cause it's affecting the heart muscle and you'll see A raised B and P. Um again, it's affecting the heart's ability to pump. Um So you can see some of the symptoms of heart failure such as dyspnea in, in young patients, which is unusual ecg can be nonspecific. So, tachycardia arrhythmias um commonly. So ST and T wave changes. So, um ST elevation of depression and T wave inversion. So again, it can kind of mimic um A CS in, in terms of its, its presentation. But again, a CS in a 24 year old is fairly unusual. Um and a again, the, the COVID infection is all pointing you towards myocarditis in terms of treatment. So, treatment of underlying cause, but usually if it's viral, it's it's more so supportive um to the treatment of the heart failure of the arrhythmias. Um So, again, treatments like ace inhibitors, beta blockers, you're, you're treating the underlying complications. Um what are the complications? So, heart failure is a common one arrhythmia. So it increases the risk of sudden cardiac death and a late complications. Again, this can come up in a but a late complication of myocarditis is dilated cardiomyopathy. Um So that's uh acute myocarditis. Ok. So again, this is a bit of a trickier S pa um but let's give it a go together. So, a 45 year old man is recovering from a recent episode of acute pericarditis. Two weeks ago, he presents with worsening chest pain, dyspnea, palpitations and feeling faint. An ecg shows alternation of the cures complex um amplitude between beats, which of the following signs would you not expect to find on examination? So, a a paradoxical rise in JVP on inspiration B an abnormally large drop in BP during inspiration, C A prominent X and Y descent in his JVP waveform D, muffled heart sounds in a raised JVP and E hypotension. So just while you're answering again, this is um a two-step SB. So again, step one is trying to figure out what the actual diagnosis is and then um based on that diagnosis, trying to figure out which of these signs you wouldn't see um on examination. So just while you're answering, I'll um answer the question. So what is a uh normal troponin level that excludes pregnant pathologies? So nowadays, um we tend to use high sensitivity troponin T. Um And again, I think the usual um is, is, tends to be less than 12, I'd say um or less than 14. Um So yeah, for a high sensitive vitro t, less than 14 tends to be normal. So anything above 14, um is indicative of, of some sort of underlying pathology, whether there's a CS or myocarditis. Ok. So we have nine responses. So let's um, go through the answers. So, what is the diagnosis? So, in this case, it's someone who, who's recently had pericarditis and you're presenting with chest pain, dyspnea, palpitations, feeling faint. So, again, fairly nonspecific, but um the ecg shows al alternation of cures complexes, um amplitude between beats. So this is uh something called um electrical Terance and that is um pathognomonic of something called cardiac tamponade. So the, the, the diagnosis here is cardiac tamponade which will come on to. But what's the right answer? So the right answer here is see a prominent Y descent um in his JVP W form. So let, let you go through them one by one because I know this is quite confusing. Um But this is quite a typical um SBA. So I think it's, it's worth doing some of these signs. So essentially um they have electrical alternates. So uh in cardiac tamponade, you have a pericardial effusion. So a build up of fluid around the heart which is compressing the heart. Um and as the heart beats, it can swing um within that fluid which can cause alternation of the QS complex beats. So that's electrical alternans. So what is a, so a paradoxical rise in JVP on inspiration? So, this is known as smal sign So, smal sign um can be seen in um cardiac tampon out. It's more common with constrictive pericarditis, but it can be seen. So, essentially why is that the case? So usually when you take a deep breath in, um it causes a negative intrathoracic pressure and it draws blood into the heart, but essentially in constrict and, and that should cause um a drop in your JVP usually. Um because blood's going into the right atrium, but essentially in um cardiac tampon, no, in constrictive pericarditis because you have um constriction um of the of the heart. Um it, it doesn't fill properly with blood and that's why you see a paradoxical rise in JVP on inspiration and an abnormally large drop in BP during inspiration. This is Pulsus paradoxus um which again is seen in cardiac tamponade. Um So why is that the case? So, again, um, during inspiration, um when blood is drawn into the heart because the heart is compressed, um because of the external pressure from the uh pericardial effusion, the, the ventricle can't expand properly. So the stroke volume is decreased. That's why you see a decrease or a drop in BP um during inspiration. So, d before you come on to see, so D and E so muffled heart sounds, raised JVP and hypertension. So, all three of these symptoms together um is called beck triad and this is a and this is the, the classical presentation of cardiac tamponade. Um So you expect to see all three of those. Um and then a prominent wide descent in the JVP waveform. So this is actually seen in constrictive pericarditis and it's absent um in cardiac tamponade. So in cardiac tamponade, there's no wide descent um in the J BP. So again, I know this is all a little bit confusing. Um but we'll go over it in the next slide and lastly, so how do you manage cardiac tamponade? So, the management is urgent pericardiocentesis. So that's a needle which goes into the pericardial um effusion and it just draws out the fluid. So that's the main management for cardiac tamponade. Um So, essentially, as I said, it's accumulation of uh fluid within the pericardial sac, it's a pericardial effusion, but it's specifically causing compression on the heart and impairing its ability to function. So, diagnosis, although it can be done clinically, it's usually during echocardiography which shows um the pericardial effusion um and the tampon physiology. So it shows that the heart isn't able to um function properly. And the management is urgent pericardiocentesis to drain the pericardial fluid along with supportive measures. Um So that's cardiac tamponade. So what's peri uh constrictive pericarditis? So, this is essentially um w um when the pericardium. So the parietal and visceral pericardium becomes thickened, stiff and fibrotic over time. And essentially this thickened pericardium um restricts the heart's ability to expand and fill with blood properly during the cardiac cycle leading to impaired cardiac function. So it can be caused by any of the causes of pericarditis or viral infections, uremia. But the for exams, the important one to know is TB um so classically be someone who comes from ATB endemic country like India Pakistan. Um and on chest X ray, you will see per uh pericardial calcification. So you can see um this white line which goes around the heart. So, pericardial calcification along with um coming from like atb endemic country is pushing you towards a diagnosis of constrictive pericarditis. Um And again, on exam SBA questions, you'll classically be asked to compare cardiac tamponade with constrictive pericarditis. So again, just remember some of the buzzwords and cardiac tamponade, the Y descent is absent. Whereas in constrictive pericarditis, you have a prominent Y descent. Um Pulsus paradoxus. Again, that's classically seen in tampon but not constrictive pericarditis smal signs. So the drop in JVP uh raising JVP on inspiration that's can be seen in both but more common in pericarditis and the classical features. So for cardiac tampon noid, it's electrical alternatives we discussed on the ECG in beck triad and for constrictive pericarditis, it's pericardial calcification on chest X ray. Um And very quickly the last thing. So, so C signs. So uh the raise in JVP inspiration, there's one other condition which can cause it and that's restrictive cardiomyopathy. So, in restrictive cardiomyopathy, um essentially, it's not to do with the pericardium, but it's to do with the actual heart muscle as well, which is in the name cardiomyopathy. So, it's due to infiltrative diseases like amyloidosis, sarcoidosis and hemochromatosis, which essentially it's um stiffening of, of the heart muscle itself. Um And in the UK, the most common cause of restrictive cardiomyopathy is amyloidosis. So that's another cause of Kaline. Um So I was gonna go over JVP Waveform but I can see we're running over. So I think just for the sake of time, we'll, we'll skip the JVP Waveform. Um Classically, I think in exams it can come up, but I think it's, it's fairly low yield. It's pretty, pretty tough to, to understand. Um So, so just, just for that reason, we'll, we'll skip the JP wave form for now. Um um So essentially the next SBA. So a 78 year old lady presents to Ed with Syncope. She has a history of Angina pectoris and is usually on Bisoprolol. Um She was recently started on a new medication for her Angina and she was still getting chest pain on exertion, but she can't remember the name. Her ECG is below. What medication was she likely started on? So that's your ECG, was it a, a long acting nitrate ba short acting nitrate C A dihydropyridine calcium channel blocker, D digoxin or ea nondihydropyridine calcium channel blocker. OK. So I see we have about five responses just for the sake of time, we'll uh we'll crack on. So, so, so what, what can we see over here. So it's someone with Angina who's come with syncope. Um They're usually on Bisoprolol and they were started on another medication for the Angina. So what can we see on this ECG? So essentially this is an ECG showing complete heart block. Um So as you can see, you can see P waves, but the P waves aren't followed by QR S complexes. So there's complete association between the P waves and Qs complexes, which is um yeah, consistent with complete heart block. So um she's on a beta blocker plus a new medication has now given her um complete heart block. So what is that? So that new medication is a nondihydropyridine calcium channel blocker. So that's your verapamil and dilTIAZem. So if a beta blocker is given alongside a nondihydropyridine calcium channel blocker such as verapamil or, or dilTIAZem when there's a risk of complete heart block. So I just remember in any patient on a beta blocker or something like verapamil or dil dilTIAZem never CP prescribed them because of the risk of um complete heart block. So that was the, the answer. So, so very quickly. So, ischemic heart disease and angina. So what is ischemic heart disease? This is another term for coronary artery disease, but essentially, it's due to gradual narrowing of the coronary arteries, which leads to less perfusion of the myocardium, um which can then cause chest pain at times of increased demand. So that is what Angina is um chest pain at times of increased demand due to narrowing of the coronary arteries if and this narrowing of the coronary arteries, which are due to these atherosclerotic plaques. If they rupture and cause occlusion of the artery, then no oxygen or blood can reach that area of the myocardium. And that is your A CS or your acute coronary syndromes. Um So let's just quickly come on to angina. So, angina um has three typical features. So cardiac chest pains, that's a constricting discomfort in the front of the chest or a central heaviness or tightness which often radiates to the neck, shoulders or jaw. It's precipitated by physical exertion and it's relieved by rest or GTN within five minutes. If they have all three of these, it's classical angina. If they have two of them, it's atypical angina. And if it's just one on its own, then it's unlikely to be angina or cardiac chest pain. Usually the the diagnosis is um classically clinically. So based off these three features, um you can diagnose angina, but if you were to do um some sort of diagnostic test, then the first line is a CT coronary angiography. So any question asking for the the first line diagnostic test um for angina, remember it's CT coronary angiography. Second line, you have sort of functional imaging testing for reversible myocardial ischemia. So things like uh myocardial perfusion scintigraphy. And then third line is an invasive coronary angiography which where you actually go in with a catheter through the artery into the heart and inject dye into the coronary arteries. Roughly that's very invasive and it's, it's third line. So what is the treatment for um Angina? So all patients with anginal chest pain should be started on low dose aspirin plus statin. If there's no contraindications, aspirin wise guidelines, we start all of them on aspirin and a statin. And the first line is either a beta blocker like bisoprolol or a non dihydropyridine calcium channel blocker such as verapamil or, or dilTIAZem. Um as monotherapy, if they're still getting chest pain on monotherapy, then you go to a beta blocker plus a dihydropyridine calcium channel blocker. So those would be things like n Nifedipine, amLODIPine. So as I said, never give a beta blocker with like verapamil or dilTIAZem. So if you wanna do dual therapy, then it's with a beta blocker plus Nifedipine or amLODIPine. Um And then again, if they're still getting symptoms um or they can't tolerate it, then you go to sort of third line drugs like long acting nitrate Ibra nicorandil or Ranolazine. But really if they're still getting symptoms on a beta blocker plus a cal blocker, then you really should be thinking of referring them um to for, for a specialist assessment. Um So that's angina. So now let's go through another S ea um oh, so just very quickly, I see we're getting close to 7 p.m. I'm happy to continue. I think it just really depends on our moderator as well. But if you guys aren't getting bored, if you're finding it useful, we can crack on a bit. Um I think we're on slide 26. Ok. If I it is OK. I don't know. So perfect. So, so we have 30 minutes perfectly fine. OK. So next b so a 65 year old lady with a background of hypertension type two diabetes, um CKD two and a grade two astrocytoma presented with a 14 hour history of chest discomfort and feeling clammy. The initial troponin is 324 and you were awaiting a repeat. A previous ECG from last year was reported as normal. Her ECG today is shown below. Her observations are heart rate, 100 and four BP. 88/62 respirate 16, that 95% on air temperature of 36.6. Her hospital that she's currently at is a PCI center. Given the likely diagnosis. What is the management? So a would you admit to the ward for medical management with dual antiplatelet and low molecular weight Heparin B PCC fibrinolysis D calculate sixmonth cardiac mortality before deciding management or e urgent referral to a rapid access chest pain clinic. It will give you a few seconds um to go through and decide your answer. Ok. We have two responses so far, we'll just give it another couple of seconds before we crack on. OK, fine. So, um I see a bit of a spread of answers. I think the most common one was B or PC. Um Percutane primary percutaneous coronary intervention. So, so let's just go through this again. This is a trickier question. I just want to put it out there that um these, all of these S PA S are on the trickier side. And I think um your, your standard MC QS or S PA S in exams might be a bit easier. But again, these are the sort of ones where there are more learning points um, for a session like this. Um, so don't get too disheartened, just know that the, all of these MC Qs are on the trickier side just to make this, um, a bit more challenging. So there's more learning. So essentially this is someone who's come in with, um, chest pain, feeling clammy, a raised proponent of 324 um, for, for, um, from their backgrounds. Um, you can see they have, they have risk factors for a CS and what can you see? So a previous ECG was reported as normal and today, um, we can see that they have new left bundle branch block. I think for your case as a finalist doing ba always treat new left bundle branch block as a semi until proven otherwise, as a medical student, new left bundle branch block is always treated as a semi. So with a raced component, obviously, we're waiting for a repeat. But with this ecg we're um we're thinking of stemi. Now, um how do you treat stemi? So, a stemi is treated with e um cardiac reperfusion therapy. So you're trying to restore blood flow to the heart. So it's either through a PC or primary coronary intervention or thrombolysis. Um So how do you decide between the two? So usually if the patient presents within 12 hours and they can receive PCI within two hours, then you always go for PCI in the first instance. OK. Um So in, in this case, um they've presented after 12 hours. So essentially what the guidelines say if they present after 12 hours, but there's still evidence of ongoing ischemia or cardion shock, then you should still consider PCI as the first line treatment. So they presented 14 hours after the, the 12 hour mark. However, having said that they're still having ongoing chest pain, their ECG is still ischemic and they have a raised opponent. So they still have ongoing ischemia. So the PC would still be um the first line, why not thrombolysis? So again, it could be considered although PCI would be preferable, but there is one contraindication to thrombolysis in their history and that is they have a grade two astrocytoma. Um So just threw that in there. Um Just if you were, if you had any doubt between B and C, that was just to make be the more clear answer. But essentially, there are a few absolute contraindications to um thrombolysis. Those are things like a previous intracranial hemorrhage, an ischemic stroke within the last three months having um a malignant brain tumor, like an astrocytoma, recent head injury, active bleeding, aortic dissection and a coagulation or bleeding disorder. So, with these sort of things, then you wouldn't go for thrombolysis. So that's why B is the answer and it's going through the others. So A and D would be considered for Tey and unstable Angina. And E you'd only really consider with, with stable angina or cardiac sounding chest pain first or further investigation. So e you wouldn't really do if they're having a CS. So yeah, so that's why the answer is B in this case. Um So very quickly within A CS. It's an umbrella term which covers three different conditions. Um So those conditions are unstable angina and stemi and stemi. So with unstable Angina. So you, you can see ecg changes such as ST segment, depression or T wave inversion or you might not see any. But the important thing is there is no troponin rise. So if there's troponin rise that automatically takes you to an Temi or sty, what's the etiology? So with unstable Angina, you'll have incomplete occlusion of the coronary artery which can lead to ischemia of the heart muscle, but there's no infarction. So just while I'm going through, can someone put in the messages the difference between ischemia and infarction. Um it's important to know the difference. So if someone just wants to send a message with the difference between the two. So remember with unstable Angina, you, you may see some ECG changes but there is no troponin rise. Then with NSTEMI again, you'll see at segment depression um or T wave inversion. Rarely, you might not see any but you probably will see um ST segment depression in version, but there will be a dynamic troponin rise. Um Exactly. So, infarction is death or necrosis of myocardial tissue. Um And that's what differentiates unstable angina from NSTEMI and semi. So in Nstemi again, there is incomplete occlusion. Um but there actually is infarction now of myocardial tissue. Um but what differentiates Nstemi from stemi is that um yeah, exactly. So in a blood supply plus infarction equals necrosis. Um So in Temi, the infarction is limited to the outer layers of the muscle. Um So the myocardium, myocardium and epicardium, but the innermost layer of the heart muscle, the endocardium um is still spared. But with stemi, you have complete or total occlusion of the blood vessel with transmural infarction, meaning all three layers of the heart muscle are um infarcted. And then obviously, as with an Nstemi in antemi, you will see a troponin rise as well. But what differentiates that as you will see ST elevation in two or more contiguous leads. So, contiguous is just a fancy word for neighboring or adjacent um but essentially that's to do with your cardiac territories which we'll come on to. Um And how do you define ST elevation? Um Again, now, this is a very fine print and is it worth committing this to memory? Maybe? II don't think it's a very high yield, but just for the sake of this talk. So in leads V two or three, that's what we look at first. So if it's an under 40 male, it's above 2.5 millimeters. If it's an over 40 male, it's 2.0 millimeters. And in any female, it's 1.5 millimeters. So if you see ST elevation V two and V three above um this length, then it classifies as a semi and in all other leads, any ST elevation above one millimeter is classified as a semi and of course, any new left bundle branch block as a student always treat that as um ST elevation mi I until proven otherwise. Um So these are your definitions of the different A CS syndromes. So, next SBA um so a 71 year old female presents with central crushing chest pain and clamminess. Her ECG is shown below. She was successfully managed with PC and transferred to the cardiac care unit. Subsequent um 12 EG monitoring shows complete heart block. The patient is not experiencing any symptoms from this. How can this be managed? So, a conservative monitoring B, transcutaneous pacing, C transvenous pacing D pacemaker insertion or e atropine. So again, just wanna answering. So I just come in with um a well, well, central question, chest pain and clamminess. That is her ECG, she had a PC, she was transferred. Um And um now her ECG ECG shows complete heart block. Um OK. So we have seven responses. So let, let's go through the answer. Um First of all, um this one, I wanna say what sort of um what sort of um stemmy this is based, based off the ECG O on the chart. Um which sort of cardiac region is, is affected with this. Um With this study this very quickly, we can see of ST elevation in, in two, in three and in. So that's pre predominantly where we see the ST elevation. So does anyone who say where they think um inferior? Exactly. So 23 aVF um um so it's suggestive of an inferior stemmy. So she's had an inferior stemmy now has complete heart block, but she's asymptomatic. What do we do? Well, in this case, it's, it's conservative monitoring. So remember um after an inferior M I, because inferior M I can affect um essentially the, the blood flow to the A V node. Um you can commonly see um uh complete heart block. But if they're asymptomatic with no hemodynamic compromise, then um conservative management of conservative monitoring is OK. But this differs from an anterior Mr. So in an anterior M I, if there's type two or even complete heart block and this is an indication for a temporary pacemaker. So just remember after an inferior M I, it is common to see complete heart block, it's usually transient and it can be managed conservatively if there's no symptoms or no hemodynamic compromise. But if it's anterior, um then obviously it's an indication for temporary pacing. So again, commit this to memory um because it, it is very, very important for you to know your, your territory. So as you guys said, 23, aVF is suggestive of an inferior M I, which is affecting the right coronary artery. V one and V two is an anterior M I um which is the left anterior descending and then V five, V 61 and VL is um a lateral M I. So the circumflex artery and if you see a combination of so V 123456, then it's suggestive of an anterolateral and that's usually the uh left common coronary artery. So, before it branches out into the anterior descending and circumflex, um if there's an in uh an occlusion there, then it'll affect both anterior and lateral. Um So those are your coronary artery territories and it's very important because this comes up all the time in BA S. Um So, yeah, just remember your coronary artery territories um stemi management. So, again, we'll just go through this very quickly. But for all patients with A CS, regardless whether it's semi and semi until angina, all of them will get loading dose of aspirin of 300 mg. Um And then they'll get oxygen only if it has 94 below 94%. So before everyone used to get oxygen, but now the latest guidelines, only if they're hypoxic, then give oxygen otherwise don't. Um Again, morphine, again, used to be given to everyone. Now, only if it's severe pain, then give morphine. And obviously, along with metoclopramide, this can cause nausea and nitrates for all patients, either sublingual or IV. Now with semi, as you said earlier, the key with semi is there's a complete occlusion. So you want to reperfuse uh or reestablish blood flow. So it's uh coronary reperfusion therapy which gives you two options either PCI, which is when you go through um with the catheter, I ideally through the radial artery. Um and you get rid of the blockage mechanically and you put in a stent or a fibrinolysis, which is with drugs such as um alter place nectar plate and these are clot, busting therapies. Um So how do you decide between the two? Um So if they presented within 12 hours and PC is possible within two hours, then the preference is always for PCI with a drug eluting stent. So again, these are stents which prevent re thrombocyst. So nowadays, there is always the, the preference to go with PCI. However, if they present within 12 hours and PC is not possible within two hours of the time they can give thrombolysis. Then in that case, give uh give uh thrombolysis. Um But obviously, it's remember to important to remember the contraindications, which she went over in the previous question. Um If they're receiving PC, and then again, you give them a, a second antiplatelet agent. And historically, it always used to be clopidogrel. Now there's newer ones like pros decry or I think for, for the case of OS, it, it isn't as important. But for SBA, sometimes they can ask you to be a bit more specific. So if they are on an oral anticoagulant, then you give pros um sorry if they're not taking an oral anticoagulant, you give pros um because it has a higher risk of bleeding. Otherwise, if they are on an anti oral anticoagulant, then you give clopidogrel. Um and then during PCI, you give unfractionated heparin that has um a reversal agent and it has a shorter half life. But if they're receiving fibrinolysis, then you give an antithrombin at the same time, something like Fondaparinux and then you get a further antiplatelet like decor afterwards. Um Again, I know this is a bit confusing but I think STEMI is one of the biggest um conditions in cardiology. So for SBA S, it's worth just memorize, committing this to memory. So for SBA S take a screenshot of this, just memorize this um because they can ask for specifics for SBA. So I think it's one of the few times where I'd actually say it's really, really important to know the, the management inside out. Um OK. Next SBA so a 59 year old was admitted following an an lateral ST elevation, myocardial infarction and received fibrinolysis with alter place. She is reviewed in the cardiac ICU and the repeat ecg um after 90 minutes shows a 35% resolution of the ST elevation. What is the most appropriate next step in the management? So, A would it be repeat fibrinolysis with, connect to places B would you go back in and do PCI again? Um C would you just repeat the ECG in three hours? And if, and if after three hours, there is still a 3% reduction, then you go for PCI D no further action or E would you start a GTN infusion? OK. Four responses. We'll give her another few seconds and then we'll um we'll go ahead with the answer. So, um OK, fine. So this is someone who's come in with a semi they've had um PC. But um the E CG after 90 minutes still shows um ongoing ischemia. So they have 35% resolution of the ST O. So what do we do? So the answer is B so PC, so essentially as per uh the nice guidelines after PCI, an ECG should be performed at 90 minutes following um thrombolysis or following PCI. And if there's still persistent myocardial ischemia, so, if there's less than 50% resolution. Uh sorry, sorry, my, my bad. So someone who's had fibrinolysis um and then they've had an ECG for 90 minutes. So, um if there's still persistent myocardial ischemia after 90 minutes following thrombolysis, so that's defined as less than 50% resolution of ST elevation. Then the next appropriate step is to proceed to PCI um to ensure adequate um reperfusion. So as we can see 90 minutes after fibrinolysis, they still only have a 35% resolution. So, because it's less than the 50% threshold, then you proceed to PCI. Um So that's important to remember. Um OK. So a 68 year old man presents with central crushing, chest pain for four hours. An ECG shows ST segment depression and T wave inversion with a dynamic shock rise. He is subsequently diagnosed with non ST elevation M I or NSTEMI, which of the following factors is not routinely taken into consideration when deciding further management. Is it a the E CG findings B troponin level C renal function, D history of angina or E BP? Ok. So we have a few responses. It seems like uh we have a, a range of, of all of the responses. Again, this is a bit of a, a tricky question, but this is someone coming in with NSTEMI. And um do any of you guys know of any tools decided uh any tools used to decide how we um proceed with patients with um Nstemi. So are there any sort of scoring tools you guys are aware of that are used? Um The grace score? Exactly. So again, someone who's coming with an N sty, so to decide what we do next with them, um we calculate a grade score. So what does the grade score take into consideration? Um So the grade score takes into consider consideration their age, their heart rate um at presentation, their systolic BP presentation, their renal function. So the creatinine and E CG findings, essentially, that's the presence or absence of ST segment deviation and then troponin would have raised uh troponin and then whether they had cardiac arrest at admission as well as um the presence of heart failure. So actually everything here except for the history of angina fly enough is taken into consideration. Um So the only thing in terms of previous cardiac history is to do with um whether or not they have heart failure. So all these things together make up the grace score. So if anyone comes in with an end to me, then the grace score is, is you should decide what we do next. So let's go into that in the next slide. So again, as with sties for all A CS patients, we give them uh 300 mg of aspirin, aspirin. If they're hypoxic than oxygen, if severe pain, then morphine splenogram and then nitrates. So for an NSTEMI, so if there's no immediate PCI planned, then all of them receive fondaparinux. And the only indication for an immediate PCI um is if the patient is clinically unstable, so they hypertensive, if there's cardiogenic shock, then in that case, you have to rush them for immediate PCI. But if that's not the case and there's no immediate PCI needed, then all of them receive from the paradox. Now what's um then used is the grace score um which is the most widely used tool which predicts the six month mortality and then that's used to decide what we do next. So if they're low risk, that's um defined as a grace score less than 3%. So that's less than a 3% chance of an adverse cardiac event at six months. Then you go for a conservative management with a dual antiplatelets on the paranox um and medical management. However, if you intermediate or high risk, so greater than 3% 6 month mortality risk, then in that case, you should aim for PCI within 72 hours. Um But you don't wait for the PCI. You, you just in, you initiate dual antiplatelets straight away, either with pros or tag or and unfractionated heparin. Um Again, uh a little bit complicated, but essentially, if you boil it down, um it, it's um not, not too, not too difficult. Um Again, I think this is worth memorizing and, and committing to memory, um an unstable Angina would be managed in and sort it the same way as an end. So to do with, with the grace score. Um so for both stemi and ST I think it it's worth um just memorizing this as it it does very commonly come up. So secondary prevention. So again, all patients um should be offered dual antiplatelets, either aspirin plus another ECB clopidogrel. Now again, things like Rosugol are more common, but again, dual antiplatelets and an ace inhibitor, a beta blocker and high dose statin. So 80 mg of, for example, atorvastatin and the dual antiplatelets are considered for uh continued for 12 months, followed by just aspirin monotherapy after that. Um If they do have coexisting heart failure, then you would add on an aldosterone antagonist as well. Um Again, post M I management does come up very commonly in S PA S and OSK both. So it's important to know the drugs and in terms of lifestyle factors. Um this will I think definitely get you good marks in in ACY to mention alongside um drugs which shows you being more holistic. So again, men, things like diets are following a Mediterranean diet which is high fruits, veg, extra virgin olive oil, fish, seafood 2030 minutes of exercise per day or until you feel slightly breathless and smoking cessation. So, again, mention this for, for any post in my patient in an O as well. Um OK. Next, um so a 78 year old lady had an inferior posterior stemmy two weeks ago. She is now presented with a two day history of worsening, shortness of breath on exertion and dizziness on examination. A pansystolic murmur is heard over the fifth intercostal space in the mid axillary line. What is the most likely cause for her symptoms? Is it a a ventricular septal defect? B, left ventricular free wall rupture, C aortic dissection, D rupture of the pa papillary muscle or e left ventricular aneurysm. So again, it's another um two-step B. So first trying to figure out what exactly the uh murmur or the symptoms are suggestive of. And then we're trying to um see what the most likely cause for that is. Um So you have four responses so far, who was given another few seconds? So we can press on. Um OK, fine. So um let's crack on. So, essentially a pansystolic murmur over the fifth intercostal space in the mid axillary line. So that is a pansystolic murmur in the apex. So the the apex is the mitral region. So, pansystolic murmur in the mitral region is suggestive of mitral regurgitation. Um And of these answers, the only one which should cause mitral regurgitation is rupture of the uh papillary muscle. Um uh and then that would cause mitral regurgitation. So, another common one was aortic dissection. So, an aortic dissection would cause aortic regurgitation. Um So, again, that would cause an early diastolic murmur her over the, the aortic region, which is the second intercostal space, um right sternal edge. So again, uh this is a common complication of post Temi. We have rupture of the papillary muscle which can cause mitral regurgitation. So, a good pneumonic to remember your post Temi complications or post MRI complications is Darth Vader. Um So, again, death arrhythmia and specifically, I want you to remember. So, ventricular fibrillation or VF is the most common cause of death following M I. Um obviously, you can have ruptures of various things. So, ventricular free wall rupture. So that would cause cardiac tamponade. Then we go back to bex triad um with cardiac tamponade, um rupture of the septum. So if it's the intraventricular septum, that will cause a ventricular septal defect, which causes a holosystolic murmur. Um and then rupture, rupture of the papillary muscles can cause mitral regurgitation. So, again, tampon on recovered heart failure. So the heart failure can be directly just due to necrosis or ischemia of the myocardium. But it also be indirectly due to things like mitral regurgitation or a um ventricle aneurysm. So bowel dis disease were recovered. So, left ventricular aneurysm. So this is uh another a post semi complication which can cause persistent ST elevation following an emi uh an M I um and left ventricular failure. So, an aneurysm is essentially just weakening of a muscle which then causes it to, to balloon. Um and essentially once it balloons, it can cause stasis of blood which increases the risk of thrombus. So, in patients with uh left ventricle aneurysm, you consider anticoagulation because of the increased risk of Thrombus um Dresler syndrome. So this is autoimmune pericarditis. So it's again due to um release of certain cardiac um antigens into the bloodstream, which can then cause um a autoimmune response. But it's important to remember that Dresler Dresler syndrome happens 2 to 6 weeks following an M I. And commonly you can see um pericarditis in the first few days, but remember that isn't Dresler that's just um pericarditis due to um I guess I injury or, or uh of, of the muscle. So if it's um 1 to 2 days following an M I, that's not Dresler. Dresler is 2 to 6 weeks after stemi um embolisms. Again, that's the, the mural thrombus we covered above and then recurrence of semi or mi regurgitation you've covered. Um So let's just uh it's 727. Um I think there's about 10 slides left, um which I imagine would take another 15 minutes, I think by 745. So do people wanna finish at 730 or are you happy to persist for another 15 minutes? I think we just have to cover tachyarrhythmias variety, arrhythmias and af um So if you're happy to persist, we can go for another 15 minutes and hopefully wrap up by 745. Ok, perfect. Um Cool, cool. Sounds good. So SBA um so a 24 year old male presents with a background of generalized anxiety. Uh with a background of generalized anxiety presents with a 30 minute history of palpitations and chest pain. His observations are as follows. So heart rate of 100 and 64 BP of 88/62 respirate of 20 sat of 98% on air temperature of 37 E CG. Shown below. What is the most appropriate management? Is it a adenosine? 6 mg, B, adenosine 12 mg C carotid sinus massage, de synchronized DC cardioversion or E valsalva maneuver. Um Sorry, let me just quickly create a pole. Um Let see. Mm OK. I'm sorry, this is all you pull. Thank you. OK. So just for the, the sake of time, I think we'll just um try and crack on. So this is someone who's presenting with um looking at the ECG um and SVT or a supraventricular tachycardia. And we'll go on on how you can uh differentiate that in just a minute. But there's a few key things to note. The first is that he has chest pain and the second is that he's hypotensive. So both of these are adverse features. So anyone presenting with an S VT with adverse features, um you, you go for synchronized DC cardioversion. Um All of these, so ABC and E are all options for SVT, but if they have any adverse features, then you go for synchronized DC cardioversion. So what are uh the adverse features? So per um rhythm arrhythmias. So for all patients with a tachyrhythmia, meaning their heart rate is 100 faster than 100 BPM. Start with a basic ABC assessment to make sure their airways, ok. And their breathing are high for the oxygen and then you come on to assessment of circulation. So, adverse features. So shock. So that's systolic BP less than 90. So syncope or collapse myocardial ischemia, which again can be seen on an ECG. But I think for the case of finals SBA S chest pain usually is, is a sign of myocardial ischemia for the purpose of SBA S at least and then heart failure. So things like pulmonary edema, pitting edema, um any sort of adverse features, synchronized DC cardioversions up to three shocks. Um So how do you differentiate the tachyarrhythmias? So you first look, is it broad complex or narrow, complex? And is it regular or irregular? Um So you have your broad, so a regular broad complex tachycardia for the sake of filing SBS um always assume it's uh VT. So ventricular tachycardia differential. So in, in reality, can be other things like an S VT with bundle branch block for the for the purpose of finals S PA sa broad complex tachycardia is regular, is always um ventricular tachycardia, obviously VT um can cause cardiac arrest. So if it's pulseless, you go down the A L um CPR route, but if they have a pulse and there's no signs of adverse features, then you give amiodarone 300 mg initially over 60 minutes, then 900 mg IV over the next 24 hours. So as I said, if there's no pulse A S and CPR, if they have adverse features, then a synchronized GC shock and if there's none of that, then you give Aurone 300/60 then 900/2 24 hours, then a narrow complex tachycardia that's regular. So that's what we came across. That's your SVT sorry, there should be an, there should be an S over here. Um And that can be an RT. So um atrioventricular reentrant tachycardia, that's your things like Wolf Parkinson White where there's an accessory pathway between the atria and the ventricles. And the other is an atrioventricular nodal reentrant tachycardia and that's where the reentry happens within the, the A V node. Um So for that, again, if there's adverse features like, you know, SBA synchronized DC shock, otherwise start with a vagal maneuver. So things like the valsalva blowing into a syringe or carotid sinus massage. If those aren't effective, then you can give adenosine. So 6 mg, if not effective than 12 mg and again, 12 mg. Um You don't give ade adenosine and asthmatics in the, in them. You go for verapamil. So adenosine causes transient blockage of the A V node um which for SVT S can revert them back into sinus rhythm, but it may also un un uh uh unmask an underlying atrial flutter. So that's the common one in BA S. So if despite adenosine, um they, they, they still have tachycardia, then usually it's due to an underlying rhythm like an atrial flutter. In which case, you rate control with beta blockers. Now, a broad complex tachycardia that's irregular. Again, I think for the purposes of finals SBA S, you're very likely to come across them as things like AF with bundle B block or AF with ventricular preexcitation, um very unlikely to come up in a finals SBA. And in those cases, you need expert help. The one which can come up is torsades, um which will come on to later SBA. Um Just remember that. Um And then finally, a narrow complex tachycardia, it's irregular. Um Again, for your cases, it's pretty much always gonna be af which will come on to um whenever onset is less than 48 hours, you can cardiovert with either electrical or chemical cardiovert. Otherwise rate control anticoagulant. Come on a lot more detail in the AF section. So again, this is your tachy arrhythmias. Um So next question, a 42 year old lady presents with a 20 minute history of palpitations and shortness of breath. She is otherwise hemodynamically stable. She has no known structural heart disease. ECG is shown below which drug should be avoided in the management of this condition. A lidocaine B procainamide C, amiodarone D flecainide or E verapamil Ok. So just for the, the sake of time we'll crack on. So it's a split between um C and E. So essentially the diagnosis here is a ventricular tachycardia. Um So which drug should be avoided in ventricular tachycardia? So actually the answer is E verapamil. So ABC and D are all potential treatments for VT obviously with D flecainide, if they have structural heart disease, then avoid flecainide. But in the SBA, it says she has no known structural heart disease. Um So it can be used of the, of the top four. Amiodarone is the most common um uh antiarrhythmic used for ventricular tachycardia. But the top four can all be used, but e should always be avoided in ventricular tachycardia because there's a risk um with precipitating um cardiac arrest. So, yeah, in ventricular tachycardia always avoid um verapamil. Um So there's two main types of ventricular tachycardia. The first is monomorphic as you can see in this SBA. And this is again, most commonly seen post M I and then monomorphic um VT. Again, amiodarone is usually first line and we've covered that the other is polymorphic um which is usually due to torsades. So torsades is usually precipitated by Long Qt syndrome. So again, long QT can be congenital where there are certain um electrolyte abnormalities which can commonly cause long QT I think those are worth knowing. So, hypomagnesemia, hypokalemia, hypocalcemia can all cause long QT and precipitate torsades. And hypothermia can also precipitate Torsades very quickly in the, uh, chat. Does anyone, anyone want to tell me what the, the treatment is for Torsades or the first line, uh, medical management for Torsades? What would you give? It's a good suggestion. It's a good su suggestion. So, again, um, uh, amiodarone would more be for a monomorphic. But, yeah, exactly. So, for Torsades specifically IV, magnesium sulfate, um, 2 mg would, would be the, the first line medical management for to. So yeah, exactly. IV magnesium sulfate, hold on. Um I think cardiac arrest we won't come into in any great detail, but just remember there's a shockable rhythms which are pulseless um VT and VF and they are non shockable rhythms which are asystole and P EA which is pulseless electrical activity which when you see a normal sort of heart rhythm, but there's no, there's no pulse. Um So again, if it's shockable, then you can give a single shock followed by two minutes of CPR. The usual ratio to remember is 30 compressions to two ventilations um drugs. So again, um in your uh in, in a non shockable rhythm. So as in P EA, you gave adrenaline mammogram as soon as possible. But in VT or VF arrest, it's given after the third shock, then after that, it's given um every other shock. So 1 mg is given every 3 to 5 minutes, then amiodarone is only given in your shockable rhythm. So pulseless BT and VF, you give 300 mg um after the third shock. So again, um in your shock bill rhythm after the third shock, you give 1 mg of a uh adrenaline and 300 mg of amiodarone and for amiodarone, another 150 mg can be given after the fifth shock. Again, just one of those things um which is just worth committing to memory and then your reversible causes are your four Hs and your four Ts. So as you're doing A S, you're trying to correct all these potential reversible causes. So, hypoxia, hypovolemia hyperthermia and you have metabolic disturbance, it has to do with um calcium, potassium and glucose and then your teas or thrombus. This, this could either be um like a stemi or it could even be a pulmonary embolism. You have cardiac tamponade tension, pneumothorax and any sort of toxins. So, again, you're trying to reverse all of these causes as you're doing your A LS algorithm. Um So worth knowing for BS. Um OK, so now we're gonna come on to our Brady arrhythmias very quickly. So, a 72 year old man presents to the ed with an episode of syncope and ongoing chest pain. His heart rate is 52 BPM with the rest of his observations within the normal range. An ECG shows sinus brady bradycardia with a prolonged pr interval of 230 milliseconds. He has received two boluses of 500 mcg of IV atropine with an unsatisfactory response, which of the following is not an appropriate next step. Is it a transcutaneous pacing? B transvenous pacing C A further bolus of 500 mcg of IV atropine or D isoprenaline infusion e adrenaline infusion titrate two response. So again, this is um part of your Perret algorithm for Brady arrhythmias. Um So for both um the tachy arrhythmias and bright arrythmias, um Russ UK are very good um guidelines with a very easy to follow um spreadsheet. Um So I think, yeah, that's really good resource recess UK guidelines. Um So again, this is a bit of a bit of a tricky question. Um but we'll just go through the answer very quickly. So it's actually B transvenous pacing. So again, I've taken a screenshot from the recess UK guidelines for Brady here. So, in anyone with um Brady arrhythmia, um So the first line is obviously atropine 500 mcg. So if you have a symptomatic Brady arrhythmia, first line, you give them 500 mcg of IV atropine. If there isn't a satisfactory response, which in this case, there isn'tt then all of these are potential options. So you can repeat um atropine 500 mg IV up to a maximum of 3 mg. So, so far this patient has had 1 mg. So they can be given up to another 2 mg as 500 micro boluses. So um that's why it's not C and then isoprenaline adrenaline infusions can be given as well. So that's why it's not D or E and transcutaneous pacing can also be done. Um If none of these things work, then you seek expert help and you go to transvenous pacing. So that's why the answer is B so as I said, you first always give 500 mcg of IV atropine. If there's no satisfactory response, then you can repeat atropine up to 3 mg, um isoprenaline adrenaline and transcutaneous spacing. If nothing works, see expert help and then arrange transvenous pacing. So that's why the answer in this case was b um again, it's worth remembering um what the risk factors for asystole are in bradycardia. So if they have Mobi type two heart block or complete heart block, and these are both risk factors for asystole. Obviously, if they briefly had asystole, um that's a risk factor. And finally, a ventricular pause of greater than three seconds. If you have any of these things, then even after a satisfactory treatment of the initial bradycardia, they should still be um observed. So is there a reason to go straight to transvenous pacing instead of isoprenaline or adrenaline before? Um again, um I think for, for our purposes, um I think just following the, the recess UK guidelines would be adequate. But I think um actually as an F one in anyone with bradycardia, if the initial 500 mcg of IV atropine isn't effective, then I think at this stage is when you would escalate your senior. Um And then any of these in um interim measures would be decided by, by seniors really a as, even as an F one, as an F two, you wouldn't really be deciding on these. I think obviously as per the guidelines, these are the, this is the algorithm to follow. But um I think in, in reality, if the initial atropine isn't effective, then really you leave the, the decision uh up to a senior, whether you go for adrenaline or preline or trans um transvenous pacing. So again, I think that's um kind of yeah, down to more sort of senior senior level. Um again, uh worth worth knowing these just for the sake of time and not gonna go over this line in too much detail. Um But yeah, know the difference between first degree, second degree Mobi type one and two and third degree. Um just very quickly if they have first degree or second degree Mobitz type one, these are usually asymptomatic and generally run a benign course, we don't necessarily need treatment unless the patient is very symptomatic. But for Mobitz type two and for third degree heart block, um again, the the risk of a is much higher, you are more likely to be symptomatic. So these do tend to necessitate treatment and usually it's with a pacemaker. Um So just worth knowing the distinction between the bottom two and the top two when it comes to treatment. Um OK. So a so now we've moved on to AF which is the final section. So we're almost done. I think there's just 22 or three slides left. Um So a 24 year old female presents with a three day history of palpitations. She has recently been recovering from a chest infection. She is hemodynamically stable and ECG shows atrial fibrillation. She has no other medical conditions and is otherwise. Well, what is an appropriate treatment option for this patient? Is it a immediate synchronized DC cardioversion? B3 weeks of anticoagulation prior to electrical cardioversion, C four weeks of amiodarone prior to pharmacological cardioversion, D transthoracic echo and electrical cardioversion or E rate control with a beta blocker and a beta blocker and anticoagulate um with do A OK, fine. So it seems like the overall majority have gone for E which which um I understand and then the other two are B and D. So again, this is a trickier question. So just keep that in mind. But the answer is um B so let's just go over that very quickly. So, um again, so this is someone who has AF and they have af for more than 48 hours. So in this case, they have a three day history of AF. So first of all, let's just go to e because most of you have gone for E so rate control with beta blocker and anticoagulant with do A. So again, I think with anyone presenting with af for more than 48 hours, that is a reasonable um potential management plan. I think in this case, because it's a young patients, a 24 year old with a potentially reversible cause such as chest infection. I think you, you do tend to go for a more of a rhythm control as opposed to rate control um given those two factors, but rate control is still potentially an option. But in terms of anticoagulate with a DOAC. So to decide anticoagulation, you use a score called the chads vas score. So in this case, because she's female, she'd score one but she wouldn't score any other uh points on the child's vas score. So one in a female is below the threshold for treatment with a DOAC. So again, if it was two, then you would consider anticoagulation, but in her case, she only scores for being female and nothing else. So she's below the threshold for treatment um with anticoagulation. And because of her age, again, you, you'd prefer to go with a rhythm control over rate control. So that's why um it wasn't e although II II can definitely see why that would seem like an appropriate management option. Um So fine, in this case, we're gonna go for rhythm control because um so first of all, with a immediate synchronized GC cardioversion. So again, if you had any adverse features, so shock myocardial ischemia, um syncope, et cetera. So any of those um adverse features a would be the correct option. But in her case, she has no adverse features. So it wouldn't be immediate synchronized cardio version. So that leaves us with BC and D. So because she's had um af for more than 48 hours, there is a theoretical risk of clot formation. So before cardioverting, you wanna make sure that there's no clot, you can do this in two ways. So b so the correct answer was three weeks of anticoagulation prior to electrical cardioversion. Um So this is one way in which you can show that there's no clot before you cardiovert. Then the reason why D was incorrect is it's so this answer, transthoracic echo and electrical cardioversion. So usually it's a transesophageal echo which is done um Just more, a lot more sensitive to rule out a left atrial appendage thrombus. Um And then you can immediately electrically cardiovert. So that's why D was incorrect. And then in terms of c so four weeks of amiodarone prior to pharmacological. So again, if there's a high risk of failure for cardioversion, so if they have a previous failure or recurrence of af then you wanna prime them for four weeks. So you give them four weeks to either amiodarone or sotalol um prior to electrical, to not pharmacological, the electrical cardioversion. Um So that's why the answer in this case was the, again, this is a bit of a tricky question, but uh just purposely made it a bit tricky just to uh again, in include more learning points. Um So again, as with, for af as with other arrhythmias, if there's any sign of hemodynamic instability, immediate synchronized DC cardioversion, but if they're hemodynamically stable, so if they presented less than 48 hours, you can either do a rate or rhythm control on a case by case basis. But in this case, it's a young, uh I mean, if it's a young patient reversible cause you usually go for a rhythm control. Um But so in our patients, you presented uh more than 40 hours of three um days ago. So either you do rate control, but as I said, it's a younger patient um with a reversible cause where you go for rhythm control. And if you're planning rhythm control, they either need be anticoagulated for a minimum of three weeks prior to cardioversion or transesophageal echo to exclude a left um atrial appendage thrombus. Again, if you do go for rate control, um beta blockers can be used but obviously not an asthmatics or calcium channel blockers and digoxin if, if there is coexistent heart failure. Um if you do go for electrical cardioversion, amiodarone and flecainide are used, remember for flecainide, if there's any structural heart disease, then you shouldn't use flecainide and then lastly catheter ablation. So again, this this can be used. Um So if the patient hasn't responded to um pharmacological cardioversion or they don't want to be on antiarrhythmics. Then you can use, sorry, then, then you can use um catheter ablation. So it's either radio frequency or cryotherapy ablation of the tissue just around the pulmonary veins as this tends to be the focus um for the fibrillation and prior to ablation, it should be anticoagulated for at least four weeks. Um And even if sinus rhythm is restored, anticoagulation is still required as per child's VSC, which is on our last slide. Um So we've come on to our last SBA of the session. Thank you for bearing with me. I know it's been a long session. I see a lot to cover in cardiology. So a 76 year old lady who was admitted for a community acquired pneumonia was found to be in af and was started on rate control treatment with Bisoprolol. Her medical history includes peripheral arterial disease for which she is on a statin and aspirin. Um A and she also has BPV. She is known to have recurrent falls. What decision should be made regarding starting anticoagulation? Is it a start anticoagulation treatment with Apixaban and stop Aspirin B. Start anticoagulation with Warfarin with bridging low heparin for five days. Is it C start anticoagulation with warfarin and stop Aspirin D do not start anticoagulation given she is already on an antiplatelet or e do not start anticoagulation given her false risk. So I'll give you um a little bit of time just to answer that. Um Once again, this is purposely a tricky question. Um So don't stress too much. It's just to prove a few different um take home points. Um So we'll just get some time for you guys to answer that and then we can um go through with the answer. Mm OK. So I can see a combination of A&E which are both um very fair responses. So um OK, fine. So, so let's go through the answer. So again, this is a very tricky question. So um don't stress too much, but the correct answer is a start anticoagulation treatment with Apixaban and stop aspirin. So, so let's just quickly go through why the why this is the case. Um So essentially in any question to do with um anticoagulation with af um always, you know, first of all, you need to calculate the child's va score which will come on to in the last slide. So in this case, she scores two points for her age because her age is above 75. So that's two points, one point for being female and one point for having peripheral vascular disease. So she has a child's vas of four. So, um yeah, so she does have an indication for anticoagulation. And the other score to keep in mind is the orbit score. So the orbit score um is essentially the risk of bleeding. So I said childs VSC is due the risk of of stroke due to AF and orbit is the risk of bleeding to the balance both, so her orbit score in this case is two. So one for her age and one for being on an antiplatelet. So we'll come on to that on, on the final slide. Um So in this case, because your child vascu is four anticoagulation is indicated. Um Now, so do A are now first line for A for Af and Warfarin is second line. So just because of that B and C are incorrect because now anyone with Af who is being anticoagulated, the first line is, is your dox. Um So now, um you know, so B and C is incorrect. Um and then D do not start an coagulation given she's already on an antiplatelet. Um So in this case, there is an indication for anticoagulation given her child FSC is above four. So in that case, D is incorrect. So now A is, is where it becomes um uh requires a bit of a, an explanation. So essentially, if someone has stable cardiovascular disease, so in this case, she has peripheral arterial disease. Um So if she has stable cardiovascular disease plus an indication for anticoagulation, so in this case, af then you just go for anticoagulation monotherapy. So in this, in that case, you would stop the aspirin and continue just monotherapy with uh the do so with Apixaban um where it becomes a little bit trickier is if they've had a recent acs. So if there um post semi or post PCI. In that case, there is a stronger indication to continue the antiplatelet. So in that case, you would give both the anticoagulation with um the the antiplatelet. Again, that decision is usually made by a cardiologist but again, stable cardiovascular disease with an indication for anticoagulation such as af you stop the anticoagulation, uh sorry, you stop the aspirin and continue with aspirin um and monotherapy now for the last one. So I think it, it it's very fair to say do not start an coagulation given a false risk. But there's specific nice guidelines that say do not withhold anticoagulation only solely due to patient's age or due to um risk of falls. Um Obviously, it is something you take into consideration, but just due to falls risk are just due to age. Those two things alone shouldn't be a reason not to give and the coagulation. So again, um that's what the latest nice guidelines suggest. Um So again, this was a, a very tricky question. Um So, so well done. Um So this is our final slide. Um So again, anticoagulation um In af you, you calculate the child's vat score, um zero, no treatment with a score of one in men, you can consider treatment but in women, no treatment because they, they've only given, been given that score of one due to their, their gender. Um And then two with both men and women, you offer uh treatment and then you always have to balance ble uh uh stroke risk with a bleeding risk and that's it used to be has a bladder. Now, it's been replaced by the orbit score. So again, you get points for age of having a low hemoglobin or hematocrit bleeding history, uh renal function and antiplatelet. So a score of 0 to 2 is low risk. So our patient in the previous SBA had a score of two, which is theoretically low risk, three is medium and 4 to 7 is high risk. Um Again, there's no set guidelines on how you use the orbits scores. Again, it it does come down to a clinical judgment. But remember the, the nice guidelines specifically say, don't withhold anticoagulation solely because of age or solely because of a false risk. Um And then lastly, now, Doac are first line. So Apixaban and Doxy or Furoxan and dabigatran are all first line now for preventing stroke risk in Af and Warfarin is second line. Um OK, so thank you. That is the end of the lecture. It was almost two hours. Thank you so much for, for bearing with me if there's any questions feel free to ask. Um But yeah, otherwise, uh and any feedback would be greatly appreciated and thank you. Thank you so much, Ishmael, that was a really, really good session. Um I think everyone can agree with me. There was some really good questions um content was on point. Um And Thank you everyone who attended as well. Uh I appreciate it went on a bit longer than planned, but uh definitely a really useful session. So, uh yeah, thanks again for, for taking the time. Um Do please give feedback? It's really helpful for us and for uh doctor Ismail as well. Um And our next session in the series will be on the 23rd of April and it will cover orthopedics. Um So just keep an eye out on our Instagram. Uh we'll post uh the link for that session to register soon. Um And hopefully we can see most of you there, but again, um is now thank you so much for doing the session and you have a good evening everyone. Thank you, take care everyone all the best for the exams. Bye.