Computer generated transcript

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

And I believe you've all would have seen what this ECG shows just a second doctor. Con we've just gone live again. Um Sorry for the interruption, folks. We're back now. Uh Any comments on the ECG S anyone? Yeah. Um It's someone's written sign of tachy. Yeah. Now I can see both together. So it's, oh, I can see both. Great, great. All right. Thank you. It's all good. Thank you for your help. Yeah, that is correct. The there is sinus tachycardia without any uh acute S tt abnormalities. Uh So we, what, what would be the management for this patient now that we've seen that this patient has uh no acute s tt abnormalities and the pa patient has been diagnosed to have unlikely uh cardiac chest pain, so no answers yet. Mhm So what we are going to do is from the cardiac point of view, we are going to reassure her that this patient does not have any significant. So, reassurance is, is one of the most common. Yeah, somebody has answered reassurance. So reassure the patient that there's nothing sinister going on. But apart from that, we'll have to obviously work around because I'm only uh, teaching you from the cardiology point of view. But, and if the scenario suggests anything else, like if the patient has any risk factors for, uh DVT or PS, then you'll have to think about those side of things. But from this presentation, it doesn't seem like anything sinister is going on and the patient doesn't, is very, very young and there's no other uh, comorbidities or any risk factors would, which would put, put her at risk of having DVTs of peas. So reassure and if you want to see what the cause of it, the sinus tachycardia is, you can check her hemoglobin to rule out anemia because she's in that age bracket in which there's chances of pregnancy there. So you can rule out pregnancy by doing the beta HCG or checking the last menstrual period and things like that. And if you're suspecting there might be some element of pe you can check the D diers. And so, and so go moving on to the next case. Uh Oh yeah. So the, the, the, the second case is a 58 year old gentleman with past medical history of diabetes, hypertension and smoker. He presented to a, with a central crushing discomfort which started when he woke up and it gets worse when he walks around. Pain has continued for the last 30 minutes and is radiating to his left arm. What do you think is the diagnosis? Yes. Since it qualifies the whole definition of uh angina, central crushing discomfort. As I said, the, which gives it one point, pain gets worse when the patient walks around. It is the second one we haven't mentioned the third feature. So Angina is there. If we ask further, we, we need to take the elaborate history like w what are the rate uh aggravating and relieving factors as this patient uh suffered any such pains previously as well and things like that. So, a good history uh is obviously the, the f the first and foremost thing in in order to s consider what's going on. So I would consider it as an acs as somebody as a few people have already commented there. So I believe you all are aware about what acs is. Acsi can just give you a brief uh discussion about ACS, acs is acute Coronary syndrome for people who are not aware. Uh It is an umbrella term which includes uh M I or ST elevation mi is non ST elevation, MS and unstable Angina. So these are the three things. So how do we know which patient has ST elevation mi, which patient has non ST elevation MI S and which patients have uh unstable Angina? Yes. So ECG is the first thing as somebody has mentioned. ECG I and if so E CG two point, yes, brilliant. I think all of you are brilliant. All of you know that so E CG will tell us whether this patient has ST elevation M I uh non ST elevation mi I or uh unstable Angina. So we did an ECG for this patient and oh God, I'm so terrible at this. So when the ECG was ordered, it came back like that. I hope you all can see my screen. Yeah, that was the patient's ECG. Yeah. So what does it show somebody has mentioned uh normal sinus rhythm, isolated TV, inversion and lead V three. Yeah, that is correct. So this patient has normal sinus rhythm without any acute S TT changes. So how do we know it's a non sty somebody has mentioned nonstemming. Nonstemming is some something which we can only uh decide after doing the cardiac enzymes, whether it's the troponins or in, in other some parts of the world where troponins are not readily available, there are other cardiac enzymes. But I think we talk about the UK. So we rely on uh on the troponins. So if troponins are negative, first set of troponins are negative, we qualify it as unstable angina. But if the patient with normal ECG or ECG with some abnormalities, apart from ST elevation and raised troponins, we call it non ST elevation mis. However, if the patient has normal ECG or any subtle ecg changes or ST depressions with normal tr serial troponins, it would be called as unstable Angina based on the, the history which he's presented with. So moving forward after a few minutes, the patient's chest pain started getting worse. So we repeated an ECG for this patient. So now what do you see in this ECG? Yeah. Yes, sure. That's correct. Uh The ECG shows uh ST depressions in almost majority of the leads starting from if we look from above lead lead, one lead, two lead VL has T wave inversions but not significant ST depressions and then almost all the anterior leads. Yes. So this patient has ST depressions. And when we did the cardiac enzymes, the cardiac enzymes were quite significantly elevated. So we treated this patient as a non ST elevation mi I good job everyone. Uh it's not, it's not anterior wall M I yet. So for I will I will come uh come back to your question what the anterior anterior wall M I looks like on an ECG. So there is another patient, third scenario, a 70 years old lady with no significant past medical history presented with epigastric pain for 20 minutes. ECG was requested by an sho on the ward which shows this patient M I and inferior lead. So ST elevation mi I and I don't know whether you're supposed to know the, the territories of the coronaries which supply, which uh areas or not. So I will just briefly discuss that as well. If somebody's ECG shows ST elevations like that, that you can see here, ST elevations in lead 23 and aVF so we call it inferior uh ST elevation, Mr and in 90% of the cases. It is the R CS, the uh the culprit or vessel. If somebody has got S TL in anterior leads, we call it anterior S TLV. Mr in leads V one to V six, any of those major. So it, it depends which one is it, if it's anterolateral anterior or Antero, depending on which territory is. So generally V six represents the anti uh walls of the heart. And le is most likely the culprit artery if somebody shows ST elevation in lead, one avil or one VL along with V five V six. So it is lateral wall M I and usually it is the circumflex or any branch vessel. Um M I moving forward to the next slide. Uh We ha we similar presentation similar history. If the patient had ECG like this, then as I was talking earlier, if ST elevations in anterior leads, it is anterior wall M I. So the culprit artery would be led. So he has got ST elevation M I. What is the main main management? How are you gonna proceed? What gives the most benefit to the patient in terms of uh mortality? And yes, PC is the, the correct answer back in the days when we did not have this uh primary facilities, primary PCI facility available. It's even now if, if the primary PCI is not readily available uh within a certain window period, you'll have to uh consider the patient for uh thrombolysis and then transfer the patient to a facility which can offer primary P uh um for PCI facility. Um and, and do the stent things and all, all of a, all of that. Apart from the uh mechanical treatment, there are some drugs which we give to patients with the elevation mis and non antielevation mis and uh jelly all A CS patients. What are those? There are four main drugs which we give the first one. First and foremost is anyone yes. Aspirin is the correct answer. So we have to load the patient with 300 mg of aspirin as soon as we have made our uh diagnosis of ACS. So load the pa patient with as uh clopi is a LA is later on. Uh Yes, yes, yes. So some of some of you have answered it correctly. So, aspirin loading dose is three stat and then now the guidelines have changed. So there is a second class of uh antiplatelet drug, which we call P two Y 12 inhibitors, which involves clopidogrel, uh pros and tag. So these are one of these medications we have to give on top of aspirin after we have confirmed that we are taking this patient to the Cath lab. So now the guidelines have changed that uh we have to load the patient once we have seen the Coronary Anatomy with P two Y 12 inhibitor. But if there are any delays, like we, if the patient especially for patients who are uh qualifying for primary PCI like patients with uh acute ST elevation MRI we have to load them with a second antiplatelet therapy. Once we have done the diagnostic angiogram, uh if the patient does not have uh um is not going for a prime PCI. And we are just considering for conservative treatment, we're not stenting the patient. Then we have to, we, we can consider giving either tard or, or uh pros or clopidogrel depending on the situation. So they, they all have their own uh pros and cons and adverse effects. So yeah, a apart from this Aspirin and P two Y 12 inhibitors, we have to also the statin, a high dose of statin is recommended, which is if you are giving atorvastatin, atorvastatin is the class one recommendation and we have to give them 80 mg of atorvastatin guideline says 40 to 80 mg. But uh class one recommendation now is 80 mg of statin. On top of that, we have to give them uh some medications which are for secondary prevention, which would include ace inhibitors and uh uh beta blockers. Yes, Fonda paradox is also part of that, that uh the the treatment strategy, but Fonda does not give any mortality benefit. It's only to prevent any further uh from uh thrombotic events from happening in that uh period because once somebody has a ST elevation, mi the following 48 hours are the most crucial for to develop more uh problems uh related to the thrombosis. So I've discussed about aspirin, uh P two I 12 inhibitors like clopidogrel pres or tachy and uh statin beta blockers and ace inhibitors. These are the main medications which we have to consider. And then after doing an echocardiogram, we decide what other medication the patient would require depending on the function. So going on to the next. Yes, I hope I've made sense to uh somebody said uh sorry, can you clarify when we give P two I inhibitors? Is this with aspirin? So previously, I was talking previously, we used to load the patients with aspirin as well as with P two Y 12 inhibitors. Even now I have worked in different trusts in which the their own trust guidelines suggest to give both of them together in A&E. But I if you talk about your exam purpose for regarding the guidelines and everything, so you only load the patient with aspirin in a and or or ambulance or whatever. And once the patient has gone to the cat lab and we have done the diagnostic uh angiogram only after the diagnostic angiogram is done, we load the patient with P two Y 12 inhibitors. Is that clear? Thank you. So, moving on to the next case, uh a 46 year old man with past medical history of hypertension and smoker, he presents to an with a one week history of cough, sorry. He presented to his GP uh with a one week history of cough who gave him some antibiotics to treat his upper respiratory tract infection. And he sent him home four days later, he presented to A&E with a left-sided new chest pain which eases off on sitting forward. WW. However, it gets worse when he breathes. What do you think is wrong with, with this? Yes, absolutely. Some, some, some people have onset pericarditis. So this is the demonic features of pericarditis. Uh the patient with any uh yes, every everyone is right, acute pericarditis. So anyone who presents after a viral infection uh with, with pleuric uh nature of chest pain, especially if the pain gets worse when they lie down flat on the bed and it gets eased, eased off and they lean forward or sit forward is uh suggestive of pericarditis and some people not, not always the case, but some people if you listen to the heart, you can appreciate a rub, a pericardial rub as well. Ok. Good. Yeah. So what is the mm uh How do you diagnose pericarditis? What do you see? What are the ECG features of pericarditis? Yes. There will be a global ST uh segment elevations with pr uh depressions on the ECG. Yes, global ST elevations, pr depressions on ECG these are the pneumonia features of uh the pericarditis. It was an ST elevation mi I it would involve certain clarity. However, in uh pericarditis, there wouldn't be any um uh proper um territory involved. Like I discussed previously, 23 aVF isn't uh is elevated. Then we call it ST elevation mi uh in the inferior leads if it's globally elevated, especially if it's um the, the, the uh if, if it also shows if it also shows uh pr depression uh in those leads, then we, we call it uh pericarditis. Yes. Pr depression a shock. Ok. So any questions so far? No. And what is the management for uh pericarditis? We give the patients a high dose of nonsteroidal antiinflammatory drugs, which is Ibuprofen. Yes. And we also do an echocardiogram uh just to see if just to rule out any pericardial effusions. Alongside with that, we can get, we can get uh t wave inversions in pericarditis as well. So normally uh pericarditis, the pathognomonic ECG feature is global saddle shaped ST elevations and pr depressions pr depressions are more hallmark of uh pericarditis than ST elevation. But you will get uh you, you, it's not necessary to get everything on every patient and every ECG. So you can get in some patients, you will get ST depressions and uh some people you'll get uh ST elevation with pr depressions. The main main, main feature I would emphasize is the, it is important to take uh a very good history. Uh History is the, the the is of utmost importance. So we II said we will give uh colchicine or non steroidal antiinflammatory drugs and we do the echocardiogram to see, see if there's any underlying pericardial effusion. Well, because sometimes there is like for, for whatever, there are so many reasons for pericarditis, uh different types of bugs and Q fever and everything. They can also cause pericarditis. But there might be some element of underlying pericardial effusion and depending on patient's stability and depending on pa patient's stability of the patient's BP is also on the lower side, then we think of pericardial tamponade and for that there is a dextroid. I hope you all know about dextroid. Anyone wants to comment on what be dextroid is. Yes, one feature is raised. JVP. Mm. Second feature is a low BP and third is a muffled heart sound. Very good. So I think we ha I have very intelligent smart audience here today. So good. These are the three main features which suggest the patient might have uh is might be tampon. Nodding. No. So I will give show you a few ECG S as well. I think we've covered a few topics now just to shall we do some ECG S now? Say yes, no. OK. Yes. OK. So I will start with some tachyarrhythmias. So uh definition of tachyarrhythmias, as we all know, uh the normal heart rate is between 60 to 100. So anything above 100 would be considered a tachycardia or tachyarrhythmia and any heart rate below 60 would qualify for a bradyarrhythmia or bradycardia. We will be discussing about the signs and symptoms. Essentially all uh tachy and brady arrhythmias can have similar signs and symptoms like uh palpitations, dizziness, lightheadedness, shortness of breath. Some people can present with chest pains as well because of the supply and demand mismatch. Uh uh Whereas some people can present with syncope or presyncope and then I will discuss some classification of uh tachyarrhythmias and approach and mechanism and also some ecg manifestations of it. So this is just a, you all can see my presentation, right? Yeah. So this, this is just a surgical guide for E CG um which you do not have to take seriously definition of tachycardia. As I said, is heart rate above 100 would be considered tachycardia. Uh Any patient with arrhythmia, irrespective of whether it's a brady arrhythmia or a tachy arrhythmia can present with all of or any of these uh features like palpitations, dizziness, chest pain, dysnea, syncope or presyncope or sudden cardiac death. Uh Initially, first of all, we have to check whether the patient is hemodynamically stable. If there's any, we have to take a proper um consolidated history of previous Mr S or coronary artery disease, any history of syncope in the patient as well as in the family of the patient. Uh Apart from that, we have to check if the patient has previous uh heart failure or reduced LV ejection fraction. And if we can uh get any previous ecgs to compare with, uh it's, it's always an add on. And the, then we, we uh look at the ECG to describe what sort of uh tachycardia. The patient has. The first feature is the signs of unstability. Let me, I showed you the slide. So let me see if, if not anymore, you can see here. So what are the features of uh unstability in a patient who's presenting with a tachy or brady arrhythmia, especially a tachy arrhythmia? Yes, hypotensive. But there is a number, a magic number for hypertension. What when do you call it unstable for uh tachyarrhythmia? Because that decides how are we going to treat the patient? Yes. Systolic below 90. That is correct. Yes. Diastolic below 60 systolic below 90. That is one criteria. What are the other criteria for the other criteria include any signs of heart failure, patient who may, may come in with any chest pain that is also on criteria. And the third feature is confusion. Mm. Syncope does not necessarily qualify a patient for uh DC cardioversion. So it's, it's not one of the uh feature. It is one of the red flag features, but it doesn't qualify the patient for DC cardioversion because a lot of patients uh can present after having an uh syncopal episode. But if the patient is confused or if the patient is uh uh not orientated or patient has is, is his patient's gcs is low, then obviously, we'll have to think about it as well. What, what is the cause behind it. So these are the main uh features of uh instability. So whenever a patient presents to you, um you will be working in A&E wards or wherever, even in GP surgery, you will, if you see a patient's ecg uh with uh tachycardia, the first thing you have to look for is whether the arrhythmia is a broad complex tachyarrhythmia or a narrow complex because they both direct you towards a different direction of treatment. So, if the QR S is narrow by narrow, I mean, it's less than 100 and 20 milliseconds or less than three small boxes. Uh Then we call it narrow complex. If it's uh more than three boxes or more than 100 and 20 milliseconds, we call it as wide complex tachycardia. Then then after looking at the, the size or width of the QR S, we have to see whether the, the arrhythmia is regular or irregular. Uh coming to this, um the, the, the, the tree of uh narrow complex tachycardia, if it's an irregular, narrow complex tachycardia, it's most likely afib, especially if there's no P waves present. However, as other possibilities may include multifocal atrial tachycardia, atrial flutter with variable conduction. And if the heart rhythm is regular, then it's most likely sinus tachycardia or SVT atrial flutter is very, very obvious on the ecgs. Once you've, you've seen a uh ECG with flutter, I believe. No, you wouldn't forget it ever in your life So it's, it's, it's very uh easy to, yeah. Uh if the patient has broad complex tachycardia, then again, this th this step is the same here. So whether the R rhythm is regular or it's irregular for irregular rhythm, again, the most likely cause is atrial fibrillation. But because it is a wide complex tachycardia, so af is not supposed to be wide complex there. So there is some additional pathology behind it. So which is most likely bundle branch block or pre excitation v ventricular fibrillation is is very different to atrial fibrillation. In VFIB, there's no formed complexes in uh and and I I'll show you some ecgs of it to, to uh see how to differentiate between the two if the rhythm is regular with broad complex tachycardia. Most, 1st, 1st and foremost, thing is to rule out underlying ventricular tachycardia because rest of the rhythm disturbances are not life threatening, ventricular tachycardia and VFIB are the lifethreatening rhythm disturbances. Uh I don't think I need to go into the details of where these nodes are located. So, classification, I think uh you're all aware about if name says atrial uh with arrhythmia, it's coming from the atria. The name says ventricular, it's originating from the ventricle. Uh However, some of them do not have that name like uh paroxysmal supraventricular. So, supraventricular means anything, any rhythm which is originating from above the level of the ventricle or above the level of the AV node. So, that is uh that could be paroxysmal torsos and uh also originates from ventricle. It doesn't have a name on it. So, mostly the mechanisms are either a automatic or triggered activity or reentry. So, these are different mechanisms. I think you, it's, it's beyond your level to know about these. Uh So I'll just skip it. Mm. Yeah. So these are the different um I think it's a little bit, it's very, very helpful once you've uh read it. So if the patient has uh if, if you're looking at the ECG with the heart rate of more than 100 you have seen that it is a narrow complex tachycardia with Q RS complexes less than 120 milliseconds. And then you look, the first thing you see is after the seeing that the patient is regular, if it is regular only, then you call it a supraventricular tachycardia. So if the supra there is supraventricular tachycardia, first thing you see is that whether the patient has P waves or the B waves are absent. So if the P waves are absent with irregularly irregular rhythm, then the diagnosis is straightforward and it's a atrial fibrillation and nothing else. If P waves are present, I hope you're old with me. Let me see. There's no question. Yeah. So if the P waves are present and the morphology of uh the mm P waves and the access of P waves are normal, then it's either sinus tachycardia or supra, nodal reentrant, tachycardia or sinus, nodal reentrant tachycardia, if the morphology is abnormal or the axis keeps changing, so it could be atrial flutter if you're looking at the sawtooth pattern on the ECG. However, if the P wave shows three or more morphologies with irregular or regular, it doesn't matter uh more if the, the, the P wave has three or more morphologies, it is most like multifocal atrial tachyarrhythmias. However, if there's anything in between them, so it could be either VRT or uh nodal reentrant tachyarrhythmias. So after once, uh once you've done, you've checked for the regularity or irregularity and you're looking at the P RP, uh looking at the P waves. If, if you've seen the P wave, uh they are present, then you calculate PR and RP intervals. So, in this case complex here, so this the start of the R wave to the beginning of the P wave, it's the RP interval. And from the beginning of the P wave to the beginning of the R wave, the following R wave, it's the pr interval. It is to decide whether the patient has short RP, tachycardia or long RP tachycardia. If the RP interval is lo uh longer, it is shorter than PR it's short RP tachycardia. However, on the other side, if it's longer than PR interval, it is L RP tachycardia. So L RP, tachycardia could be a, any of those. It is usually either sinus tachycardia or a atypical Avian RT and short RP tachycardia. Once you've got short RP tachycardia, I would say just cause pick AVNRT. If you've seen that the RP interval is shorter than the PR interval, it's most likely AVNRT because VR AVR T it is very difficult to see the P wave. So this is the ECG. So it's at your level, you do not need to know the difference between VRT and AVNRT. It is just uh the origin of where the origin of that tachyarrhythmia is really, it doesn't have any uh significance at your level. It is only relevant if you're in electrophysiology and you have to do ablation. So you, you need to know where to ablate. Uh Otherwise, the treatment is essentially the same for both of them unless there's white WPW syndrome, which II will explain in a minute. So this is the ECG any comments what's going on. And this ECG, well, it's a sinus tachycardia. I showed this ECG before as well in, in the, in that young lady with the tachycardia. So it is a sinus tachycardia because the P there is the morphology is uh similar in every complex. So this is P wave, there's AP wave and then it is followed by a very nice complex. So if you see it's present in every Curis complex and there's 1 to 1 conduction every day is followed by a QR S complex. They are all narrow Curis complexes. And obviously, we have to treat the underlying cause we do not treat the sinus tachycardia. I can't see the ECG mm. Right. This was the ECG which I had showed earlier as well. Can you see now? Right. Mm So it's a sinus tachycardia as you can see the, these are very nice, beautiful P waves. Every P wave is followed by a Curis complex with 1 to 1 conduction, one P and then one Curis complex, one P one Curis complex and it is at the rate of almost 100 and 23 and 150. Yeah, between, yeah, roughly around 100 and 20 BPM. OK. And then going to the next slide, what do you think is wrong in this E CG? Yes, it is an S VT. But as somebody was asking me, what is the difference between AVNRT and VRT here, I would explain. So if you look at this ECG here, there is a small blip after every C is complex here in lead V one, which is called pseudo R wave pseudo R wave in V one. And if you look at lead two and three, there's a small blip following every R wave. This is a pseudo S wave has everyone seen that. And if you go back to what I was explaining to you here, so this P wave P wave or the pseudo R wave or pseudo S wave is essentially AP wave which is submerged in inside that Curis complex and it gives a false P appearance. So if you look at here, so this p this, this notch was here following. Uh So it is a very short RP interval with a very prolonged pr so short RP, tachycardia is most likely, as I said, it's AVNRT, but sometimes atypical AVT can also have that appearance. Ok. So a BNR TS uh usually they have an abrupt onset, has more uh female uh preponderance And the rate is usually between 100 and 40 to 260. It's a narrow, curious complex and uh uh unless there is an underlying bundle branch block or an accessory pathway. And on, as I said, there's a pseudo R wave in lead V one or V two and pseudo S waves may be seen in the inferior leads, which is very good. This is one of the best ecgs I've ever come across with a very beautiful uh pseudo R wave in V one and pseudo S wave in 22 and three. OK. Moving on to the next uh ECG. So it is just this, this uh slide is just showing you the different uh pathways of uh how this tachycardia originates. What happens is, so if, if this is the consider this is the AV node and there is a slow circuit and a fast circuit so fast would, would there, there is some sort of abnormality in this area and it's not, there is some delay in conduction. So this is the fast part, we would, would conduct the electrical circuit here and it will go and uh cause the normal sinus rhythm. However, a heart muscle is a type of muscle which uh sooner or later gets the electricity and shows that uh its its appearance on the ECG. And once that has already gone there, this area is still in its depolarization and it goes, this electrical current slowly conducts to it. And by the time it has reached there, this, this has already passed that repolarization phase. So it will get conducted here and it enters into a uh reentry circuit and it keeps giving signals and electrical activity. OK. So after that, uh what is the treatment for these AVNRT S or supraventricular tachycardias? If somebody is coming in with supraventricular tachycardias, what is, how do you manage them? Yes, vagal maneuvers is correct. But before, before doing any treatment, always, always, always remember you have to ask or, or check whether the patient is stable or unstable because both of bo the stable patients. Yeah, good question. We uh if the patient is unstable, you have to uh zap the heart with DC cardioversion. And if the patient is stable only, then you do these uh vagal maneuvers and uh whatever drugs you have to give. So uh unstable patients have a very easy uh management, easy in terms of exams, but but not in terms of managing the real patient. So uh the answer is very straightforward, just cardiovert them and do a repeat ecg after that. However, if the patient is stable, you can consider doing some vagal maneuvers. There's a list of different vagal maneuvers in which one of them is carotid sinus massage. You can ask the patient to blow inside a 20 or 50 cc syringe or you can ask the patient to cough as well as hard as they can. Sometimes that terminates the or, or in, in some uh communities like in Japan and China, they submerge the patient's face into cold ice water that also uh relieves that uh tachycardia. So uh bagel maneuvers are the first line. If that fails, then we think about the uh drug or uh medications. Uh The first line is adenosine. So now it has changed when I prepared this slide. It was 12, 6, 1212. But now the guideline says first day six, then 12 and then 18 mg in the UK. But in, in the America, it's still the same. If anyone wants to go to America, it's still 6, 1212. Uh Other treatment modalities may include uh rate limiting calcium channel blockers which are dilTIAZem or verapamil and beta blockers or amiodarone can also be considered. So how does this vagal maneuvers and adenosine works? So when I was telling you about the atrial flutter, these are the flutter waves. If you, if you hide the R waves at the top and you only look at the baseline ecg strip, you see that sore tooth appearance at of the baseline. So these are the flutter waves and it is be because this one is showing 2 to 1 conduction, this one is showing force to one conduction and some, some are showing 3 to 1 conduction. So we call it atrial flutter with variable conduction. So if you've done this carotid sinus massage or you've given the adenosine and it breaks the rhythm, then, then you see what the underlying electrical activity is or sometimes you can just terminate that uh vicious cycle of tachyarrhythmias. This is the next patient. Uh What do you think is going on here? Ok. Uh It's not V TVT has to be, as I said, VT is on is always broad complex. However, this ECG is showing a narrow complex tachycardia. As you can clearly see, the curs complexes are not wide enough to be classified or considered as a broad complex category. So, mm someone has said as sweet, the TORS tors is, it's not like the torso is very different. Again, it's a broad complex and it will have a twisted uh ribbon appearance. Uh That is why the name is most likely it is WPW. But at this moment, we will still call it supraventricular tachycardia, as you can see in some of these ECG leads. Uh There is some uh delta will appear uh visible as well. So the the baseline is a bit erratic. So it's not uh I think it's not the best ECG to look for. So I do not blame you guys. I should have uh selected a better one. I had a few nicer ecgs. So we'll, we, what we did is because it, we, as I said, it, there's the, there's, there's no difference in, in this management as long as the patient is, if the patient is unstable, you just uh shock the heart with DC cardioversion and you just terminate that uh tachyarrhythmias. If the patient is stable, do those steps either vagal. If vagal has failed, then give the adenosine, it will show what the underlying rhythm is at least. And when we did that, the underlying rhythm was like this and here you can clearly see the delta waves. So if you see in lead, lead to or, and in fact, in any lead, there is a very short pr interval with a slurred of stroke of R wave which is EWW, which is VRT or orthodromic type of RT. It's I think it's a bit too above the level of M sra. If you were pulling for higher specialty training, I would have gone into the details of it. But for your level, it's, it's enough to know this is WPW syndrome or orthodromic RT. Mm Yes. So this is another patient. Uh this, this patient also presented with some uh uh this patient actually presented with a stroke and when we did the ECG it showed this and on further questioning, the patient confided that he's been having this uh palpitation for some times. So what is, and what does this ECG show? Goodbye? Yes, that is correct because it is a tachycardia. First step was to see whether it's a tachycardia or bradycardia as I explained earlier, it because it's a tachycardia because as the heart rate is above 100 we have to then look for whether it uh it's regular or irregular. And this is clearly lead to showing that this uh tachycardia is fairly irregularly irregular and and um closer in uh looking, there's no uh visible P waves here. So we call it atrial uh fibrillation. Yeah. Yes. So, and in the management is first, we have to see what the the cause is majority of the times it uh there's no cause fine and age is the most common risk factor. You might come across with a question that what is the most common cause of atrial fibrillation or may? What, what is the most common risk factor? And age is the top one. If age is not there, then select hypertension hypertension is also one of the most common causes of atrial fibrillation. But since the patient is coming with tachy with uh tachycardia and symptomatic tachycardia, so you have to look for electrolytes, whether the potassium magnesium, calcium and all electrolytes are uh within normal range, then you also have to check for thyroid function test because hyper hyper or uh hyperactive thyroid can also cause atrial fibrillation, sometimes fever or sepsis. It can also induce uh atrial fibrillation with fast ventricular response. Some of the recreational drugs or alcohol binge is also one of the very uh especially alcohol binge is a very common uh cause of uh triggering the atrial fibrillation in uh in western population. Then acs per pericarditis, myocarditis. In fact, anything which can irritate, the heart muscle can trigger atrial fibrillation. So the management for atrial fibrillation, first and foremost, is to find out whether the onset is within 48 hours or is le more than 48 hours. If it is within 48 hours, then we can safely consider electrical chemical uh cardioversion. However, if the onset is for more than 48 hours, then we just leave them on a rate controlling medication in which may be beta blocker, calcium channel blocker or amiodarone. If there is some sort of urgency or emergency, for whatever reasons, then we can consider doing a transesophageal echocardiogram to see if there's any uh blood clot. If there is no blood clot fine, then we can consider a DC cardioversion. Uh irrespective of whether it's within or more than 48 hours. If the toe shows any uh uh blood clot in anywhere in LA or LV, mostly it's in, in uh la appendage. We uh uh anticoagulate the patient and then plan for elective TC cardioversion after at least three of uh regular uh anticoagulation. So, if the onset is, as I've already explained, uh that we can consider doing a DC cardio if it's less than 48 hours. So whenever you start on anticoagulation, always check these two scores. Some people do not use has fat and they, they, they use the orbit score for atrial fibrillation, bleeding risk. Mm It's spelled as O RBI T orbit and you check whether these patients are high risk of bleeding or high risk of uh thrombosis. So, high risk of thrombosis is with Shard VSC. And now they've uh according to the current guidelines, if the Shard VSC is m more than one in males or more than two in females, we recommend starting anticoagulation and anticoagulation means any of the DUA or Warfarin. The DUA are uh may include Apixaban, Rivaroxaban, dabigatran or uh or any of those. So there's no uh preference of one over another. It could be anyone because they, they all have similar uh benefits and risks as well. However, if you, if, if, because of poor kidney functions or uh by patient's choice, they do not want that, then you can put them on a Warfarin which is an uh a Vitamin K antagonist. And uh but, but the only caveat with uh putting a patient on Warfarin is to uh regularly monitor their I NR S and it has to be uh therapeutic before consid uh for at least three weeks and at least uh no more than uh ₹2 s have to be subtherapeutic before considering for a DC cardioversion or uh electrical conversion. Then atrial flutter, the management for atrial flutter is them as atrial fibrillation, like anticoagulation rate control, explaining the patient about the stroke risk and putting them on uh one of those anticoagulants, which I've already explained to you under the heading of atrial fibrillation. Uh However, the ECG can be quite uh different from what the atrial fibrillation. ECG looks like. And if you hide these uh r waves here, you see that. So tooth pattern and uh if you look at it, you can tell that there is some variable conduction going on with some, some being conducted with a 1 to 1, some 4 to 1 and some 2 to 1 conduction. Uh Anyone knows what's going on here on this E CG. This is a 58 years old gentleman uh with COPD and hypertension, he came to the clinic with uh so he was uh short of breath and the doctor arranged uh 20 the this 12 lead ECG and they found that there was some abnormalities there. What's going on. T mhm Not really. Somebody has answered atrial fibrillation for atrial for, for this ECG to be called atrial fibrillation. The P waves should have been absent. No, it's not atrial fibrillation. So as if you closely look at lead two, there are at least three different morphologies of P waves, the rhythm is irregular. I think that is why you're confusing it with atrial fibrillation. But if you look at, look closely before every C is complex, there is ap wave. But when you look at P waves morphology, the morphologies are, there are at least 3 to 4 different morphologies. So it's a multifocal atrial tachycardia, which is a benign rhythm and you do not have to worry about it. Only thing is we have to just treat the lung condition. It, this multifocal atrial tachycardia is most likely due to a lung pathology could be uh lung fibrosis or uh COPD. Uh Like in this patient, I mentioned this patient had COPD. Is it clear to everyone? See it's very beautiful m multiple morphologies of P waves, but each P wave is followed by a Curis complex. So it's not a heart block either. It's not atrial fibrillation. Here are some uh the, the list of causes of different types of SVT S. And uh the ECG features of uh of uh different uh supraventricular tachycardia for sinus tachycardia, P wave morphology will be normal and every P wave will be followed by AC is complex for a V nodal reentrant tachycardia, P waves are not visible or if they are visible, they will either be inverted P waves immediately, they can be immediately before or after curious complexes depending on whether it's a short uh P tachycardia or a long uh P tachycardia then we have RT in RT, the P waves are visible between cures complexes and T waves. As we had she seen previously in atrial fibrillation, the rhythm would be irregularly irregular. The RR intervals will be irregularly irregular and there will not be any organized atrial activity or P waves. And this is the commonest tachycardia in patients with uh who are over 65. As I said, atrial fibrillations, most common risk factor is advanced age. Atrial flutter can be in any age from right from birth till very old. Uh the visible flutter waves flutter. The the if, if somebody's ecg shows heart rate which is constantly at 150 I would say choose a flutter as the diagnosis unless proven otherwise, unless you're certain that there's, this is not atrial flutter because what has in atrial flutters flutters rate is constant at 300 BPM with a sore tooth appearance which I shown earlier. And whenever there's a 2 to 1, usually it will flutter is a 2 to 1 conduction or a 3 to 1 conduction. Depending on that, the heart rate would be 100 and 50 BPM if it's 2 to 1 conduction and 75 BPM, if it's a uh 3 to 1 conduction, 0 100 BPM. If it's a 3 to 1 and 4 to 1, if it's a uh 75 beats from the neck, then we have uh multifocal atrial tachycardia, which I had shown to you. Now coming to the more sinister type of tachycardia, which is a wide or broad complex tachycardia. OK. So if the broad complex t um by now you're all aware of what broad complex or wide complex tachycardia means the C is complex is wider than 100 and 20 milliseconds or more than three small uh squares. Uh If it is regular, then we call it ventricular tachycardia is and back to a monomorphic type of ventricular tachycardia. If it is broad but irregular VT we call it torsades or polymorphic. VT. Other types of wide complex, regular tachycardias include a VRT and antidromic type. Previously, we discussed the V RTV, however, antidromic or a AV broad complex. But if given a choice and depending on the patients, especially if they have risk factors for if previous heart attack, previous M I previous heart failure choose ventricular tachycardia because 01 ventricular tachycardia is sinister. It can, can take the patient's life if you haven't managed lately. Vert is, is very unlikely to take the patient's life. So it's not, it's a, it's a benign rhythm, I would say, then we have to regular broad complex tachycardia because of uh hyperkalemia or any supraventricular tachycardia with an underlying bundle branch block or pre preexcitation like BP W irregular broad complex tachycardias could be due to torsades or uh ventricular fibrillation or irregular like a atrial fibrillation with bundle branch block. So this is the, the chart which shows how to uh diagnose a wide complex tachycardia. Again, you have to first see whether it is if it is wide or wide in 20 milliseconds. First thing is to check whether it's regular or irregular, irregular, wide complex tardia. Again, it's atrial fibrillation is proven otherwise. And this wideness is because of the underlying bundle branch block. But if the reg if the broad complex tachycardia is regular, the first thing is uh before doing the vagal man maneuvers, you have to uh uh to check whether the patient is stable or unstable. If the patient is unstable, treatment is the same shock the heart and uh or DC cardio the patient. And uh uh and always remember whenever you're shocking the patient, unless uh the patient is in VF you have to um synchronize the uh uh do, do the synchronized cardioversion, not unsynchronized cardioversion. So if it is regular, you have to check whether the C RSC S during a tachycardia are identical to non tachycardia. Like if you have any previous ecgs to compare with, if the patient has underlying broad co uh be the uh bundle branch block or broad complexes on a normal ECG as well without tachycardia, then you can safely say that this patients has tachycardia but it is wide, not because of VT but it is because of the underlying bundle branch block. But I, as I spoke earlier, if the patient has any previous history of heart problems, especially MRI S or stenting, then choose ventricular tachycardia unless proven otherwise. II, if you, once you've checked that the patient has regular ro complex tachycardia, you have to check whether this um atria and ventricles are related in a 1 to 1 pattern. Like every P wave is followed by a complex or not. If yes or you're not sure about it, then you have to check for the curious morphology in precordial leads which are leads V one to V six and whether they have any right or left bundle branch morphology or not, I hope I'm not going very fast, slight, not moving. I'm sorry, I'm so sorry. So bundle branch blocks, I was talking about uh wide complex tachycardia, whether it's a VT E RT irregular torsades. And this chart I'm I was showing that wide complex tachycardia. You have to first check the regularity. If it's regular or irregular, irregular would fall under atrial flutter fibrillation with under bundle branch block. And if it's regular, it would fall into VT unless proven otherwise, especially if patient has previous heart problems or previous MS. I hope it is. You hope you can all see the slide now. Yeah. OK. This chart um I was showing if the there is to one relationship between atria and ventricle or if you're not sure whether the P present but are still regular. If it was irregular, you will treat as atrial fibrillation. But if it is regular RR interval whether or not you see the P waves treat them as wide complex tachycardia, which is most likely ventricular tachycardia. OK. I think this is a bit too much for you guys. You do not need to how to diagnose VT on. Mm this, this, you know on ECG. So what is going on in this sl what's, what's wrong? What do you see in this? What is the abnormality? Yes, that's correct. It is a ventricular ectopic or some people call it premature ventricular exer or preven premature ventricular ectopic or PVC or PV ES A VP CVV, whatever it is. So some people call it V VC. Some people call it PVC. So premature ventricular excitation and if it, the E CG is done and it shows anything like this, what is the abnormality? Yes, that is correct. It is ventricular by and as you can see every there is one normal C is complex followed by a bar looking complex which is broad and it is definitely coming from the ventricle and it's there is a pattern to it. Like every do curious complex is followed by that premature ventricular complex, then normal, then premature ventricular. So this pattern is called ventricular by OK, if you're having this pattern, there is a normal sinus rhythm followed by two sub bizarre complexes like two ventricular ectopics. The pattern is what is the pattern called like this is called bigeminy. What would it be called, if there was a cure complex followed by two premature ventricular ectopics. Yes, that is correct. So, it's called uh trigemini. What if there was a normal complex followed by three such bizarre looking complexes or three pvcs? Any anywhere there is no such thing as a ventricular triplet, we call it ventricular tachycardia. So if the heart rate especially is above 100 and there are any three ventricular topics coming together, it is called ventricular tachycardia. If that tachycardia persists for more than 30 30 seconds, we call it susar tachycardia. If it uh terminates on its own by medicines or by DC cardioversion within 30 seconds, we call it nonsustained ventricular tachycardia. OK. Threes of more than three ec ventricular beats at the rate of more than 100 BPM. If it's less than 30 seconds, it's called nonsustained VT. And if it lasts for more than 30 seconds, we call it the same ventricular tachycardia. So this is uh uh an ecg of a patient who had monomorphic VT. As you can see, it's a broad complex tachycardia. It's very uh the complex as we, we we are unable to appreciate any P waves there, but it's definitely broad complex tachycardia and some ECGS mm in some patients you can appreciate a capture beat as well, which is I'll come it. So the, the, so some on an ECG you can see these capture beats, capture beat is actually you'll have this sustained broad complex tachycardia and suddenly a very normal beautiful QR S complex, uh normal looking Curis complex will be captured uh in that ECG will be called a capture beat. And it is a Hallmark, one of the Hallmark features of uh ventricular tachycardia. Sometimes what happens is you do get normal beats and ro complex tachycardia and beat was neither looking like a normal Curis complex nor it goes with a VT, it's called a fusion beat because what's happened here is that VT almost terminated there. And this new thi this so normal sinus rhythm is taking over. So this rhythm is called this, this beat is called a fusion beat. And this is another uh sign of uh ventricular tachycardia, then we have the Joseph sign which uh or, or the Garda sign, you have to just measure that you don't need to know that. So it's, it's about the calculation and measurements of that uh intervals shoot. So uh about uh different types of V TSI. If I, I've shown you this ECG with the mo monomorphic VT, and then there is a type of PT called polymorphic VT if the polyphoralis ischemia. However, if the QT segment is prolonged in a baseline ecg for whatever reason, because of any electrolyte abnormalities or any drugs with the patient is taking any QT prolonging drugs like antipsychotics or antibiotics, which may prolong it, then it is termed as torsades, de pointes. OK. So uh briefly summarizing the treatment, if the patient is more dynamically unstable, then uh the, the treatment would be DC cardioversion. And the examples of uh uh uh instability or hypotension, altered mental status, chest pain or heart failure. Amiodarone is the treatment of choice for resistant VT S. Uh And however, if the patient has gone into cardiac arrest or pulseless VT, then to give them uh we have to shock the heart according to A S algorithm. OK. Torsades de pointes is treated with magnesium. I think this is just the algorithm which I've just explained to you. Yeah, I'm sorry. II don't know what's happening. There's some problem with this computer. Were you let me share the window again? Yeah. Right. This is the the slide I was talking about regarding the monomorphic VT. So thi this is a regular broad complex tachycardia. These are the features which I have woken about regarding fusion and capture beats. So here it is the normal uh bye. This is the normal looking Curis complex submerged between uh broad complex tachycardia. So because we have captured a normal bee, we call it a capture beed. If there is a fusion of broad and a narrow complex beat, it doesn't really look like a normal sinus beat, it doesn't either fit into that BT uh type of complex, then we call it a fusion beat. And these two are Hallmark features. If you can capture them on the ECG, then you can safely diagnose patient as ventricular tachycardia. As everyone is, everyone take with me getting everything. What, what I'm teaching? Brilliant. Do anyone has any questions or anything? WPW again? OK. So somebody asked me to show the slide for VT. So this is the monomorphic VTI was talking about regular broad complex tachycardia. This is a monomorphic BT and then someone has asked me to show WPW, this is the ECG for WPW. This was when the patient presented, uh when the patient first presented with the tachycardia. And this ecg after the tachycardia was uh so with uh adenosine, OK. If uh just just one more question exam, they ask you what is the permanent treatment for supraventricular tachycardia? Irrespective of what that is uh whether it's RT or AVNRT or whatever it is, what is the permanent or long term mm Treatment for those tachycardias? Yes, that is correct. Ablation is the permanent solution for it. But in 3 to 5% people uh is in fact, uh more than that 20% of people, it can always come back in, in later life. But first ablation has 80% chances of uh permanent resolution. However, if the patient goes again for an a repeat ablation, the chances are much more, it's more than 95%. So that's about it. Really. Is there anything else or any, any other topic? II think we have, we still have 1520 minutes. Is there anything else, any other topic which you want me to discuss in comparison to smi any changes to guidelines for management. It's mainly in, it's in ST elevation M I and non ST elevation M I. The one feature, 11 management step which is different is the time frame for intervention for ST elevation M I primary PCI or thrombolysis. Thrombolysis is not indicated in non ST elevation. MI IPC S are indicated for both ST elevation and non ST elevation. But the time frame is different. For ST elevation. You have to keep that uh window period of the, the this door to uh balloon or door to needle time of 100 and 20 minutes. If you can uh cannot achieve that 1 20 minutes, then you have to consider thrombolysis for non ST elevation M I. You can do an early invasive uh coronary angiogram and uh a stenting uh within preferably within 72 hours of time. Uh Otherwise, the treatment is essentially the same go over heart blocks and ECG changes. I haven't got any. I can, I haven't got any ECGS of heart blocks unfortunately, but I can show you I can Google some imaging, I can teach you. So what happened or I can just just uh tell you what the difference is between heart blocks. There are three main types or categories of heart blocks. First degree heart block is the the pr interval. Sorry. Hello, wait, I'm just trying show you some ECG OK, know, so this is the ECG I got for there. Is it, can you see my image here? No, I don't know how to show ECG OK. I will stop. Yeah. If you look at this ECG this pr interval which is starting from the P to the start of the, the R wave here. It's longer than one large square or one large box box or five small boxes which is within that one large box. If it is larger than large box, which is 2 100s, 1 small square is equal to 40 milliseconds. If you multiply five, it's 200 milliseconds if it's longer than that, constantly throughout that rhythm strip. If it is like that, we call it first degree heart block. Uh Where is green on? Did you guys see the ECG? See I Yes, brilliant. So if it is longer than that, it is called first degree heart block. And for first degree heart block, you essentially do not treat it unless the patient is very symptomatic with that, which is very, very, very, very, very unlikely that the patient will be symptomatic with a first degree heart block. Uh The second type of heart block is the Mobitz. The type in, in Mobitz category, there are two different type is a Mobitz one which is shown here in this ECG. If you look at this here, there are, there's one P wave submerged literally immediately after that T wave and there is one P wave here. Which is immediately the next QR complex. These are two P waves. So we know there is one QR complex missing here. So if you follow it, so this pr interval is the shortest pr interval followed by a slightly longer pr interval here which keeps prolonging until there is a drop beat. And this pattern follows, it is called a second degree Mobitz type one heart block. OK. If we do not have this pattern and the pr intervals are otherwise static weight, let me show you more bits. Yes. Like here if there is pr intervals are otherwise fixed, but there are dropped beats. Like here there, there is AP wave, this is AP wave and there is a dropped beat. Here, there is no conduction of the PP wave into a Curis complex. We call it Mobitz type two. Mobitz type one does not normally require any treatment, but Mobitz type two and third degree heart block, third degree is the complete heart block or complete a V dissociation. If you have that, then this is the ECG for complete heart block. So sometimes you can get ecgs with MS. So always look for other patients as well. Sometimes they can have M I alongside with a complete heart block, first degree or second degree heart block. Like here, this patient has est elevation mi I but if you look at these P waves and this pr interval here it's quite prolonged here, pr interval is a bit shorter. Here, it is long but not longer than this, but it is definitely longer than this. So it is an underlying uh complete heart block or third baby block. Like here, this pr interval is very short. There is no QR S after this P wave here interval is much prolonged here. This is the shortest. So there is no association between AP wave and a QR S complex. So it is called complete a V dissociation or third degree heart block. Mm mm Yeah. And see you can see it, this is AP wave, this is ap wave, this is AP wave, this is AP wave. If you look at these pr intervals, these are not fixed. Some P waves are coming literally submerged into the Curis complex. Some have a very short pr interval, some have quite long and some do not have any Curis complex followed by following. You can see, right. Some people are saying we can see, some people are saying we can't see, I don't know, can see, can see Gansa, we can see you not in uh wait, let me share the entire screen. I hope you can see it now. So this I'm talking about P wave P wave is complex P wave P wave here, if you see this P wave is immediately f uh followed by Curis complex here, there's no uh Curis complex at all here, it's a very long pr interval. This pr interval is quite short, but there is a cure is complex for. So there is complete a v dissociation. And if you look at this ECG here, we can see it, we can OK. So if you look at this ECG here you see there is an ST elevation M I of inferior leads 23 aVF along with that sometimes what happens is if especially in uh in all the stress of exam, you only look for one pathology, but sometimes there is a hidden second pathology as well. And some, some you might come across with options like this patient has ST elevation in the ST elevation M I. And then there would be another option saying uh inferior ST elevation M I with a complete heart block. So you have to pick that option here. OK? I hope I've made that clear. So third degree or complete heart block and Mobitz type two AV block require a permanent solution uh which is normally a, a permanent pacemaker. One more thing if, if uh there is a patient who uh has a very slow heart rate or a bradycardia and you look at the ECG they have a third degree or a complete heart block, but they may not. And uh on top of that, uh they're not maintaining their BP whilst you're arranging for a permanent solution, a permanent pacemaker in the interim period, you have to cover them with something. It could either be a transcutaneous uh pa pa pacemaker. It could be a transvenous pacemaker which is, uh, through the temporary permanent, uh, temporary pacemaker wire which you have to put through one of the, one of the large veins or, um, you can also consider giving some medications like atropine, uh, which is very, very short acting or, uh, phenylephrine, which, uh, you can start the patient on with. Ok. I hope I've covered quite a few topics in cardiology. If you still have any questions you can pop in whilst we, I'm here. Hello. Hello. Yes. Hi, Doctor. Hi. Hello. Hi, Mario. Yes, I can. I think you've, I think you've muted yourself. No, no, no, I can, I can hear fine. Oh, no, I think it's fine. Thank you very much, Doctor Khan. No, it's a pleasure. Thank you. Let me know if you need any further as well. It was quite a bit short notice and then I had some family affairs going on so I couldn't really prepare slides really well. No, no, it was great. Thank you so much. I think you've covered most of the topics on our list. I tried. Yeah, it was really good. Thank you so much. No problem. It's a pleasure. I hope people learned something from this session. No, definitely. It's been really helpful. So, thank you. Bye bye. Thank you. Thank you. Bye bye. Um We're gonna put the uh feedback forms on the uh chat so please do fill it up. Yes, please Thank you. Thanks buh-bye. Thank you. Good luck for your exams. So, just to echo what Mario said, we, we bring a feedback form out for this latest session, so please defer it out. Uh We're now gonna have a lunch break so give you a bit of a more time. Uh Our next session is gonna come back at 215. So, uh that's when we plan to go live. So please come back for around then. So we'll stop, bro broadcasting now. Ba.