Transcript for:
Essential Medical Study Strategies and Topics

[Music] [Music] [Music] Hi guys, hope you're doing great. Uh I think that every MCQ that you solve will make you one step uh closer to victory. And uh you don't have to you know in every 1 hour that you're studying it may not be productive but then you have to show up every 1 hour because see uh suppose in this 1 hour the productivity is less maybe in the next hour I can compensate by focusing more. So it is about like showing up every single day and every single hour in my opinion and your productivity will keep on fluctuating like we talk about waxing and winning course for so many medical illnesses. Uh I can say a similar curve can be present with respect to concentration as well. So uh my suggestion at the moment is that you are building yourself for a grand finale and uh the next few days are going to be a test of your grit and discipline that is uh going to be put to test and you are like standing on the edge of greatness I would say. So with these words I think we can get started for today. Uh I would be just waiting for your quick comments uh in the chat box with respect to whether the audio and the visual part is perfectly fine and then we can go ahead with our subsequent part of the discussion. Uh we'll be focusing in this particular section mainly on the cardiology and the neurology component which form the core with respect to the questions that come on uh general medicine and uh just a word of wisdom here that is like there are only two days in a year that we cannot do anything that is yesterday and tomorrow. I mean every single day uh we can be putting our best foot forward and that helps in resulting that results in optimal results. So yes guys uh just waiting for a quick confirmation from your side and then I think we are good to go for uh today. Uh the main focus would be to do a bit of theory revision as well as I'll be putting some multiple choice questions in between as well. So that would help you uh ace your skills both with respect to theory as well as multiple choice questions. So uh yes yes CVS I'll be doing guys uh thank you so much and those if you might be having any issues with audio you can just close and go back to the video again uh because sometimes there can be like a local relay issue as well. So this would cover all exams guys uh even if you're sitting for FMG exam if you saw the level of the last FMG exam it was it was crazy crazy difficult. So I think that u u I mean we can we can focus on the theory part. uh the PDF of this would be available subsequently. I think they'll be sharing the links subsequently and you can just register on that and uh you'll get a PDF of the same. Okay. Uh thank you Dr. Sakshi. Uh uh the session uh will be variable doctor depending on your uh I would say responses uh that the duration will be decided. So we start with uh uh yes doctor I'll be I'll be speaking primarily in English only. that would be the major meth that would be the major uh mode of communication except for a few uh some some in between words from the mother tongue otherwise like it's going to be uh core English aspects. Okay. So let's hit the comment button with respect to the first question for today and I'll be expecting answers from you guys. Uh Dr. uh I'll I'll let you know where to get the PDF like let's focus on the core aspects at the moment like let's not uh focus only on the PDF part because it's more important to listen to the theory component okay so we are having a patient who is u having exertal disna 60-year-old man uh he's faint while dancing fainting while dancing in a marriage party and you are having a heaving aex beat and there's anrotic pulse and a systolic murmur and then I'm getting like lot of varied inputs there though I think uh uh Jay was the first one to mention Jay Bora was the first one to comment on the correct answer for this one. Guys, uh this is not hypertrophic cardiomopathy. Hypertrophic cardiomopathy will be presenting much more younger usually between 20 to 40 years of age and uh then in that condition you will not be having an anacrotic pulse. But the pulse that is found in hypertrophic cardiammyopathy and has been discussed so many times is pulses bispharians. So uh I think you were able to identify the question right away on reading the word anacrotrotic pulse and systolic murmur. In fact, if you watch the movie Terminator, then Aranoid Schwarzenegger, the lead guy, I mean, I think all of you, especially guys listening to here who love watching action movies, I think you are a you would be like Terminator series is like that gold standard thing with respect to action movies and Arnold Schwzenegger Mr. W, he developed valvular aotic stenosis and post that valvular iotics, he had to undergo a trans catheter aotic valve replacement. So the first and the foremost thing is this is a very easy question that I'm starting with so that I can uh help you guys get into that warming mode just like athletes practice on a daily basis first of their warm section and then they get into hardcore data. So guys the diagnosis in this case based on anacrotic pulsenous systolic murmur is going to be valular aortic stenosis. Uh I have also explained the word sad pneumonic for it that there is syncopon exertion there is angina and there is dysnia. I mean sad is a pneumonic to remember the manifestations of valvular aotexis opening to sir can you comment can I can you quickly comment in the chat box what is the uh what is the normal uh valvular orifice for the aotic valve normal is like approximately yes guys normal would be like you know about 2.5 square cm and in aoticosis anything less than this would be causing critical uh reduction in the blood supply to the i aota so therefore there can be development of synoponic exertion there would be a concatant development of angina because the person would be having left ventricular hypertrophy. Though in this question there is no mention of angina but then uh I mean these are three primary reasons why these patients would be coming to us and the highlight of this condition is that the murmur will decrease on standing in hypertrophic cardiammyopathy the murmur tends to increase on standing. The murmur of hypertrophic cardiammyopathy is totally opposite of all other murmurss. I've said that statement multiple times. I'll re reemphasize that once again. All murmurss decrease with valaba standing and amilateral inhalation. The logic and the rationale behind it is that less blood would be coming in the heart if the less is going to come in. Therefore the intensity of the murmur will decrease. That explains answer as option number A for this question. And yeah Dhanushi you're perfectly righter perfectly right with respect to mital valance. But there it is like longer right. So one is going to be louder another one is going to be longer. The gist of the first question is that don't assume answers to a question when it comes to option number B, C and D. That is asymmetrical septal hypertrophy, banana-shaped cavity of the left ventricle and proper law. They are all features of hypertrophic cardiammyopathy. And this question can be ruled out on the basis of age. That's number one. And the second thing that I think you can be using to rule out hypertrophic cardiopathy is the pulse finding which is pulses bisfarian. The ABCD of pulse is what I can say at the moment. anacrotic pulse, visarian pulse, corrians pulse and dicrotic pulse. I'll be writing the pneummonic of ABCD subsequently for the types of pulses. But a good job to all of you who got the scoring question correct and now we would be uh yes yes uh the uh you getting a hang of it. Let's move on to the next question the second one for today before I focus on the theory part. This is just a warming session so that I can get you uh all warmed up for the main session and the theory that we'll be doing. Okay. So we have this young female she's having these palpitations and dizziness uh after playing lawn tennis and she's had like such multiple episodes for past 2 years and he says like what would be the ECG finding that would be I mean this particular ECG is signifying which particular condition okay so uh yes guys a very very straightforward this is a repeat question from the inet exam and what you can pick up in the ECG of this patient is I'll try to replicate it I mean uh in the in the V1 right uh What you can see is a presence of a very deep SR and then you can not note that notching that is present before there is a T-wave inversion that is coming that notching that is happening is what is called as an epsilon wave. This would be seen in the terminal part of this would be seen in the terminal part of the QRS complex. So that helps you identify that this is uh this is going to be arythmogenic right ventricle hypertrophy uh arithmogenic right ventricle dysplasia. Along with that, yeah, you can see a T-wave inversion happening in all the leads right from like V_sub_1 to V5. All the leads are having a very symmetrical T-wave inversion. That can explain the presence of a subendocardial eskeemia in these patients. But if you look at all the options when it comes to I'll just uh uh just make it more symmetrical. Option number A, hypertrophic cardiammyopathy will be having left ventricular hypertrophy. And for diagnosis of left ventricle hypertrophy the depth of the S-wave in V_sub_1 and the height of Rwave in V5 or V6 should be more than 35 mm and that criteria is not getting satisfied. I don't see deep S waves in lead number V1 and I do not see like very tall waves in V lead number V5. So uh that would be ruled out bugata syndrome. Well well that would be having that characteristic cove pattern of ST segment elevation. And I'm just going to draw that cove uh uh segment cove ST segment elevation with a T-wave inversion. In fact, Bugatta will be having any of the two possibilities that I am currently making before you. One of them is called as a CO pattern. The second is called as a saddleback pattern. And since buga has already been asked in the exam in the previous year. So that can rule out option number C as well. You can see two types of ST elevation shown in this line diagram. That's going to be the first which is called as the co- pattern and the second one which you can see is a saddleback pattern. And this is a sodium channel defect. So prior to this in the paper they asked regarding bugarda which is a channelopathy but in the the recent paper they decided to ask regarding ARVD. And as far as the details of ARVD are concerned uh there would be uh saddleback is a feature that is seen with both two and three. You were right. And co- pattern would be for type one bugata the total three varieties. And what is Uhul's anomaly? Then Uhul's anomaly is when there is no right ventricle or there's a very thin I would say right ventricle. I mean there is no mo myocardium in the right ventricle. So two very close differential diagnosis in this question are there. One is arithmogenic right ventricle dysplasia. Second is Uhul's anomaly. Uh anomaly means that the RV moardium is not there. So patient will present in pediatric age group. Patient will not present at 25 years of age group. It would be a pediatric presentation with that of right ventricle failure because imagine if the right ventricle muscle is not there only the endocardium and the epicardium are fused to each other. If you don't have muscle in the right ventricle man, it's going to cause features of right ventricle failure in a pediatric age group. So keep that thing in your mind also that if they give you features of RVF in a very pediatric scenario with absence of right ventricle mocardium that's what we going to get answer as uh that would change the entire domain of the question. So since we are having a younger patient at 25 years of age and usually athletes nowadays right if they're having a sudden death the reason for this can be arithmogenic right ventricle dysplasia and what you mean by arithmogenic right ventricle dysplasia is what I show you in my subsequent slide yes that is desmoplain that's the gene that they're going to ask you and they're also going to give you a slide of this condition so look at the pecularity of the image that I'm showing you at the moment this particular image is having a fibro fatty this particular image that I'm showing before you is having a especially the fat component know the fat part is much more visible I mean you you know from pathology the fat is washed off so all those white spots are present I mean normally we see these these kind of images with respect to a fatty liver but what I'm telling you at the moment is that there is a fib fibro fatty replacement in the right ventricle and because of this fibro fatty displacement in the right ventricular uh right ventricle especially in the area adjacent to the epicardium You see epicardium followed by muscle. Epicardium followed by muscle. In the muscle there is a fibro fatty right ventricular I mean fibropati deposition present and this contributes to development of a voltage gradient. You can comment in the chat box what type of uh arrhythmias would be seen in arythmogenic right ventricular dysplasia. The name is ARVD as somebody commented very rightly. The no this is not a tabbyat doctor. This is not a tabbyat that we're talking we are not talking about syndrome at the moment. Nako syndrome would be having bully hair and all those things. This is simply a patient who's an athlete. She plays lawn tennis and she had uh I mean multiple palpitations and luckily she did not die otherwise there could be an I mean she's she's participating in a lawn tennis rally and you due to the excessive strain on the heart that there can be a possibility of death in this patient also. Yes, one of the common one that is seen in this patients is uh I mean this is a disease related to desmosome. So desmoplac defect is one of the common ones that we see in this patient. But like the comment I would like you to hit the comment button. What is the common arhythmia that would be seen in this condition? So it would be a ventricular tachicardia which is the usual cause of death in these patients. Uh not yeah ventricular tachicardia can then degenerate into ventricular fibrillation. But this slide number one that I've shown is for ARVD. And let me know what is the treatment for this condition as well. Quickly hit the comment button. I would like everybody to simultaneously hit the comment button. Tell me the treatment of choice for arythmogenic right ventricular uh dysplasia. The condition would contribute to sudden cardiac death. So I think uh absolutely absolutely beta blockers uh I am getting ICD plus beta blockers. Okay. So uh in this condition well there would be no role of beta blockers. I would say the main treatment for this patient is to put in an ICD that is implantable cardioviator is the main treatment that would be required for arithmogenic right ventricular dysplasia. So it is implantable cardio doctor it's not implantable pacemaker right pacemaker is obviously for brad ariththmias but in this condition because there's a there is like a possibility of development of tachihythmas that is why implantable cardiova defiabitor would be required then another very common slide that they give and I think madam would have have also discussed it that is going to be having that helter skelter appearance of the myioytes so this is very straightforward the helter skelter appearance h for helterkelter for hypertrophic cardiammyopathy And then you can see hypertrophed meiocytes. In fact, this is again a very big pecularity that if you find that some of the myioytes are damaged and some of the myioytes are going to be hypertrophed myioytes because they give this integrated questions where you would be having some clinical domain and some pathological information present. So this is helter skelter. You can see the crisscross appearance of the helter skelter as they mention. And if he says hypertrophit myioytes then I can I have the answer again? Uh quick comments in the chat box. Yeah, myocardial disarray. I mean that's the word that we use in medicine. Myocardial disarray. Pathology people use the word heltokeal appearance. But yes guys I mean uh no no this is not a ninja. Ninja would be for dilated cardiammyopathy. This is hypertrophit myopath. Yeah boxar nuclear because of the fragmentation right because of the fragmentation. Those nuclear are crushed. Normally the nucleus is going to be round. It's crushed because of the hypertrophidytes and hypertrophytes are a feature of dilated cardiammyopathy. The pecularity in dilated cardiopathy is that the heart is dilated but the muscles are hypertrophic. Only some not all majority of ones are damaged. Majority are damaged. So the remaining myioytes will show a compensatory hypertrophy. So we can see a asymmetry with respect to the myioytes which are present and then they have given this last image in which you can see a very characteristic jumbo jumbo size atria present. Yes guys um yeah yeah yeah uh jumbo size atria would be present right super dilated super dilated uh atria present in this case yes guys uh the last slide please can I have the answer please what is the type okay I can get a banana there I am getting a lot of inputs uh guys there is fibrosis in the muscle of this patient come on come on you're not supposed to get this right this patient is having a normalsiz left ventricle if you compare with The cavity of the right ventricle. If you look at the cavity of the right and the cavity of the left, it looks equal. Equal. Now the cavity of the left and the right ventricle is equal size is equal. But atria are bigger than ventricle. Normally like it is the ventricles that are bigger than the atria. But in this case it's the atria that are bigger than the ventricles. And what you are also seeing in this particular case is a lot of I would say pink amyoid material deposited between the myioytes. So this is like a slide for restrictive cardiammyopathy. And one of the important causes for this is going to be amoidosis. That is why the pathologist will say pink amoid material deposited. Pink amoid material deposited. In fact, this is the rarest type of cardiammyopathy. And the most common cause for the rarest type of cardiammyopathy happens to be amoidosis. Uh the features are going to be standard with respect to congestive heart failure. And I'm also going to use this opportunity to mention regarding the ABCD of pulse. So I'll just write it on this particular slide. I mean A is for anacrotrotic pulse. That would be a feature that would be seen with respect to valvular aotic stenosis. Then is alphabet B is for bisparian pulse. The third one is collapsing. That is super easy. I mean collapsing pulse nobody makes a mistake. And then we get a twice beating pulse. When what when I say the word twice beating pulse both in systol and diastol that's called as a diorrotic pulse. Quick answers here. When it comes to anrotic pulse it's going to be valvular aotic stenosis. Bispharian is hypertrophic cardiammyopathy. Collapsing pulse is going to be valular aotic regurgitation and when it comes to dicrotic pulse then dicrotic pulse would be seen with respect to dilated cardiammyopathy. Yes, you're right in patients like beta blockers and dejoxin. Well, deoxin I'll say is absolutely contraindicated in these patients because the heart functioning is severely compromised. Now among all these cardiammyopathies we'll also quickly revise regarding taco to superubcardiopathy and the pneumonic you can use to remember taco to superubcardiamopathy would be uh tuned tu n e d and that is for taco to suba means a jar to trap the octopus. So the left ventricle of this patient would be bulging out like this. Uh this is mainly because of unexpected uh emotional trauma like death of a loved one. That is why we call this condition as broken heart syndrome as well. And there is a catacolamine surge that is happening in this patient. It is a catacolamin search that would be responsible for taco to superubcardiammyopathy. The diagnosis of this condition is usually made in the kathlab. The diagnosis of this condition will not be made in the routine emergency because ECG of this patient will be showing a ST segment elevation. The cardiac biomarkers in this condition will be super elevated. So we will think that this is a case of ST elevation MI. But when we send it to the Kath lab when they do a coronary angography in this patient, the coronary angography of this patient would be normal. So that's why I've written no obstruction of the coronary circulation. It's a differential diagnosis of ST segment ST segment elevation MI. We'll now cancel the PCI procedure. We'll not do a primary percutaneous coronary intervention in this patient. Rather, we will manage this patient conservatively. Quick comments in the chat box. How would you manage the cardiogenic shock of this patient? Yes, normal catlab findings. Quick answers for taco to sububca cardiammyopathy which is like a representation for a jar that is used to drop the uh octopus. Yes. Uh guys uh as far as ST elevation is concerned doctor for this condition uh it's not necessary postmenopausal woman. It can be anybody right. Uh takoto means intense emotional trauma contributing to damage to the heart. Okay. So yes we will not be using uh dobutamine in this patient. Traditionally we use like dobutamine or we use dopamine or we use uh norepinephrine. All of these are absolutely contraindicated for management of this condition. The cardiogenic shock in this condition will be treated by use of intraotic balloon pump IABP. Uh we we do not use uh inotropic drugs because they'll increase the catacolamine levels. Now by catakolamine excess is the reason for the pathogenesis of this condition. It is the catakolamines that are causing damage to the heart. So if I'm going to be like you know using drugs that are going to increase the catacolamine levels that's going to be counterproductive. So it's it's intriotic balloon pump and yes impella is another device that we can be using very good answer and then we'll be able to manage these patients effectively and then subsequently like we'll be able to uh you know in majority of cases recovery if the diagnosis made on time then the recovery of this patient would be done. So we are sorted for like talk the the type of cardiammyopathies. I mean in this particular slide I've tried to focus on various types of cardiammyopathies including the one that is asked in medicine and one that I discussed on the previous slide is athogenic right ventricle dysplasia which is a hot favorite of our examiners. Now I put up a question before you and uh this would help us solve the questions on berbers as well. Grahamsteel murmur there the two classical ones that they love to ask. One is Austin flight the second one is Grahamsteel murmur. So uh yes guys quick comments in the chat box with respect to grahamstale murmur will be seen in which of the following conditions? Absolutely correct. Grahamststeel murmur is a feature of pulmonary artery hypertension. When there's a pulmonary artery hypertension this can contribute to development of a mild pulmonic regurgitation and this mild pulmonic regurgitation would then be contributing to development of a early diastolic murmur. So that's a grahamstale murmur. In contrast u I'll be asking you for Austin flint also but don't hit the comment box for Austin Flint at the moment. My next question to you guys is what is the I mean the cutff for pulmonary artery hypertension pressure more than how much on catheterization would be a diagnostic of pulmonary artery hypertension like the normal mean pressure in the pulmonary artery uh yes I we'll discuss Austin also guys give me a second my question to you guys is and I would like everybody to hit the comment button simultaneously pressure more than how much is pulmonary artery a tension your answer would be given as more than 20 mm of mercury can you tell me What test is done to check for whether you should give calcium channel blockers to the patient or should you be giving bosentin to the patient? What test would be done? Anything more than 20 mm of mercury. I'm talking about mean pressure being more than 20 for diagnosis of pulmonary artery hypertension. What test would be done for identification of the fact that should you give calcium channel blockers? Yes, we'll be giving uh we'll be giving inhaled nitric oxide. That inhaled nitric oxide would be called as a vaso reactivity test. What I imply by the word vasor reactivity test is that we'll be using this test to we'll be making the patient use inhaled I I stands for ino stands for inhaled nitric oxide and on basis of this we can then decide what is the treatment to be given one can be calcium channel blocker second is going to be bossent or ambryent if they don't say anything in the question then your straightforward answer is ambrecent is the drug of choice for pulmonary artention otherwise like cool you can mention that as I mean first line drug to be introduced as calcium channel blockers in the patient as well yes vasor reactivity test inhaled nitric inhaled nitric oxide related MCQ I'll use a separate color to ask you this in which condition would you be checking for exhald nitric oxide in which medical condition would you be choosing exile nitric oxide for your diagnostics yes guys waiting for your answers in one was inhaled nitroxide second question is regarding exhald nitric oxide yes bronchiala we call it pheno fractional excelation of nitric oxide is useful for diagnosis of asthma so I had very good inputs here with respect to the two very simple test. So just take care of that question when he says inhaled versus exhaled nitric oxide. Now as far as ostan friend murmur is concerned again we'll be talking about you know the uh the type of murmur that would be seen in this case. Of friend murmur is always going to be seen in patients who are having severe variety of valvular aotic regurgitation. And once you have this severe aotic regurgitation there's like a large volume of blood coming back in the heart. And when you have that large volume of blood coming back in the heart, it would result in development of a mid diastolic murmur. Therefore, what you need to do is remember some hacks. So I'm going to tell you quick hacks to remember mid diastolic versus early early diastolic murmur. The pneumonic that we have discussed for metastasic murmur goes by the name of CAM where C would be standing for like caricums murmur. I hope everybody remembers that. Then it's going to be Austin Flynn murmur and then is going to be mitroenosis. That's anyway a hot favorite of our examiners. And the last one would be a flow murmur. So these are like simple pneumonics which can be used to make our life easier with respect to mid diastolic and early diastolic murmurss. The pneummonic for the right hand side is gap where G would be standing for Graham steel. That's the only one that he'll be asking you for the right hand side. Then is for iotic regurgitation of the mild variety and then is going to be the pulmonic regurgitation of the mild variety. So pretty straightforward questions present here. uh comments in the chat box again. Caricum's murmur is seen in which medical condition? It's a characteristic murmur, right? It's a murmur related to valvalitis. It tells you about the damage to the mital web reflect and this would be seen with respect to romatic fever. For ostinfen murmur, as we've discussed, it's a feature for severe variety of valvular iotic stenosis. mitro stenosis anyway like we'll talk about this subsequently also there has been a question on mitalenosis last time on FMG exam with respect to the intensity of the murmur and the duration of murmur I I'll describe those technical aspects of intensity and duration of murmur or mitroenosis and then flow murmur example can be like atrial septile defect where like the blood will go from LA to RA and then from the RA to the right ventricle and ground steel murmur is mainly because of pulmonary artery hypotension and this pulary artery hypotension would then result in mild pulmonic regurgitation those less blood would be coming. So that's why like there's a early diastolic murmur that would be happening and if they give you a diagrammatic representation the same uh then for early diastolic murmur the line diagram would be something like this S1 S2 and S1 and you'll be noticing that the intensity of the murmur will tend to progressively decrease. You can see a declining trend for early diastolic murmur whereas mid diastolic would be like much more longer with respect to the camneimmonic that I have mentioned. So since you have got this and romantic is again what they love to ask you. So let's do another question. Uh this would be two questions that have been asked in uh uh I think the second one the second one is the FMJ exam but let's handle the first one. Yes Dr. Lithia you're right that would be a seagull murmur known case of heart disease with recurrent sore throats presence with shortness of breath. On examination there's a hyperdynamic precardium with a water hammer pulse. There is like pistol shot sounds over the femoral arteries. I mean I know the comment box is just going crazy with that pistol shot sounds and femoral arteries. Uh that's going to be valular aotic regurgitation and there's a pansytoic murmmorina patient. So there are two two lesions given in this first and one is that of aotic regurgitation and the second one is that going to be of mital regurgitation. So it should be option number a romatic heart disease with aotic regurgitation and mital regurgitation is what is occurring in this patient. The most common valve involved in mital romatic heart disease is mital valve. The second most common word is aotic valve. So I mean this is like the reality of India that even today after so many years of independence we still have sore throats. We have patients suffering from um romatic heart disease. So we call it the disease of poverty. It's a heart disease of poor people. Uh quick comments in the chat box with respect to uh romatic heart disease. Which valve is not involved? Romatic heart disease valve which is usually not involved. There are only four heart valves. Now mital triaspotic bulmonic. So yes guys, which valve is unlikely to be involved? Mital is the most common one. Aotic is the second most common one. Which valve is unlikely to be involved? So usually that is not involved is the pulmonic valve but you can still be having pulmonary artery hypertension because of long-standing mital stenosis in this patient. So absolutely correct. Yes, I loved that. Triuspit regurgitation to anodox triricuspid valve is the one that is involved in it is mat mital valve involved iotic valve involved. trios sequence mat pulmonic val usually romatic heart disease involve so cool man let's do the next one a patient has been diagnosed with mitalenosis what will decide the severity of mitroenosis and uh I'll just do a line diagram here meanwhile I'll be waiting for you to hit the comment button in in mitalenosis what will happen is pressure in the left atria will be more because a quick diagram here representing the same the opening in this area this case is narrow right this is going to be a narrowed opening so there's going to be a higher pressure in the left atri of the patient and due to higher pressure there would be a loud opening snap that's the first thing that's going to happen in this patient loud opening snap then there's going to be a murmur that will peak in intensity and then is going to have a secondary spike that's called as a preystolic accentuation because after S1 there's going to be stol happening but if I'm going to modify this diagram by making this obstruction even more narrower more narrower it will cause an increase of pressure if the pressure will increase further the valve will open much more earlier as compared to normal and therefore what you can see in the line diagram is that the total length of the murmur is increasing. I mean just check it out man. Uh if you look at this diagrammatic representation the length of the murmur previously versus the length of the murmur now the length of the murmur has increased and uh therefore what you can also see in this line diagram is that the gap between the S2 and the opening snap has progressively become reduced. So I had very good inputs from this one. This is very classical teaching that is given in Hutchinson clinical methods and the same question has been asked multiple times. So what you get in this condition is a increase in the length of the murmur and a reduction in the S2 and the opening snap gap. It is the reduction in the S2 and the opening snap gap that would be seen in this case. That's because of the length of the murmur that would be increasing. So cool guys uh I think uh this was a very good input from you guys with respect to microenosis. we will have to treat these patients with percccutaneous mital balloon valvotomy. That would be an indication for severe variety of mitroenosis. I mean every time we have severe mitalinosis we go in for a percutaneous mital balloon valvotomy. But if it becomes calcified severe mitroenosis then we will not be in fact I can just add a quick slide to this uh uh yeah I think you have to watch RR for this like if you are even an FMG student man this is a question from the last time's FMJ exam only. I mean it's a screening exam but they're asking you how to evaluate the severity of mitalinosis. Okay. So a quick inputs here the quick inputs for you guys are like this uh like you know if a person is having a severe percutaneous mitro balloon severe mitalenosis and it becomes calcified also. Uh wait for my question guys wait for my visual cue. uh severe calcified mitalenosis. We do not do a perccutaneous mital balloon valvetomy because the balloon is going to uh cause the valve to break into pieces and those fragments will then go into the brain of the patient. We can have like emolic stroke kind of a presentation. So in this patient what we will do is deploy an artificial heart valve that is a prosthetic heart valve and when we plan for a prosthetic heart well there can be two possibilities. one you can talk about metallic and instead of metallic we can also talk about biological prosthetic valve but what I mean by biological prosthetic valve is that it can be from a pig's heart so I can use the word porine it can be coming from a cow's heart so I can use the word bovine or it can be coming from a catar also question for you guys is if a cataboric heart valve is being used in a patient what is the technical term for it oneliner question if it's going to be a cateoric heart valve that is used like I said porsine I've said bovine then I've said carabar so if it is a cataboric heart valve that is being used what's the technical term used for it okay yep yep if it is yeah the superior two are obviously going to be xenographing that is okay but he said what is if the cataboric heart valve then we are going to be using the word no it will not be called as a allograph guys I think uh uh some doctors immediately came up with the correct answer yesuh I think uh Dr. Fatima was the first one to come up with it that was homograph it would not be called as alograph alograph is where it's like a cousin brother or sister now when it is first relative so this is the question that was asked that if it is the biological heart well that is going to be used then like biological heart well mean cataric then it is a homograph that would be used otherwise we'll anyway be using a metallic heart well metallic heart well will need lifelong anti-coagulation so there will always be a need for OAC that is oral antiquagulation and usually the drug that would be required in this patient would be barferin and if he says what will be the target INR that needs to be achieved then the target INR that we need to achieve in this patient would be any value between something in the range of 2 to three so there are two questions I just wanted to bring to your attention one is the homograph question second is the target INR that I need to do in case a metallic heart valve is used for cases of mitroenosis so we are sorted for this question and MS happens to be an important topic uh that is usually asked and therefore I spoke about it and uh let's now talk about must know facts about JVP bit of the theory component is what I'm discussing after these questions and the first one is with respect to small signal sign you know this is always going to be like a rise of the JVP you know because this is a revision session we'll do some theory component also must know facts with respect to JVP small sign basically means a paradoxical rise because normally you would always be having is a fall of JBP but in this case it is reverse that is happening it's a paradoxical rise of the JBP that is happening the pneummonic for this is like u uh the pneumonic for this is going to be like uh cops right so the cops would mean that C would be standing for constructive pericarditis constructive pericarditis cops TP constructive pericarditis means that there is going to be a calcification present in the valve then alphabet R will be for restrictive cardiammyopathy R is RCM restrictive cardiammyopathy and then subsequently like u uh the next input would be for right ventricular failure so these are like three conditions where we'll be having to small sign RCM is a very good answer there so you can do CR or you can see these are like three situations where you would get a small sign and the MCQ will always say not seen in with respect to cardiac tempon very good right ventricle failure right he can be writing right ventricular failure by writing the word inferior wall my mio myioardial inffection he can be writing it as corpalmonil he can write the word acute corp pulmonal so it doesn't matter I mean anytime there's a right ventricle failure inferable MI corpmonil are usually the situations where because of the Right ventricle compliance being lesser. The Javp will be showing a rise instead of a fall because heart cannot accommodate the blood. Your in my heart does not have a failure. So our heart can accommodate the blood. Okay, cool. Large A waves would be seen in is again a question that has been asked repeatedly. Uh this would be due to obstructive lesions of the right side of the heart. So you can keep the comments going guys. Medical conditions that contribute to large awes. Very good. Uh okay. So I'm having good answers there also. then is pulmonic stenosis. These are like standard situations where we'll be getting is large a wave. Uh somebody commented mitalenosis also but then mitroenosis Dr. Tossi I would like to clarify is only long-standing. So if you get a question where tricuspit stenosis is also given and mitroenosis is also given. Don't select mitalosis. It is long-standing mitalenosis. Plain mitalenosis given this has has occurred in the exam. He gave TS also and MS also in the option and he said select the one where you have a large a present. So he'll not answer it as mitalinosis because mitroenosis only long-standing will cause it. So just a word of caution here I mean my job is to just keep on telling you what is the right thing and then yeah subsequently like even pulmonary artery hypertension would contribute to it. So causes the pulmonary artery hypotension like you can write down a connective tissue disorder like scleroderma. Comment in the chat box for what antibodies used for diagnosis of scleroderma guys. Then there are drugs which have been banned. These are like weight loss drugs like fenfluramines. They've been banned for weight loss. Yes. Uh okay. So scaroderma is like I think anti-entromeir antibody that would be helping up in diagnosis of this condition. Yeah. One is centromeir and the second is going to be topoisome antibody. Between the two the single best answer would be topo isomeiris antibody also called as anti-scl. So these are inputs for like yeah I had both inputs coming in centromeir as well as as well as topoisome. uh the correct answer is anticl because is going to be super easy. So most people are able to crack the question. So most of the time they'll be asking you regarding topo isomer antibody for sclerodma because there's a variant of this no crest syndrome that crest syndrome is the one where you would be having centromeir antibody C for crest C for centromeir antibody the answer would be given as poisome antibody. Yes uh Dr. Rhdraal is the correct one here. Okay cool. So don't answer centromeir guys. I repeat that again. That's only for crest syndrome and crest syndrome may not have pulmonary artery hypertension but diffuse involvement uh in sclerodma is the one which has pulmonary artery hypertension which can contribute to death. Then you'll talk about absent a keep the comments coming. Absent a waves would be seen if the heart is twitching. If the heart is twitching the answer for that is going to be atrial fibrillation. That's going to be one of the commonest arrhythmias in clinical practice. You see a wave is because of power and if the power is lost then the bad news is that you get absence of the A waves then is going to be canon a canon a waves would be seen with respect to AV dissociation. What I mean by AV dissociation is that the atria and ventricles are contracting simultaneously. Imagine atria and ventricles contracting together. So the power of the two will be added and that's going to cause like super large a waves. Uh I have put a video on this on the prep letter channel also you can check that out. We call it frog sign. Frog sign means big time pulsations in the neck in this patient is occurring. So a dissociation is what is going to be seen with tachiarythmias and bradhythmias. So if he says which brady would be causing it then a lot of people have made the correct answers there that would be complete hard block. The other name for that would be third degree heart block. So the theory part to be remembered is complete heart block. Third degree heart block stoke Adam saddam syndrome the difficulty that in medicine they use the uh different names for the same condition that causes error of judgment. So the Brady condition is one and the same thing. It is complete hard block third degree hard blockers toxin syndrome and if it says tacky then yes lot of comments were coming in for the tacky component that's going to be like uh uh ventricular tachicardia junctional tachicardia and can be seen even in PSVT also but then primary answers would be like VT and JT that is ventricular tachicardia and junctional tachicardia then we'll talk about absent x descent and for absent x descent you can see a valvular lesion here you can see blood leaking like this to the top across the triuspid well and connected to the right side of the heart would be ultimately the jugular vein and the jugular vein column should be falling downward. So you can see two vectors one is going down the other one is going up and both of these vectors if they are of equal equal strength they can cancel each other you can see one is going down other is going up so they'll cancel each other so therefore absent x descent because x is going to be related to atrial relaxation there are two vectors which are fighting with each other and therefore this is a very common question that is again asked absent x descent would be seen with respect to the answer would be given as strike speed regurgitation so again very good answers and I would just like to extend your knowledge space here by just drawing a line diagram representing it. I mean this is how the normal JVP waves would be coming. It would be a c this would be a cb then is the x and the y descent. And what's going to happen in my particular case is that uh there will be like this C happening then there is no X there is no X happening in this person and rather directly from here the whole system will lift up in a triphit regurgitation of the more severe variety and therefore I have created one more MCQ for you that would be called as CV wave or maybe written in the MCQ as a giant Vwave and second what you can also notice in this line diagram is where I put the star mark there it's like suddenly coming down like it looks like a roller coaster ride right if you go to any roller coaster ride it just takes you up and then suddenly you plummet downwards so where the star mark is put that is what is called as a steep y descend so ultimately triuspit regurgitation is answer for three questions yes lancc sign is a very good answer apparent on trypit regurgitation is answer to three MCQs it's going to be absent x if you can mentally visualize this diagram now the x is going to be absent then after see what will Vwave and then there's going to be a very very prominent Y descent happening. So you need to remember this information that's going to be absent X CV wave and then a steep Y descent that's going to be a feature with respect to triricuspit regurgitation. So one they ask you about triricuspit stenosis second they ask you about triricuspit regurgitation with respect to the findings in the JVP and now we come to the hot favorite of our uh question. Very good yast you came up with a correct one absent Y descent. Absent Y descent would be when the ventricular filling will not happen and you can see it could be blood it could be fluid outside the heart of this patient and if there's blood or fluid outside the heart it will crush the heart so filling is not going to happen there's going to be obstructive shock happening so absent white descent is like a question which I think uh even if you are sleepy even if you are deep asleep and somebody wakes you up and says when do you get an absent white descent you say okay don't bother me it is cardiac tempon and we go back to sleep again uh two standard questions that I'm going to write here is steep X steep Y and then it's going to say the word steep X and absent Y. It is just technical jargon by the examiner. Don't cut the noise, right? That's the slogan that we say. So steep X is just a distraction. It's a distraction. You just need to focus on the word absent Y and absent Y is CT that is cardiac ampard. But if you get a combination of the two that would be constructive pericarditis. So two very straightforward datas that I currently mentioned before you and now is a question that is coming up. If a person is having hemopericardium like this guys got a stab injury to the chest because of this penetrating injury to the chest there is a hemopericardium then uh the person will develop obstructive shock. He will develop pulsus paradoxis the pulse will tend to disappear in the phase of inspiration. Uh how would you manage this patient? options are you have to answer it as either thoracictomy or you have to answer it as pericardioentesis. A quick answer that I'm waiting for you guys. Uh if you are saying thoracicis you can just type the word t uh uh th toottomy. Okay I give three option toocentsis uh thoraccotomy and then pericardioentesis. Yes. Okay. Okay. So I am getting lot of inputs there with respect to pericardioentesis versus thoracictomy and then I made it uh I made one another option as thoracicis. I think I have highlighted this earlier guys if it is going to be blood due to a stab injury then even if you do a pericardioentis or blood because there could be a laceration of the cardiac muscle because there could be a hole in the heart there could be laceration in the muscle. So even if you remove that blood more blood will come so it's not going to serve the purpose. So don't answer it as uh emergency pericardioentesis in this patient. Do not answer ecardraphphic guarded pericardioentis. Your answer would be given as thoracictomy. We need to fix the bleeding. We need to fix the damage to the heart. So the technical word that we'll be answering is emergency resuscitative thoracictomy. I emphasized this point multiple times earlier. We are doing a quick revision today that for suppose I was saying to you lung cancer patient is having peric cardioent lung cancer patient is having tamponad or if a tubercular pericardis patient is having cardiac tamponad what will you do then it is understandable that we can be doing pericardioentis in a patient. So for medicine causes but if he says medicine causes like one of the cancer that can metastize to the heart is old cell cancer. So if he gives you a scenario of a malignant paricardial eusion or if it is tuberculosis so he says infective ideology responsible for those hardcore general medicine causes where there's going to be tubacular pericarditis followed by pericardial eusion followed by development of cardiac temper because more fluid will accumulate around the heart. So if it's going to be old cell cancer and tubacular pericarditis in those circumstances guys what you are going to do is pericardioentis that would be done echo cardioraphic guided and from where would you insert the needle? Yes guys comments in the chat box where would you insert the needle in paricardioentis options are second intercostal space fifth intercostal space 7th intercostal space. Yes guys we are doing a echoc cardioraphic paricardioentis in a case of tubacular pericarditis who went into tamponard needle would be put in through second space fifth space seventh space or would you be using zernal approach okay fine I think everybody got it right zonal approach guys don't answer fifth space that is for like you know that tension he thorax management that we'll be discussing in the later part of the day in the session too so it is always a zonal approach now I mean if If I want to approach the heart, I don't want to go by the lungs. If I want to approach the heart, I I don't want to go through the lungs. As simple as that. So that's why it is zistnal approach that would be done. It is sub subzoid and we'll aim for the left shoulder of the patient. It would be guided procedure. Then we'll put in a pigtail catheter and through that pigtail catheter because if I put in a needle, it can touch the heart, it can damage the heart also. So we we'll just go poke the paricardium. Then we put a ptail catheter and through that we can remove the pericardial fluid, send it to laboratory estimation. we can do CBN also so that we can identify the ethology per se. So that is when we are sorted with respect to like uh the causes that could be asked and uh let's talk about another question at the moment. Uh okay constructive pericarditis finding uh uh doc it's coming up that JBP finding constructive pericarditis is coming up once again the steep X and the steep Y but since you asked it okay I'll just pause for a while while these guys are figuring out the answer to this question is that in constructive pericarditis doctor what happens is because there's a calcification outside the heart imagine it to be like a eggshell so because there's like a thick zone of calcification out of the heart the filling of the heart in the late part of the diastol is compromised so the heart will compensate by increasing the filling in the early phase. So what you get in patients of cardiac tampon constructive pericarditis is that the early diastolic filling is exaggerated to compensate for the decreased filling in the later part of the diastol because later there is a calcification outside the heart. So that rapid ventricular filling that is exaggerated rapid ventricular filling that is exaggerated is responsible for the finding of steep y descent in this patient. I'll do more justice for this as we move on in the discussion but at the moment since the question came up I thought I should just speak about it. Uh that was like a impromptu answer that I cannot stop myself from saying considering that these are genuine queries and very academically oriented queries. Okay. Uh what is the most specific ECG finding that is seen in patients of pericarditis then ST segment guys is seen ST segment changes are seen in so many conditions. Now ST segment changes are found in so many conditions. Uh therefore it is not an ST elevation with concavity that is to be answered like this is what happens in this condition. I just draw it before you so that we can discuss it subsequently. What you are seeing is a slight twist with respect to the baseline. What you're noticing is a slight twist with respect to the baseline. What you are seeing is okay let me just zoom it in. You can see a normal ECG that I've drawn and then subsequently you can see this ST elevation with concavity that is happening. But along with this you are also noticing this characteristic finding that I'm showing that is the peer segment of the patient is going down. Right? So the most specific ECG finding that you get in pericarditis specific one is sensitive. Sensitive is obviously correct. If I say what is the sensitive ECG finding for pericarditis acute paricarditis then never an issue then answer will be option number A. But specificity is something that is like you know see exclusively for this condition that would be like a PR or segment depression. So the answer in this particular question would be given as option number C. Uh that is going to be like a PR or segment depression guys that party sign and all those things are for myocardial infection. No, it is concavity. I agree to whatever you guys are saying. You see option number A. Boys and girls, listen to this carefully. Acute paricarditis is inflammation of the ventricles in the atria. We get an ST segment elevation with a concavity and we simultaneously get is a PR segment depression that I have highlighted in this particular uh sketch. So yes, one of the early findings that we see in pericarditis is ST segment elevation with concavity. But if he changes the question to that of specificity, then it is going to be answered as sphere segment depression. party sign we'll talk about in the subsequent part of the ECG. So acute pericarditis the most common cause for this is anyway idiopathic but one of the ECG findings a very characteristic one that is asked for this would be though with COVID also know we were having pericarditis people were having chest pain but then the differentiation can be made and usually like in pericarditis the chest pain will radiate to the left shoulder the the nerve that carries the pain to the left shoulder is usually the frenic nerve okay so uh I think uh we are right with respect to no not B but it would be C yeah we can have viral coxsaki B Coxaki parvo viruses those are other viruses which can contribute to development of pericarditis. Yes, viral can be there. Exactly. COVID, Coxaki, parvo virus. Those are like the viruses which are responsible. The answer to this question is option number C. Doctor, it's a PR segment depression for the most specific finding with respect to acute pericarditis. It's C as an answer for the specific finding and uh like the common finding that we get is anyway the ST segment elevation with the concavity. The correct answer I'll put remove the tick mark from here so that there is no confusion. The sensitive part is obviously the first one but the specific part is a PR segment depression. uh no in this case sore throat may or may not be present so we can't predict it then uh uh next up is pericardial eusion there can be two reasons behind it the common ones in India is either going to be TB or if it's not going to be TB then it's going to be yes yes Shoubam Gallot you you made it very correct uh the chest pain going to the back doc that is for iotic dissection now if it's chest pin going to the back then it's going to be iotic dissection every time you read since you put that up I just want to highlight every Every time you read a question of a hypertensive patient and the question says that the chest pain is showing radiation to the back especially if he sparks spot radiation to the intercapular area. Whatever else he may say subsequently does not matter. This is more than sufficient to crack the question of the tear in the aorta that is going to be iotic dissection. So uh in this case uh like what I was describing was the pain relating to the left shoulder but it is aotic dissection that would be answered for pain in the intercapular area and as far as the investigation choice for iotic dissection is concerned since I spoken about it let me just complete it here only for the investigation choice for iotic dissection the answer will depend upon the blood pressure values like if the blood pressure is crushing and it is very very low then I would like to do a bedside eco cardioraphy or we can do a transissopagel eco cardioraphy but uh if the BP of the patient is normal to low but is at least not on a crashing state then we can do is a CT angography. CT can be done again very fast and in a CT angography what we can check out is the tennis ball appearance and then uh subsequently like type A and type B iotic dissection type A will always need surgery type B we can go for medical treatment with levital and subsequently a surgery in the patient can be planned. So uh I think since the question mentioned about somebody asked about radiation in the back so I I I thought it imperative to mention about it and coming back to the uh agenda that we are having at the moment like tubercular pericarditis uh there's going to be TB then there's going to be malignancy it can be breast cancer it can be malignant melanoma that can be used uh esol Dr. like you know yeah we can be using esmol but then because of the extreme vaso constriction know that alpha part also has to be neutralized so between esphol and lealol I think a better answer would be given as leitol for a h because hypertension is the trigger now and there's extreme amount of vaso constriction happening so alpha will not be neutralized by giving asmol so you're right like asol can be used if the b is dramatically low but then overall to treat the hypertension state of this patient it would be levital as a better answer Okay, as far as pericardial eusion is concerned, there would be two ECG findings which are very very characteristic. One is low voltage ECG. Can I have the diagnosis diagnostic criteria low voltage ECG? Quick comments in the chat box guys. What is uh the definition low voltage ECG? Your answer would be that the height of the Rwave and the depth of the S-wave would be less than 5 mm is the definition of low voltage ECG. That would be one of the characteristic features that would be seen low voltage ECG. another finding. Okay. Sure. Sure. Sure. Sure. Offline B. Okay. And then is going to be another ECG finding that will come because the heart is dancing in a bag of fluid. You see it's a dynamic motion to and fro movement of the heart. Heart is dancing in a bag of fluid you know slloshing like waves in a scene. waves are thin. So because of the waves created the voltage recorded by the electro electrodes will keep on fluctuating and therefore this finding would be referred to as electrical alternance. Electrical alternance is like a very characteristic finding that's again seen with respect to pericardial eusion and when it comes to the X-ray findings in this patient the cardiothoracic ratio will be increased. Somebody mentioned very rightly water bottle heart and if somebody's money-minded then he will not say water bottle. If if you are like you know survivor with respect to you know sports then you say water is the most precious thing. If somebody is like not exercising and somebody's money minded then money bag. So water bottle and money bag appearance are like u two very characteristic words. At this junction, I just want to emphasize to everybody who's participating in this discussion guys, every question you solve is going to take you closer to the final victory and every hour's productivity will keep on changing because I continuously keep on getting these queries like you know focus attention span decrease to persist that is all that is required just sit there right don't go out you know we go out and chill no man nothing doing nothing Because if you go out, you're going to watch Instagram, it's going to uh take out your energy. It's going to decrease your attention span. So just persist. That's my message at the moment. Uh you will be able to uh remember things guys. Uh it comes uh gradually. Normal cardiothoracic ratio will be 0.5. Heart occupies 50% of the space in the chest in you and me. Heart occupies 60% of the chest with respect to children. The normal values of cardiothoracic ratio with respect to adult and child are 0.5 and 0.6 in this condition because there's going to be water outside the heart in this condition because as you can see there is like water outside the heart. Therefore the appearance is looking very peculiar. That's why we call it a money bag or a water bottle heart at the moment. And uh like for this particular condition we have to be proactive and do the investigational choice. If he says investigational choices then the answer is none of them. And the answer is eco cardioraphy. Eco cardioraphy can help you identify a pericardial effusion from a low pressure cardiac tamponard to a cardiac tampon because ultimately the complication of this pericardial eusion would be specifically development of cardiac tamponard where usually they'll ask you regarding the following aspects. Uh as far as inet is concerned guys this is it came up in the chat. My only thing is that uh it's like scuba diving they just go more deeper into it like I I mentioned a technical term right that has been asked in inert exam that is called as low pressure cardiac component I mean when I write this or when I speak about it the query of most people is boss cardiac is characterized by high pressure on the heart every time you say like this now how come there is low pressure so here it is only atrial collapse if it's going to be low pressure cardiac tempon guys then only atrial collapse will be occurring If only atal collapse will occur, there would only be a 30% decrease in the filling. If there's a 30% decrease in the filling, the BP will decrease by only 30%. So in this condition, you will not be having a unrecordable blood pressure. You will only have hypotension. So therefore, because you will have hypotension and not a unrecordable BP pulsus paradoxus will not be seen in patients who are having low pressure cardiac ampard. I'm starting this topic of cardiac tempon by saying a very peculiar thing that if he says the word low pressure cardiac temponutard then we don't have pulsus sparadoxis because traditional data for the topic of cardiac temperance is presence of pulsus paradoxis low pressure cardiac temponut simply means that there is going to be less there there's only atrial collapse happening and subsequently if I say the word subsequently if I say the word cardiac amponard that means it's high pressure and that's when the pulsus paradoxus finding would be Quick comments in the chat box. Impulsus paradoxes the inspiratory fall in systolic blood pressure should be more than how much? I'm writing SVP I. I means inspiratory fall or systolic blood pressure. When do we say pulses paradoxes? For checking pulsus paradoxes, it is normal breathing that is recommended. This was again a question that was asked in any set exam that when you are checking for pulsus paradoxes, what will you ask the patient? Deep inspiration, deep expiration, mid inspiration or simple normal breathing. We will not ask the patient to do a deep breathing because if he will do a deep breathing the inspiratory blood pressure will fall substantially and it can even cause synop in a person. So it is like normal breathing that would be required. Normal fall is like at least 10 mm and in this patient you will say more than 10 mm. That's a good answer just to discriminate and they've added two points extra. So a better answer will be to say it a little more than normal. In you and me the inspiratory blood pressure falls by less than 10 mm and in this patient it would be like more than 10. So the more specific answer will be 12 mm and it is normal breathing that is required in cardiac amponent the person's BP will become unrecordable. So he will use the technical word that is obstructive shock and then he will ask you regarding the JVP findings. Please comment in the chat box to small sign will be seen or will not be seen. You have to seen seen not seen please comment in the chat box to small sign waiting for your answers. Yes we'll be having is a steep X and we'll be having a absent Y. You have to tell me who small sign will be seen or will not be seen. Absolutely it will not be seen because there is absent Y. Now absent Y means that there is like no filling occurring in the heart of this patient. So as such a small sign is a feature that is seen in patients who are having constructive pericarditis. It is seen in restrictive cardiammyopathy. It is seen in right ventricle failure but it is not seen in cardiac. I had very good inputs here from a lot of young Gans. And therefore how will he write this? He will write like this in the MCQ elevated JVP with this he will write the word nonpulsatile elevated JVP guys in your entire career in cardiology in your entire medical domain only time you read the word non-pulsatile elevated JVP is for cardiac component non-pulsatile elevated JVP now for those of you who have listened to me I would like one more comment here tell me one more medical condition where lung cancer will be a cause and there is a non-pulsatile elevated JVP a miscellaneous Question here non-pulsatile elevated JVP is seen in opt cardiac temponent is not in options non-pulsatile elevated JVP is given in the question but there is like you know no mention with respect to any any cardiac component absolutely right the answer would be given as superior vennea thrombosis and this superior vennea thrombosis can be occurring with respect to lung cancer center lung cancers like small cell cancer squel cancer can cause a mass effect they Impress on the superior vennea they can cause superior vennea syndrome. Yes guys, the next answer would be tension heumorax also but not plain pneumthorax right it is tension heumthorax where a same kind of a situation can be seen in a patient absolutely right very good uh another question coming up since I had very good answers so I can't stop myself from answering asking you guys what is the most common cause of tension he though respiratory system is scheduled for the second session for today but yes we we are going to put up a question what is the most common cause of tension he uh Pancose tumor will cause neurological manifestations like uh uh you know wasting of the intrinsing muscles of the hand and then panc tumor can contribute to pain radicular pain occurring in the arm horner syndrome manifestations this is a central lung cancer uh which would be a better answer superior thrombosis okay trauma trauma trauma trauma so I just want to add to the word don't answer it as plain trauma that will be given in the options your answer will be given as barot trauma the most common cause of tension heis is not penetrating trauma. I I want to emphasize this guys. The most common cause of tension he thorax is not trauma. It is bar trauma. It is ventilator. No no it's not blunt trauma man. That's what I'm saying. In the options blunt trauma will also be given. In the options penetrating trauma will also be given. All three will be given. Penetrating blunt trauma will also be given. Bar trauma will also be given. But if he says what is the most common cause of tension, it is ventilator patient denergy. There is a asynchrony between the ventilator effort and the patient's effort. Maybe because adequate sedation was not happening. So the leading cause for development attention heaxis bar trauma. Guys you you have to remember this information. Uh I I had to say this because I could not wait for the second session to come up here. Two must know informations for this time. at this time is if he says cardiac temponard with hemopericardium uh if it's penetrating trauma to the chest have injury to the chest that there's no rule of paricardioentis it's a thoracictomy and if he says tension he the number one cause is going to be mechanical ventilation no no barat trauma no drum not barat trauma is not like a blast bomb blast or like underwater explosion no no no I'm talking about ventilator patient as you see we were putting patients of co on ventilator and then because the lung pressures were not Because there were limited number of doctors and there were so many patients. So when you have to ventilate so many patients, there can be errors, right? And the every patient's lung compliance is going to be different. So if the settings are not appropriate, if the settings are not appropriate and the peak inspiratory pressure is higher, then it can contribute to development of this lung to burst and that is like tension. So yes yes uh spontaneous may vital will not be affected but it is tension the vitals will be affected. The next point to be remembered is that ECG showing a low voltage ECG uh low voltage ECG or electrical alternance is a common thing that is seen. I'm writing it with a separate color because this is a common thing between paricardial eusion as well as patient who are developing cardiac tempon. So don't base your answer on the basis of cardiac temper. Don't base your answer of pericardial eusion and cardiac temperate on the basis of low voltage GCG. Check out the data in blue. That would be useful. And the chest X-ray this patient will also be showing a money bag appearance. The only difference is that the money bag will be like you know much more bigger in size. Uh don't use ECG and chest X-ray as a discriminating factor. If ever in doubt in the MCQ with respect to pericardial eusion and temponard straight away check the blood pressure values. Blood pressure values will never ever crash in pericardial eusion but blood pressure values will always be crashing. Blood pressure values will always be crashing with respect to cardiac tempard. This is like an important topic. So I spoke about it and now we speak about constructive pericarditis. In constructive pericarditis also because there is less blood coming in the heart less will be going out. So there can be an inspiratory fall of systolic blood pressure more than 12 mm of mercury. So pulsus paradoxis can be seen in this condition. Uh JVP in this patient however will be showing a very characteristic finding of small sign. So that presence of a small sign will do the trick for the question because pulsus paradoxes is going to be a common thing between both tamper and MCQ as well as constructive pericarditis. Even in this condition there would be a low voltage ECG. Yes, I'll come to pericardial shutter in a while that is low voltage ECG is a common thing. Once again cardiac catheterization in this case will be showing that square root wave sign. Now most of the time you are going to be in a position to answer the question of constructive pericarditis on the basis of the information that I mentioned but otherwise suppose uh you know this is not working out then what are the tricks that would help you solve this question are two two things first is he may write the word paricardial shutter like what happened in last time's nepg 2024 in August was that he did not use the word paricardial shutter he just used the word loud dowstallic sound so whether if he is comfortable if he writes the word paricardial ial shudder. He writes the word paricardial shock. Cool man. I mean I am sorted. I am sorted. But if paricardial shutter and shock is not given then it would be a loud diastolic sound that would be given in this patient. And along with this along with this for constructive pericarditis what we would also get up in this patient would be what somebody mentioned for the JVP that is a steep X and then would be a steep Y descent for this case. Whereas in cardiac temper it was an absent Y descent. So these are the discriminating features that would be present otherwise paricardial shutter or paricardial shock would do the trick for you. Uh another finding in the x-ray of this patient would be presence of calcification. So cardiothoracic ratio will be increased in paricardial eusion. It will be increased in tamponard but will be normal because now there is no fluid now and most of the time uh history of taking would be given if he himself mentions the fact that has been taken by the patient for like 6 months to one year. Now in the revised guidelines of natural tuberculosis uh elimination program the for extra pulmonary TV the 880 is to be given for one year in contrast to the previous time. So if he himself mentions patient has taken at for one year and now is coming with complaints of pedal edema. Why pedal edema? Because there is going to be compliance of the right side of the heart being lesser so there would be swelling in the feed. There would be subsequently left ventricle compliance being lesser. So there can be breathing difficulty. So patient has already taken it for one year. There is a pedal edema. there's a breathing trouble and then it's going to be the findings which are given in this case then these are the findings that would be given in a patient including the findings of steep exa uh steep y descent the reason for that steep y descent is that in this condition and this somebody asked earlier also so I'll just put it here the reason for this patients having a steep y descent is a exaggerated rapid ventricular filling because the late phase of ventricular filling will be compromised because of the calcification of the heart imagine this patient's heart like a eggshell and This is the only only question in the exam where they'll give you a CT test. In fact, in cardiology, CT test will be given only two times. Let me just write it down. In a cardiology MCQ if they're giving you a CT chest either it's going to be a question of chaotic dissection where you'll be able to see that classical tennis ball sign and in case like you know you are not having I mean you you not having iotic dissection in the options uh then another scenario where like a CT chest is given for the topic of interest that is constructive pericarditis normally to we don't do a CT chest for a person having a cardiac issue we'll be doing a cardiac MR right if I have the facility then it is a cardiac MRI that would be doing. So in this particular case it's like iotic dissection in constrictive pericarditis vectity chest would always be given in a question like you can see superiorly a lot of calcification outside the heart of this patient you can see like uh this is a squ what I'm trying to say is constructive paricarditis is going to be squa related to constructive pericarditis and as far as the treatment of this condition is concerned what we going to be doing is a paricardial stripping procedure what we do in this case is paricardial stripping that would help in managing our patients effectively absolutely right absolutely Right. So uh uh no no doctor not the most common cause of constructive pericarditis is not idiopathic it is tubercular it is acute pericarditis which is idiopathic in origin and it is constructive paricarditis which is a squa for tubercular paricarditis where there would be a thick zone of calcification outside the heart of this patient and the reason for steep why I explained once again is exaggerated heart is trying to compensate for the late part of the filling being affected right if you're thirsty right and you know you won't get water earlier. So you try to drink whatever you are having earlier. Similarly, heart is because he knows later. So he's trying to grab all the information earlier or getting all the all the blood inside much more earlier. That's the exaggerated rapid ventricular filling that I have currently explained to you. So cool guys, we are like sorted for the disease of the paricardium and now we are having a question for you guys. Uh you are intern intensive care unit. Patient is having PVT. So comment in the chat box for the full form of PVT and he says uh it's an open surgery doc. It is CTBS right it's not like a routine procedure that's why CTBS is a a branch where like we we say those cardiac surgeons are god no nowadays people don't take CTBS branch because they think that it is low paying job I understand like salaries of doctors are lesser but then CTBS is like god only now okay yes the full form of this would be a per uh this would be a pulseless ventricle tachicardia absolutely right pvt basically stands for the word pulseless ventricular tachicardia And now he says like what are you going to do in this case? So uh uh let me just wait for a few more comments. Yes guys uh hit the comment button pulseless ventricular tachicardia in the casualty. What what are you going to do? I'll not like do check the pulse of the patient is already in intensive care unit. If the ECG itself is showing a VT with that broad QRS complex and a Josephson sign then I'll not waste my time checking pulse in this patient. Absolutely. Yes. So I think most guys are getting it correct. Uh it's only fight between B versus C that is going on and the correct answer will be that we'll not go for scene safety. Scene safety is for basic life support. Like suppose patient is on the road and somebody has collapsed then we go for scene safety but at the moment it is not a scene safety it is straight away start CPR in this patient. So answer for this question would be option number B like he would anyway be unresponsive. Patient has become pulseless. So the correct answer for the current question on the agenda would be answered as like start CPR and subsequently a defibrillation needs to be done done in the patient only if the question yes that's the main point the patient is in the intensive care unit in a intensive care unit like checking scene safety doesn't matter no or checking responsiveness like the patient if if the if the ECG is showing a VT and you can see on the multipar display monitor that the BP of the patient is crashing that's when we write the word PVT the BP is unrecordable that's when we'll have to straight away go for defibrillation in this patient However, uh if if he's going to be like uh uh if he's going to be like a patient who has collapsed on the road, then it is obviously, you know, verify scene safety and check for responsiveness, that's like the peripheral situation that would be coming. So uh just remember SRS they they'll ask you to uh arrange them in the correct order like if he's going to be asking about basic life support if he gives you a scenario that you are on the road you went for a morning walk and somebody has collapsed you are at the airport boarding gate and somebody has collapsed in front of you and they call you up that is when you will check for scene safety like he could have fallen near electrical cables he could have got electrocuted he could be fallen near an escalator and he could have injuries to his physical injuries to his body. So there it is verify scene safety. Then you tap the patient on the shoulder. Sir, can you hear me? You can touch his hand. Sir, squeeze my hand if you can feel me. And then shout for help. By shout for help, I don't mean I'm screaming my lungs out. I need more than one hands. And then what will you do? You will activate the emergency response. What I mean by activating emergency responses that you will be asking somebody who's come to assist you to call like 108 or whatever is the 102 whatever is the ambulance number and uh the because ultimately you need to transfer the patient to the nearest hospital and then you will ask uh the person who has come for assistance to procure AED procure AED that is like uh automated external defibrillator that's the main treatment that would be done in this case so just get these steps That's right. SRS, AR and AD would help in management of this patient. Uh uh Drestler. Okay, we'll discuss in MI. Right. So just just get the steps right. Procure automated external defibrillator for this patient. Uh if you are supposed to evaluate this patient, would you first check for pulse or would you check for like you ask the person to go and get the AD machine? Now what will you do yourself? Will you first check the pulse? Will you first check the pulse or would you be first check checking for breathing? Okay. Okay sham that's a good question difference between cardio version and defibrillation uh I have explained that in a routine video but I'll do it like once I'm done first exactly we'll first check for breathing just follow the steps guys it is look for no breathing and subsequently like check for pulse and how a doctor will spend how many seconds in evaluating it is 10 seconds and if both of them are absent if there is no breathing if there is no there is no carroted pulsations present in the patient that is when you would go ahead with institution of CPR for management of this patient that would be in a ratio 30 is to two and once cycle of CPRS for 2 minutes. So these are like simple steps in basic life support that you would like that you would that you would have to remember for the patient. Also I would like to say that if you are doing a intubation then the number of breaths how many breaths to be given once you've intubated though on peripheral scene it's not possible to intubate but like suppose the patient was shifted to the hospital or the ambulance came and in the ambulance the facility for intubation was present then like how many breaths would be given per minute to this patient or like one breath every how many seconds one is the doctor will use 10 seconds to simultaneously evaluate the carrot pulsation and the breathing effort it would be one breath every 6 seconds. So the respiratory rate that we want to achieve is something in the range of 8 to 10 per minute. This is after advanced airway that is at least advanced airway that is one breath every 6 seconds is what we want to achieve. That would be 10 breaths that are need needed to be achieved in this patient. And by the time the AD will come and then we'll be putting the paddles on the chest of the patient. So uh please comment in the chat box while I make this line diagram before you that in a person who is collapsed and you're putting the paddles of the AED in which intercostal space would you be putting the paddle uh on the right hand side? This is like the left side of the patient. This is the right side of the patient. So the pads p a pad of the AED will be put in which intercostal space on the right hand side. The pad would be put on the second intercostal space. So one pad is put on the second intercostal space. It would be infraicularly. But your technical answer would be that it is manubrial angle that is second intercostal space. That's where like the p a because a paddles or pads paddles are for defibrillator and pads are for the a machine. So one pad would be put in the second intercostal space. Can you tell me the position of the pad for the left? Yes. on the left hand side it would be the fifth to the sixth intercostal space. Your answer would be it is between the fifth and the sixth intercostal space in the mid ailary line. The middle of the paddle the left paddle would be put like you know on on this side that is on the uh on the mid axillary line of the patient. So two paddles have to be put here and both of them would be connected by wires to the automated external defibrillator. So what you can see here is just a crude representation that the AED will be deployed and the paddles are to be put in the positions that I mentioned before you. The computer will do a rhythm check and then you just have to press on a button. It will deliver a DC shock that would be of intensity 200 that would always be 200 Jew by phasing 200 J by Pasicip right you just remove the sticker from the back put it on the pad. I'll just show it to you. You know, paddle is this one ma'am. This is paddle. Paddle to you'll require that insulation also. Right? So if it is a defibrillator, if it is a defibrillator, the one that we use in the hospital, no, where you have to hold it. That is called as a paddle. That is P A D paddle. Hold it in your hand and then you give a decision in the hospital premises. That is with respect to a defibrillator. But with respect to AED that is automated external defibrillator. What you're seeing here is the pads p a ds the pads that are being used right so it is like pads positions are what I have shown here at the moment and then obviously this is an automated external defibrillator that would be helping us handle our patient now the question uh paddle walla because that is in the movies they show for paddles because in the hospital premises so it is like a paddle wall only now only in the outside scenario is a a machine that would be used yeah the positions and everything would be same uh Yeah, nowadays we don't use monophysic. They're all programmed to use 200 by 360. Okay, G fine. So before we go to the next question, somebody asked regarding what is the difference between defibrillation and cardio version and that is what I'm going to explain to you. You see the computer of the DC shock is taught to pick up the peak of the Rwave. If the Rwave will come, the computer will fire the DC shock. So if the computer is trying to read the peak of the Rwave, if the computer is trying to read the peak of the Rwave, that is when we use the word cardio version or a better way to remember this would be the word synchronized DC shock. What I mean by sync mode is that the computer will try to sync with the peak of the Rwave. But now check out this rhythm. Patient is having ventricular fibrillation. You can see twitching in the heart. If the twitching is happening then the computer will get confused. We taught the microp processor of the computer to pick up the peak of the R and now there is no RV. So the computer is bound to get confused. So in those circumstances where the peak of the Rwave cannot be picked up that is where we will be shifting it to a non-synchronized we will shift it to a non-sync mode. I mean there's a toggle switch with which you can select a sync or non-sync mode and it's a non-sync mode that would be delivered which is called as defibrillation. So if I put it in Hindi, I'll say that in both Hindi and English, defibrillation may computer will not search for the Rwave. If you press on the non-sync mode, computer will not search for the Rway straight away firing. But if it is going to be you press on the sync mode, the computer will wait for the Rwave to appear. The decision in the advanced card life support is made by the doctor with respect to whether or not should you be using a sync or a non-sync mode. The minimum that I expect you to remember at this moment is Yeah. Yes. Yes. Yeah. in Casino Royale. That's a very good example. They showed a AED. I mean, that was very funny, but then it's okay. I mean, the guy is giving himself a DC shock. That's that's crazy. Okay. Uh that's a good observation. Uh Human Defibrillation. I I think you are a fan of action movies like any guys would be. Okay. So, non-synchronous DCO uh DC mode is defibrillation. And there are only two MCQs where you will be answering it as ventricular fibrillation. One is going to be ventricular tachicardia. Second is ventricular fibrillation. English defibrillation is used for ventricular fibrillation and then is ventricle tachicardia for all other tachyas. Uh in all other tachyas it's going to be synchronized DC shock that would be used. Uh Anjuman just comment did they did they use car batteries in that casino royal? I remember that scene where I think he was trying to hook it up with the car batteries or something like that you know. So that is funny if they used car batteries to give a DC shot to an individual. Okay. So cool guys, basic life support is a good answer. Let's move on to the next one for today. Uh the patient has had a ROC return of spontaneous circulation and in those circumstances where there is a ROC happening he says which of the following is a negative sense question. Which of the following is not correct about management of a postCPR returner? Like you you in the intensive care unit the guy had a PBT. You ensure that the circulation comes back. He's gone back to normal sinus rhythm. Yeah. Yeah. Yeah. Yeah. That is also funny. I saw that one Mr. Bean also using that was really funny. Okay. Okay. Very good. Very good. Uh you see uh when we have post CPR returners spontaneous circulation we want a mean artiller pressure more than 65. Understandable. Oxygen saturation is 92 to 98%. That's what we want. And usually the cause of this can be MI. So we should also be going in for like a perccutaneous coronary intervention. But there's a concept called as theopetic hypothermia. We will deliberately decrease the temperature of the body so that the metabolism of the heart becomes lesser and if the metabolism will become lesser energy requirement will become lesser and if the energy requirement will become lesser the patient will be able to survive for a longer duration. You see here the problem in this question is it is written patient is not cooperative. You see the point is targeted temperature management. I mean the answer to this question anyway is option number A because it's a recall anyway you guys would have been able to solve it but what I want to bring to your message is that it is done in those patients who are going to be like you know totally unconscious so this is yes yes yes yes it is done in comes patients absolutely absolutely so not in a cooperative patient I mean if the guy is having loss of cereal perfusion there would be brain damage right and because of the brain damage um the guy would not be in a position to cooperate So good pickup. Good pickup Leah. Good pickup Dr. Mahi. In this particular situation, the answer for this question is option number A. And this was a last time's in set question. So what I've done at the moment is like I made it uh uh like I discussed a neat PG question. I discussed an FMG exam question prior to that easy one. So what I'm trying to do is a mixed pack so that you know you you get like a idea of all of these and uh just a suggestion uh in case you have time at your disposal. I think there is time at disposal. So give a give a mock test. Make a habit of like you know doing these mock tests on a regular basis. That will ace up your preparation level. Uh it's it's uh you see the objective of doing a mock test is to you know hyper tune our senses because we can't read everything but we have to analyze. Sometimes you would know only three options out of four. Sometimes you'll know two options out of four. Sometimes you know only one out of four. But then should you answer that question where I know one out of four where I know two out of four or not that is what nobody can teach right I can teach you theory but which question to leave and which question to uh you know attempt comes with self-practice sometimes when you guess a question it will go wrong sometimes you'll guess it you'll get correct like my guesses always go wrong so I stopped guessing right what I found subsequently was because I'm not able to guess the correct answer I started answering opposite of whatever I was guessing and suddenly my score started going up so you need to figure out a method Right. My guessing power is life of learning 32 hypothermia body temperature relatively less. Uh should try a mock test of any set not exactly doctor. For FMG exam there would be a separate one. No. So I think uh it's it's optional. I I would not like to say mandatory but uh you have already cleared one exam and now you're preparing for need PG etc. Then it's it's worth recommended. Okay guys moving on to our discussion. This is just a reference. The PDF of this will be available to you guys guys subsequently for revision. I would suggest you to revise this video subsequently also by downloading the video onto your device and revising it at 2x right you have to endure me but you will be able to reinforce the information or the concepts that I have said here and some part you can skip also the parts that you are already aware of so that would help you you know help you method the that would help you uh understand the things relatively method okay so next Next we'll talk about like ACLS that is advanced cardc life support where there are three boxes which are to be remembered uh they usually ask you these questions that uh the DC shock doctor in the description of the video only know there would be some PDF where you can like register for a PDF or you can go into the app and register and the PDF would come to you or you can drop a email at marva [email protected] and I'll be glad glad to share the PDF with you even the blank one so that you can annotate on it subsequently okay uh sorted uh CPR are like you know we have to give every time after DC shock so every time we read about ventricular fibrillation every time we read about vent yeah telegram group of preplatter that's another way you can use it everywhere man this would come up this would come up so you don't need to worry about it uh thank you doctor thank you for lots of love and regards in a case of ventricular fibrillation um there would be three boxes which are to be remembered and usually the question will come like after the first DC shock what is to be done after the second DC shock what is to be done and after the third decision on what is to be given and it is going to be like CPR CPR CPR Dr. pathus follow these details very very religiously follow these details very religiously the ones that I'm discussing BLS ACLS is always asked three DC shocks are the ones that can be given in the first box you can see you are just securing IV link otherwise you can use introious access okay the comments are going down quickly comment where would you put in the in which needle will you use to get a introious access yes guys quick comments in the chat box which needle will you be using for intraosia success and I mean intraocious success is obviously the lower extremity yes in the tibia tibia 22 to 24 needle 18 cause needle okay proximal tibia okay okay so your answer would be that this would be yes it would be jamshed's needle here yes bone marrow biopsy needle so the needle that you can be using see in America they have that portable gun they the bullet that bullet that is fired It penetrates the cortex and reaches up to the medela. So it's like a a gun that is fired but in India we won't have that facility. So we'll be using a jumpshed needle. And yes it would be like a lateral to the tibial tuborosity. So your technical answer would be obviously tibia. But if he says where then it is not exactly the tibial tuborosity it is like a little lateral to the tibial tuborosity where we penetrate the needle and we get access to the bone bone marrow of the patient and bone marrow has very good communication with the venus system. So it would be like jump shaded needle tubular tuberosity where we'll be poking the patient for intro success and uh we'll anyway the CPR is continuing if the patient reverts to normal sinus rhythm great if it not then the second DC shock would be given so this is second DC shock being given after which CPR is being given and then we are giving epinephrine to the patient the concentration of epinephrine that we give is standard that will be 1 mg 1 is to 10,000 and this is being given because we want to increase the responsiveness of the electroshock we will also intubate this patient at this particular point of time. So the number of breaths to be given will be like one breath every 6 seconds or 10 breaths per minute. If in spite of two shocks is not improving the third and the last shock that we give is for uh followed up with amidron or lignocane that would be given to this particular patient and absolutely like I think everybody got it spot on that these details that we're discussing is for advanced cardiac support where these three sequential steps are asked per se for ventricular fibrillation and a pulseless ventricular tachicardia. If he says what is the type of DC shock that is given what we've learned is it would be a non-synchronized DC shock and how many DC shocks are given then it is total of three but if I change the question to the right hand side for cardiac arrest if it is a cardiac arrest or a pulse plus electrical activity uh sham intraosious in sternum will be very risky now for somebody uh like you know honestly speaking uh even trauma guys know I I'll speak to a trauma guys since you said why not give sternum but uh I I think it's too risky to insert it in the sternum. If it goes too deeper, it can contribute to a damage. Even if you're using a guard, right? There's a possibility of causing trauma to the patient. So, I think lower extremity would be a better answer. When it is when it is going to be a non-shockable rhythm, then it's even much more easier epinephrine aisto pulseless electrical activity. Examples of pulsus electrical activity can be like cardiac tampon. Example of pulsus electrical activity can be like tension heum for which specific managements are required. But in all of these patients the first line intervention would be epinephrine and followed by this anyway CPR. If in the MCQ ASAP word is not given then first answer CPR. For all MCQ's answer is CPR only as we discussed in the previous question only. If epinephrine ASAP is not given then answer is CPR followed by epinephrine to be given to this patient. And uh I mean after getting an IV excess there is no rule of DC shock in a flatline ECG like this guy had a moardial infection ST elevation MI and then he became flatline. So what we will do is repeat adine shots. There is no limit to the amount of adine shots that can be given to this patient. So it is repeat adine shots. Okay Dr. Medico I'll do that. It is repeat adine shots that would be given for this person so that we can convert this into ventricular fibrillation. Barar barber adine. The reason why we give villain repeatedly is to convert a as stol convert a stol into ventricular fibrillation and the moment you will give convert it into ventricular fibrillation you can be giving a DC shock to the patient but we don't give DC shock in a flatline ECG the main reason why I went into the right hand side of this patient is that the DC shock of the patient soldier in a patient who's coming to a crashing patient and like most of the time you know most patients who coming to us amputation bilateral unlikely. Most of the time the cases that we get patients going into arythmias are either going to be like old people with a heart attack. That is one possibility like foot mostly soldiers amputation below above both less likely maximum number of DC shock that can be given is three only doctor like you can see I put three three stars mark three star marks here. This is DC shock number one. This is DC shock number one. This is DC shock number two. And this is DC shock number three. But DC shock is absolutely contraindicated with respect to a flatline ECG. Can you comment in the chat box for uh any other contraindication for DC shock? Waiting for your answers. DC shock is contraindicated in a case of ACE stole is what I have already said. Can you tell me any other condition where DC shock would not be given? Ace stolen pulseless electrical activity is anyway mentioned. There is no role of DC shock in which of the following. Yes guys uh yeah yeah yeah pulsus electrical activity understandable that is understandable any other situation which is a complication of myioardial infection. Okay, very good. Multifocal tachicardia but crash last but even in multifocal tachicardia we might have to give DC shock is not recommended because of the recurrence of arythmia. But the technical answer here would be what is called as electromechanical dissociation. What I mean by electromechanical dissociation is a complication of myioardial inffection where the heart will burst. You see heart attack it was causing so much of transmural myioardial infection. It is so much a transmural moardial infection occurring that the heart is subsequently burst on the third or the fourth day. And the technical term that we use for that if the heart will burst even God will not be able to save this guy. That is called as electro mechanical dissociation. The meaning simple English meaning of the word electromechanical dissociation is a cartic rupture. This can usually occur on day three or day four with respect to post myioardial infection in a patient. uh yeah one complication can be MI can be LV anurism but then again if there's an LV anurism a small one I can be giving a DC shock in a patient but these are like three situations where like we are not going to give DC shock and one doctor said multifogulated teicardia doctor your point is correct totally spot on you are right there but I'm just modifying what you are saying by saying that DC shock is not recommended in multifocalated teicardia not because of the fact that it will it's contraindicated it is just that the arhythmia will tend to reoccur so I would like to treat the COPD of the patient for multiple tachicardia. Uh ECG finding of electromechanical dissociation would be electrical alternates. The doctor said what will be the finding of electromechanical dissociation because when the heart will burst when the blood will pour into the paricardial space and when blood will pour into paricardial space it will cause cardiac temponard it will cause a hemopicardium. So the ECG finding of this patient will be electrical alternate. So that's the pecularity with electrical alternates in this patient. The pulse of the patient will begin to disappear. That's the ECG finding that would be coming in this patient. Electrical alternates. Uh doctor for combined medical services know uh they ask a lot of data from cardiovascular system neurology that I'll be discussing. So I think this session will be highly productive for you. Uh because they keep on changing the questions every year. So even if you're doing those previous year questions, it would help. But then listening to this poor information would make it make you more capable of handling all these aspects. The ECG finding of electromechanical dissociation would be that of like a very good question that came up would be uh answered as electrical alternates. Okay, cool. So we are now going to talk about uh arrhythmias and the first arrhythmia that I'm going to describe before you is having a variable R interval. There are two ECGs in which you will always be getting is a variable R interval. One is multifocal ticardia. Second is atrial fibrillation. Most MCQs of this topic will always begin by describing a alcoholic and may also mention that this guy went for binge drinking. And then what you will notice is that there would be absence of P waves in this patient. As you can see in the irregular R interval there is no presence of any Pwave present in this patient. Yeah, holiday heart is one possibility. So the correct interpretation for the first ECG that you see at the moment is atrial fibrillation. This is one of the most common sustained arrhythmias in clinical practice. Now the problem in atrial fibrillation is that there could be twitching of the atria that can cause clots because they can be clot formation. I can either be going in for eco cardigraphy to visualize the clot or I can be using a scoring pattern that is called as chad s2b score to decide for the need for anti-coagulation. I mean how do you decide the need for oral antiquagulation? Either we will base it on transisophagel eco cardigraphy where I can see the clots but even if I like transisophagel eco cardioraphy will require like you know more uh intense uh uh I mean at least the patient needs to be admitted right on a OPD basis at least we can do a trans thoracic eco cardioraphy if we can see the clots it is cool otherwise we can use the scoring pattern to start the patient on oral anti-lotting drugs uh he will use the word VAF VAF means valvular atal fibrillation valvular atal fibrillation is the one that is seen in India with rheumatic heart disease with mitroenosis and the drug that should be used in this case is warferin and the target INR of this patient should be kept between 22 to three as I mentioned but if he says the word nonvalular atrial fibrillation if it is non-valular atrial fibrillation then it is the newer oral antic-lotting drugs that would be used for this patient that is like a pixaban and uh in case he talks about recent onset this was FMG exam question last time this was FMG January Recent onset atrial fibrillation with hypotension. If atrial fibrillation is of recent onset definition of recent onset is within 48 hours then there are no clots. If there are no clots and the BP is unrecordable then you can straight away go ahead when give a DC shock to the patient to treat the patient. But if it is long-standing atrial fibrillation with hypotension in need PG they have always asked longstanding atrial fibrillation with hypotension. in long-standing atrial fibrillation because there is presence of clots present in this patient in long-standing atrial fibrillation because initially to hepin like you put up a question I can initially anyway give heperin to the patient no even if I'm having issues with any other drug and there is like a sever compromised GFR in a patient heperin anyway has to be given initially for the patient so that I can at least prevent the acute onset events that are occurring in this patient so okay if it is long-standing in fibrillation Then because there is presence of clots in those circumstances what we will use is raise protocol where we'll be using esmol in this patient along with esmol we'll also be using uh anti- clotting drugs that I mentioned then we will be giving emitron to the patient for chemical cardio version and if there is no improvement with emotron then subsequently a DC shock can be given even in this case but the point is race protocol is valid for R is for rate control A is for anti-coagulation C is for chemical cardio version and E is for electrical cardioverion. That is mainly to be remembered for whenever there is a long-standing atrial fibrillation. Now I will discuss two more MCQs one of NETPPG 2024 and another one of NETPG 2023 uh with respect to atrial fibrillation. Again what he will do in both inet and nepg is that he will put up a question of atrial fibrillation and he will mention that the patient is in acute heart failure. Now he will not write the word acute heart failure. He will write bilateral crepitations in the chest. If the question will mention acute heart failure in the options like he will say in the description bilateral crepitations in both the lung fields then do not answer as small because beta blockers are contraindicated in acute heart failure that is when the answer will be given as dejoxin. So somebody commented dejoxin that is answer only to be given in a question when there is heart failure given. This concept has been asked in inet and neat PG again and again. And then in 2023 he mentioned that the atrial fibrillation patient is having ama which is poorly controlled. So again beta blockers are contraindicated and in those circumstances I can be using calcium channel blockers in this patient that is vapamil for this patient. Now we'll come to a question like I I'll say this once again vap or delta can be used for the patient. I'll answer that query of Pat recurrent episodes of atrial fibrillation options option we use laser beam to destroy the cardiac tissue from where the current is generating that is catheter ablation that is we will do electrphysiological studies and after electrophysiological studies catheter ablation will be done in a patient the second option that I have is to put in a implantable cardio defibrillator if a person is having a documented structural heart disease like cardiam cardiomyopathy like alcoholic cardiammyopathy then we'll put in a implantable cardio defibrillator but there is no documentation of structural heart disease then it is catheter ablation that can be done in a patient so let's look at the gradation of the questions FMG exams recent onset atrial fibrillation recent onset atal fibrillation so in a recent fibrillation then the answer is you can straight away give a DC shock because BP is unrecordable but if it is long-standing atal fibrillation due to hypertension due to any of the other situations before you answer Solo just check out in a question because since you guys would be sitting for any set very soon and then subsequently some guys for need PG and subsequently guys for FMG exam so keep a watch for these two facts that I'm highlighting heart failure to acute heart failure he'll write like bilateral crepitations are felt in both the lung fields of a patient third heart sound is present elevated JVP is present he will give you findings of congestive heart failure In a question of atrial fibrillation if findings of congestive heart failure are given if acute pulmonary edema is given don't answer as smallol is the message. If he says ama then it is much more easier I think then it is vapamila that would be used. If it is on a recurrent basis then cathetilation or implantable cardio defibrillation which is to be used. Yeah. Yeah. We can use debigron also epixab and dabigatron. Those are like the newer drugs that can be used for management of these patients. But your first answer would be amadron and then subsequently you can answer ibu delight for this patient. Okay. Okay. IC filter for this one doctor will not be working. Ic filter is used in those cases where there's a recurrent pulmonary imololism occurring in a patient. No. If this patient having recurrent clots going from the deep endosus to the heart, that is where IVC filter will be used for this particular patient. Okay. Okay. Fine. I think I addressed most of the queries there. Yes, beta blockers are not to be given and dejoxins are dejoxin is to be used. That's only in a situation. Uh there the DC cardioverion followed by thrombolytics. uh Anchuan can you just comment on this part again or send me an email regarding the case that you were discussing because patient might have had a mocardial infection now so in a myioardial inffection you anyway have to uh I mean give thrombolytics to the individual but anyway an do let me know regarding the case that you are talking about otherwise for atrial fibrillation that's the algorithm to be used for recent onset of the long-standing atal fibrillation anyway like thrombolysis there's no thrombolysis to be done for case of atrial fibrillation okay moving to the next Question again a hot favorite with our examiners. Here also he will give you irregular R interval. You can check out the R interval in this patient is varying. Once again considering that there is a variation in the R interval. I will check for the P waves. Now if I zoom it here what you will notice is here it is like a Pwave. Yes. Coming in but the size of the Pwave is different from the second one that I have shown or the size of the Pwave is much more different from the Pwave that is preceding it. So what we are having in this case is multif focal atro ticardia mat. MAT stands for multif focal atrocardia. This is called as MAT guys multif focal atro ticardia. And the hint of this question will mostly be COPD patient presents with palpitations and syncopal attacks. The moment I say COPD for the rate control of this patient I cannot be using beta blockers. So it is here calcium channel blockers like vapamil and tiasm will be used for this patient. In multifocal tachi cardia our objective is to treat the COPD of the patient and therefore quick comments in the chat box with respect to what treatment is given for COPD apart from long-term oxygen therapy. I mean obviously we will give oxygen to the patient long-term oxygen therapy using a oxygen concentrator but then quick comments in the chat box what is the treatment drugs that you'll be using in COPD. Can you tell me the longest acting beta to aist? Can you tell me the name of laba longest acting beta to exist? Yes, guys. Waiting for your comments. Which of the following? Okay, I'll not give examples then, right? I'll not give examples then. Okay. Can you tell me the name of the longest acting? Okay. Cell metrol. Cell metrol. and metall for metrol. Okay. So, uh Dr. Basak was spot on. Yes, Dr. Shriashi. Uh it is Indiaol that would be given that's a long acting beta 2 ages that will be working for like almost 24 hours. So, I just wanted to test your knowledge of pharmacology by mentioning regarding lava that would be given to this patient. We'll anyway be using llama in this patient. Llama can be like teotropion, glycopyrolade. There are so many of them that can be used and along with this uh what we will also use in inhaled corticosteroids that can be like budonide, blothasone uh a whole host of these drugs which are available. But then we need to treat the hypoxia guys. We need to treat the hypoxia of COPD because COPD will hypoxia will cause pulmonary artery hypertension. It will cause right ventricle hypertrophy. You know the story. So I'll just write it quickly here. I mean there is a hypoxy and COPD patient. Hypoxia will cause vasoc construction of the pulmonary artery causing pulmonary artery hypertension. This pulmonary trap potention will cause right ventricular hypertrophy and because of the hypertrophy of the heart there would also be damage to the right atria and because of the damage to the right atria there can be creation of this arrhythmia that is called as multif focal atrial tachicardia. The definition of multif focal atrial tachicardia will be that there will be a variable R interval as you can see and along with variable R interval the Pwave amplitude in this patient will also be variable. There are two things that have said variable here. One is going to be Pwave amplitude that is variable and second is RR interval. So now you know two conditions where there's a variable R interval atal fibrillation and multifibrillated teicardia. Just check the presence of Pwave. A Pwave is absent it is atal fibrillation. If it is present with a variable amplitude as I've shown the size is varying man. I mean look at the pointed Pwave look at the shorter Pwave. Look at almost a flattened Pwave. So because the morphology of the Pwave is totally different. The morphology the amplitude is totally variable. We call it multifocal ticardia and DC shock doctor again in you used my favorite word buster medicine. I love that right. But DC shock contraindicated DC shock is avoided in this condition because of recurrence. You know contraindicated word DC shock is not recommended in this condition because of the recurrence because of the hypoxia component which is present in this patient. Inflammation inflammation Dr. Gotham we have said like airway inflammation is a feature that is seen in COPD also you having lot of lung secretions present those lung secretions will obstruct the airway that is why like we will use inhaled corticosteroides then the next ECG which is present here yeah rope flumlast can be used subsequently like that's like a step up that we'll be using in gold classification we'll talk about gold classification in part two of our discussion okay so what you can see next is those flutter waves which are present and uh because of these flutter waves we are having that sawtooth pattern that is seen with the atrial flutter. So the next arhythmia I'll just do a ink change for this so that I can get the contrast going is atrial flutter and the treatment for this condition is same as that of atrial fibrillation. So we'll still go for rate control anti-coagulation amodron and then uh DC shock but then the intensity of DC shock that is used in this condition is the lowest intensity of DC shock that would be used that is 25 to 50 jewles is the lowest intensity of DC shock that would be used for these patients. Once we get this right, we'll next focus on the next arhythmia which is a narrow QRS tachicardia. You can see a narrow QRS teicardia with the ST segment depression coming up and then there are hidden P waves. The features that I've shown before you is hidden P waves. What I've also shown before you is a narrow QRS complex with the RR interval in this patient being substantially reduced. Considering this this would be a supra ventricle tachicardia. This is a peroxismal supra ventricular tachicardia. Question putting up to you guys. What is the best treatment for peroxismal supra ventricular tachicardia? Yes. Stable veagal stimulation unstable DC shock. Okay. Let's be a little more aggressive. Okay. Adinosine. Okay. But adinosine will not cure it. Right. DC shock will not prevent the recurrence. Adenosine and veagal maneuvers will not be preventing. Right? So if he says what is the best treatment for PSVT it is the reason for PSVT remember is a re-entry phenomenon the question is on prevention guys the question is on prevention exactly Dr. Ram got it spot on. What we will do in this patient is a catheter abilation. The best way for treatment of all arrhythmias is to prevent the recurrence of these arhythmias it is a catheter abilation. A patient is not ready for catheter ablation at the moment to prevent the episodes from occurring I can be starting my patient on a on a calcium channel blocker like vapa male. So it is catheter abilation and vapa male which would be answered. Baky the remaining answers would be if the patient is hemodynamically stable then in those circumstances it is veagal stabilization first using a caroted sinus massage followed by administration of adinosine and after giving adinosine we'll be giving a saline push to the patient so that the drug can reach up to the heart because the dose we giving is 6 mig and then maybe if required 12 mig subsequently but if the patient is hemodynamically unstable then I will not be wasting my time for giving veagal stimulation and adinosine for the patient I will straight away be going ahead with a synchronized DC shock. So there are three domains that I've covered here. One is for prevention. Prevention second is for acute presentation. In acute presentation we have divided the discussion into two parts stable and hemodynamically unstable and most questions regard uh I mean revolve around this also. Narrow curious hypocalemia. No doctor absolutely not not not hypocalemia will be having a T-wave inversion it will be having a PR prolongation it will be having ST segment depression so the findings in hypocalemia would be uh wava we can try absolutely put them we can use yes calcium channel blocker in case of adinosin sham you're right if it is an amatic we can use calcium channel blockers anyway it will block the a node of the patient the next situation or the next arythmia that I'm dealing with you is having broad Q super broad QRS complex right with that very characteristic notch that is being present. So what you can see in the ECG of this patient is a broad RS complex tachicardia and along with this broad RS complex tachicardia you are also noticing a small notch that is coming up which is called as Josephson sign even if you don't remember Josephson sign the main word to be remembered is every time there's a broad RS complex tachicardia you are going to label that as BT that is ventricular tachicardia and since all these are of equal equal size you can see the vertical height of all of these is Same same. So you will say the word monomorphic ventricular teicardia. In a question of monomorphic ventricular teicardia again if he says stable ventricle teicardia the beep is holding it is amatron. Emodron is a broadsp spectrum antiythmic drug that can be used in a patient otherwise we can use beta blocker also like I don't have emadron at the moment. I can be using beta blocker like metopol to control the fasting heart rate. But if it is a pulseless ventricular teicardia then it is a DC shock that would be given. It's a non synchronized DC shock that should be given to this patient. If it is a pulseless ventricular teic cardia it's a non-synchronized DC shock that would be total of three DC shocks that would be given. Great comments coming coming guys. You need to keep on commenting right so that you can remember all these small small nitty-g gritties and these questions are very super easy man. Super easy. There are only like hardly six seven concepts to be remembered like irregular RR interval with absence of Pwave, presence of P, presence of atal sawtooth waves, narrow QS tachicardia versus a broad QS ticardia. Those are like ultra easy concepts guys which are very very scoring and PSV we don't use amidron in PSVT because we need to act on the AV node. Now amidron acts on the cardiac muscle not on the AV node. Emidron the main mechanism is the drug works on the ectopic focus in the muscle and it slows down the firing frequency of the topic focus so I it will not block the AV node that's why yeah the intensity would be uniform 200 jou by phasing okay so moving ahead guys uh pulseless v yeah yeah yeah we we'll be using a DC shock in a patient PS asma calcium channel blocker dushri I hope I have answered Very good. Very good. So you are getting a question now which is having again a broad QRS tachicardia. But at the same time this broad RS tachicardia is having a variable amplitude. Because of this variable amplitude we are going to call it a polymorphic ventricular tachicardia. and considering a polymorphic ventricular tachicardia. The drug that we'll be using in this patient is magnesium sulfate that is a separate thing that if this patient is also having a unrecordable blood pressure then I'll go ahead with RDC shock only a non-synchronized variety but from the drug perspective it is magnesium sulfate that would be given and usually the trigger responsible for this can be electrolyte imbalance like hypocalemia and hypomagnesmia. So every time you get a question on electrolyte imbalance and arrhythmia coming up then hypoglymia, hypomagnesmia or drug toxicity. Drugs could be like hydroxychloropin drugs could be like cisopride estol. So if they give you drug toxicity like in nepg I think they put up a question on estol or I think it was on tphenadine but these are like banned drugs. Cisopide estamazol, tarfinadine, hydroxychloroquin is not banned. It is used but then it can cause a prolongation of the QT interval and it can cause a development of uh yes even class one and class 3 antiythmic drugs also. Yes, Sedhart, you're perfectly right for that. Even class one and class 3 antiic drugs can be contributing to it. So, magnesium sulfate would be used as the drug of choice. And the last one is super easy that would be ventricular fibrillation about which I've already spoken about where there would be a twitching activity. Most scenarios of ventricular fibrillation will originate from either football player dying suddenly or it's going to be myioardial inffection patient crashing in the casualty where ventricular fibrillation and the treatment for the same would be working. PH may how does it work? Magnesium is antagonist of calcium. No. So it will antagonize the effect of calcium and therefore calcium causes vasoc constriction. So it will relax the blood vessel. So PH is pregnancy induced hypertension. Vasoc constriction. Magnesium is the antagonist of calcium. it will antagonize the effect of magnesium and thereby the the good thing would be that uh the the effect of vasoc constriction will go away and the blood pressure will relax. The key word is magnesium is antagonist of calcium. Okay fine moving ahead we are now talking about a brady arhythmia and I would like you to I mean I'll just count the heart rate of this guy this is like 7 8 9. So the heart rate of this patient would be 300 divided by 9. That would be less than 40 beats per minute. Yes guys, heart rate of only 40 beats per minute. If you check out the PR interval of this patient, this this is a Pwave. I'll draw a Pwave here. This is a Pwave. Prior to that is a T-wave. The green that I'm showing is a like a T-wave inversion that is coming up. So this was a T. Then subsequently I've shown a Pwave where this is another Pwave. Let me just get the colors right so that I can emphasize the information before you. So you can see a inverted T-wave. I think everybody can I I'll do it once again. This is the inverted T-wave I'm talking about and after that in blue color you're seeing two P waves present. This is one of the Pwaves. This is the second Pwave. Right? And you can check out the PR interval. The PR interval in this patient after and before the mist beat the PR interval in this case before and after the mist beat is the one which is to be checked. Let me put appropriate colors so that we can get this data right. Keep the comments going guys keep the comments going. The PR interval after because you can see a P followed by a P here there there's a drop happening here. There's a drop happening here. I'll draw the vertical arrows for the drops. So because I'm saying drop beats either it will be mobits one word block or it will be mobits to word block or it will be a two is to one block. I repeat my statement. If I say drop beats in a question the heart rate is slow and I'm saying drop beats in a question. Either it will be mozzard block or it will be a moetss two block or it will be a 2 is to one block. There can only be three possibilities in a question. In a moits one block there is a prolongation of PR interval. So the answer to this cannot be mobits one. Now we are left with only two. more bits to hard block and two is to one block. So I would like you to now compare this ECG that I'm now making before you where the PR interval is normal. It is normal. It is normal. It is still normal. And then after T you can see a P and a waiting waiting waiting waiting waiting like a sinus pause that is coming and you are noticing that there is a drop beat that is coming in this patient and there was a drop present and then once again the restoration of activity is occurring. So guys what I want to bring to your attention is that before you answer more bits to hard block in a MCQ check out the fact that is it happening that it is alternate conduction and nonconduction versus multiple conductions and then a drop. The answer to this question a difficult one for today is what is two to one block? Two is to one block is a differential diagnosis of more bits to odd block. The first thought process of yours should always be check out the PR interval after and before the draw date it was equal equal. So it is first answer is Mobit squad block but if you check out I'll put markings now this is a conducted Pwave conducted Pwave where I put the arrows conducted Pwave so QRSV or TBR then I'm saying that the person is having let the green go off it is a non-conducted Pwave where the P is shown non-conducted Pwave then again I'm putting marking conducted Pwave let it go off now is a non-conducted Pwave alternate conducted non-conducted conducted non-conducted We call it a two is to one block which is a differential diagnosis of mobs to ad block. Mobits to block EC PR will be normal and will be normal and will be normal and will be normal. So it is like normal normal normal and intermittently there would be drops present and again the rhythm will be normal. So the common thing is obviously drops the drops that are occurring alternatively that is what you call as a two is to one block which is a differential for mogit block which I want to basically explain to you. So I think that uh this is like a important ECG especially from the perspective of the forthcoming exam. The first one on the block is going to be insert. So that's a favorite of those. Uh Mobitz one, Mobitz not two. Nobody will mistake. I'll I'll do a quick representation for Mobitz one also. You can compare on a visual scale only. I have increased the PR interval. I'm going to increase the PR interval even further. I'm going to increase the PR interval even further. So I don't think so that mobits one ever can be a challenge for anybody because if you check out the PR interval the first time, the second time, the third time, the fourth time, it's going to show a serial increase. But if the PR interval is normal, normal normal followed by drop, it is mobits 2. So this was a I think a good pick up by a lot of people who answer two is to one block spontaneously. But I'll say now compare the three ECGs together. Mobits one to clear prolongation of the PR interval is moss one on blocks 2 it will be multiple normals multiple multiple conducted followed by non-conducted multiple the word is multiple conducted P waves followed by non-conducted waves multiple conducted non-conducted you alternative in 2 is to one block guys it is alternatively conducted Pwave non-conducted Pwave alternatively conducted Pwave non-conducted if it is alternately we running then you are going to say it is two is to one block. If it is going to be like multiple normal normal normal normal conductions multiple array of drop that is when you call it move bits to hard block. So this is what I would like you to remember at this moment guys otherwise like uh what I would suggest is listen to this in the rapid revision segment as well where like I have given much more time to this here at at the posity of the time that I have at my disposal. I think I'll be able to explain this again. So, Shubam I think I was able to explain this but then uh uh uh if if it is not present then this this is a common aspect to be remembered in 3 is to1 guys there would be like two like 2 is to1 basically is a term that is used when alternative you know one conduction and then one non-conduction is present if it is going to be like one conduction and two non-conducted waves then it becomes like a 3 is to1 block that would be happening so there would be two waves P waves present in between that okay fine let's move ahead to the next one where they they have given myocardial infection. They've given an ECG of myioardial like he began by describing classical levine sign in a patient with sweating etc. So we knew that he's describing a myocardial infection and then he's given this ECG. If you scroll through the ECG, lead number one, not significant changes. Lead number two, lead number three, I can pick up a bit of like you know ST segment elevation. In lead number three, I can pick up a bit but not in lead number one and two. But uh that means that I am not being able to pick up anterior wall myioardial infection because what you are checking out in this ECG. Yes guys, keep the comments coming for which surface of the heart is involved in this particular case and what you are noticing in this chap is a ST segment depression. What you're noticing in this guy is a ST segment depression with upright T-wave. You can see upright T-wave. I'll I'll just zoom it in. You can I'll just erase it and do this activity once again. In lead number V2 and V3, there is a horizontal. Normally whenever I draw ST segment depression, it's always like this. Whenever I draw a T-wave inver ST segment depression, now it is always going to be having a curvature around it. But you can notice in the current ECG that I'm drawing, it is a horizontal ST segment depression with the upright T-wave that are shown in lead number V2 and lead number V_sub3. This is a little difficult one in a sense that the ECG findings are present in V_sub_2 and V_3 and bit in lead number V uh in bit in lead number V4 also. So there can be two possibilities in this question. Either this is going to be a non-station MI of the anterior wall. That is one possibility non-estation MI of the anti-robable that is possibility number one. Second possibility is that the person could be having a posterior wall mioardial infarction. Now how do I differentiate between the two? Differentiation is one possible by putting special leads like V7 V8 and V9. If V7 V8 V9 will show reciprocal changes then I will say posterior wall MI will say non-estation MI of the anterior wall. But if this V7, V8, V9 is not given then how would you pick up in a question is the word what I was saying verbally and I drew it also that is a horizontal ST segment depression in myioardial inffection you will always have a convexity present but if you're having a horizontal ST segment changes present this is a horizontal ST segment depression and a upright T-wave which goes in favor of a posterior wall mioardial infarction so initial impression of mine was this is non-estivilation MI the conventional way try to differentiate between the two is to look for lead number changes in V7, V8, V9 which is posterior leads but because those were like not given in the exam. So the key word to be picked up is a horizontal ST segment depression along with presence of upper T wave especially with respect to lead number V3 and therefore the answer for this particular question would be given as posterior wall myioardial infection. I agree that the previous two ECGs that I've given have been relatively more difficult than the traditional ones. But I'm trying to prepare you for like even if they give you whatever like even if the hell breaks loose, I am trying to make you up gearing gearing up gearing you up to handle those challenges. Now we will be focusing on we'll be focusing on the next ECG which is much more easier and I expect spot answers here. Again, Levine sign present. You can notice a bit of T-wave inversion in lead number B3. Meanwhile, some part of the inferior surface is also having eskeemia. There is a T-wave inversion in lead number three. Quick comments guys. I would like everybody to hit the chat button simultaneously. What type of myioardial infection is shown here. The changes are seen in V_sub_1 and in V_sub_2 and in V_3 right and okay so not significant in V4, V5 and V6 but at least like V_sub1, V2, V3. Yes. Yes. anterior wall MI and because V_sub1 V2 I can call it septum also no because V_sub1 V2 will be involving the septum part. So your answer is right antal MI. I would just like to modify by saying this is a anterior septal. My I added the word even if you said antal MI it is okay. Even if you said antal MI it is okay. But I just wanted to bring to your attention that lead number V1 and V2 specially studies the septum also. So antioepal myioardial infection will be a much more better answer. Like if he wants to make it more specific then the answer would be given as anticeptal mioardial infection where you can see that classical tombstone pattern where you can see the classical tombstone pattern and this tombstone pattern is the one that is also called as party sign. The word is tombstone or the alternative name for this tombstone is party sign. P A R D tombstone or party sign present in V1 to V3. So my my I'll I'll base my answer going more in favor of like antioepal myioardial infection. Very good Dr. Anupria that is party sign also. Now let us compare the next ECG. This is especially for if you are an FMG student and you're listening to this because I don't know what uh fascination the FMJ examiner has with ask asking this ECG of MI where okay I'll not say otherwise it will become more obvious. Yes guys can I can I comment can I expect some answers here? Especially if you're an FM. Everybody can comment. Everybody can comment. But those if you are an FMG student listening to this. Yes. Lead number two. Lead number three or lead number AVF may classical ST segment elevation present with a convexity fascination but two three ABF may changes. So very good guys. I had very good input from lot of you. I mean obviously in the chat I can't pick up that which exam are you preparing for. But then inferior MI is again something that they love to ask. So I've described three before you. Posterior wallal MI then is going to be inferior wall. Then is the anterior wall myioardial inffection. Uh this is going to be the involvement of the right coronary artery. And the leads which will be involved in this case would be lead number two, lead number three and lead number AVF. And you can also notice that in this particular case the heart rate of this patient will begin to slow down. Here it's around 75 but gradually because of the Vegas activation. Uh yeah Karthik you were right IV fluids can be given if there is hypotension. If he mentions like inferior wall MI case and he mentions there is hypotension. So this is the only type of MI where IV fluids can be given to the patient. Though this is playing with fire you know that 500 ml bolus that you're giving is playing with fire because you're trying to utilize the Frank Sterling law but uh like that's the only option that you have that the remaining part of the heart whatever is normal you're trying to increase the cardiac output by stretching the muscles. Frank Sterling law stretch the heart and the cardio contractility will increase MI will cause damage to small part of the heart. So the remaining part of the right ventricle is normal. So you can stretch it and make it work more. Though it's like beating a tired horse. That's why I said playing with fire when you give ivors to this patient. But that's what we doctors do playing with fire all the time. Right? Those emergency scenarios that we handle on a regular basis. They can go south in immediately in a moment. The moment it goes up and everything is BP goes up everybody's happy. You know when when it falls further that's when everybody's saying no you did you must have done something wrong. So that's like uh hypertrophic cardiammyopathy IV why would we give ivy fruits to hypertrophic cardiammyopathy doesn't make sense right we can give ivy fluids if he's having diarrhea dehydration not a problem okay so these were like the questions that have come up okay quick inputs here with respect to the treatment for myioardial infection presence with bradicardia and vomiting the best known is a pneumonic that is used for treatment of myioardial infection Whatever be the type of MI ST versus non-ST elevation MI bestone is the treatment that is required. Can you tell me the window period for thrombolyis? Window period for fibbronolyis in ST elevation MI and we can move on. Options are standard 3 hours, 6 hours, 9 hours, 12 hours. Quick answers there. Window period for fibonolyis in inferable M in in any type of MIT elevation MI. Yes, window period would be answered as 12 hours. Window period would be answered as 12 hours. In this 12 hours, whenever the person will come to the hospital, we will start thrombolysis within how much time of arrival? Then the answer is 30 minutes. Do take care of the fact that don't mix it with 90 minutes and all those things that people were saying window period for fibbronolyis for a patient of ST elevation MI should be kept as 12 hours and within these 12 hours if the patient will come within 30 minutes I mean whenever patient will come within 30 minutes we have to start the treatment for a case of ST elevation MI if he himself mentions that the cathla facility is available then obviously thrombolysis will not be the main strategy that I'll be using. Then it is primary percutaneous coronary intervention that I'll be using for the patient. This is like a summary of the core aspects that we need to remember for estation MI. If I don't have a cathlab facility, we will be going ahead with medicines. If it is going to be cathla facility, then it is primary percutaneous coronary intervention. Let me write down the drugs also. B would be for beta blockers. Most of the time that would be used as metopol. Alphabet. E is for inoxarin. That would be low molecular weight because I want to prevent the clot from propagating further. S is for statins. T is for thrombolyis. But this is valid for only ST elevation MI. So I'm just putting asterises here to say thrombolyis is contraindicated in let me write it also. Thrombolyis is contraindicated in a case of non-ST elevation MI. Reasons I have explained non-estivation MI. the clot would be platelet rich and here it is fibbrin rich clot. So we don't give thrombolyis in nonestation mic platelet rich clot. So it is best known pneummonic that would be used. Then M would be for morphine O is for oxygen. A is for aspirin and here with aspirin we give a second medicine that is tickr loading dose of what aspirin and tagriller. So those are dap that would be given and then we would be giving nitrates to the patient. Nitrates are contraindicated if on admission the systolic BP is less than 90 mm of mercury. Yes. So it is dual antiplateral therapy that would be used for this patient. This is all strategy that would be used for those cases of ST elevation MI in non-ST elevation MI will be using intravenous antiplatlet drugs. Quick comments in the chat box. Which antiplatlet drugs are used in non-estivation MI to destroy the plot? Yeah. Right, right, right, right. Which uh yeah, we can use and there's so many drugs no tenace, ret any of those drugs can be used for management. Yes, the drugs that we can be using in this case are like epi fibetide. Yes. Or instead of epi fibbratide we can be using canriller in the patient in non-steelvision MI it is still best known beta blocker in oxoparin statin thrombolysis it is topaban topiban that would be used we don't use thrombolysis in this patient guys it is terophabiban any of the three drugs can be used in this patient and subsequently the person would be taken off for percutaneous coronary intervention so PCI is now done for both varieties that is for ST elevation MI as well as for non-ST elevation myioardial infection. The treatment of choice for myioardial infection whether he says estation MI says non-estation MI in both the scenarios guys if he says what is the treatment of choice your answer would be given as percutaneous coronary intervention is given in both of them a word of caution thrombolysis done only in non in estation MI if I don't have a PCI facility but the T in the pneumonic for non-estation MI is for trophaban though I could be using canalin fibotide because it was fitting in the pneumonic that is I have mentioned so in half a page I've summarized the treatment for myocardal infection because your data has to be crystal clear in your mind. Right? I said you are building yourself from the final. So all your data has to be concise. Whenever you are reading my suggestion to you guys is summarize your data. Make it conciser. Every page of your notes should be having a stick on pad. On that stick on pad you should note to details so that you are able to because in the last time you know you will not be able to uh yes uh rescue PCI would be done within 90 minutes. Uh Dr. Karthik a very good question. I think it was FMG exam question. Rescue perccutaneous coronary intervention is done in case of failure of thrombolysis within 90 minutes. Like I have given medicine to the patient. Suppose I am in a small city in India 50 kilometer or maybe 100 kilometer from Gural right or Delhi. I did thrombolysis but the medicine has been given but ST elevation is not coming out. If ST elevation is not coming down then I will have to transfer the patient to Delhi in an equipped ambulance and the strategy where we are like after thrombolyis we are saying elevation is not coming down. So within 90 minutes we have to do this call of transferring him to a higher center that is rescue PCI. Though there can be lot of medical legal issues there because later will say like this. Oh why did you not send earlier? So you must always take a informed consent before you are doing thrombololises in a patient because uh lots of time you know you you should say take him to a bigger center if you want where do they do a cathlab procedure. Now they say no no no we can't go because it is like traffic jam on the highway or some uh whatever be the reason I mean you should be explaining the concepts to the patient properly and rescue perccutinous coronary intervention the cutoff here is again within 90 minutes of uh like the failure of thrombolyis we should be going in for a rescue perccutinous coronary intervention this was a question that was asked in FMG exam okay so next we'll do a question with respect to nervous system this was like the cardiac issues that we discussed so bear with me for another hour or so I think and uh you guys would be more fighting fit. Uh let's do uh Deepak uh can you when to answer question? Uh Deepak I could not get your question. Okay 90 minutes and 30 minutes. Okay, I'll explain it Rabi. Meanwhile you guys can take a break. Those guys who are tired can take a break. There are two concepts guys. One is balloon angoplasty. Balloon angoplasty is door to balloon time like patient of myocardial infection when he comes to me in the first 24 hours and I am working in a cat lab equipped hospital then I should be starting like patient came now how much is the time 217 so within 1 and 1/2 hour I should do a balloon angoplasty and I should destroy the clot this is technically called as per primary perccutaneous coronary intervention right but if a patient is coming to a hospital where I don't have facility for PCI I'll say them take him to bigger hospital they say no no it's so far away how do we take him what if he collapses I'll say we we'll give you ambulance we'll give you doctor in the ambulance and uh he can be transported baky it's your wish you want to keep him here they say no no no sir we trust you so sir okay fine we start with thrombolyis this can be done within 30 minutes of arrival of the patient this this is all within arrival of the patient to the hospital because in the hospital slip there's a punch in time. Now the computerized slip will say patient admitted at 2:17 p.m. So within 30 minutes we should start thrombolyis in the patient. ECG basic treatment best moon should be given and then thrombolysis should be started within 30 minutes of arrival. But the second point is patient had MI at 8:00 a.m. in the morning. So till how much time can you do thrombolysis? It is 8:00 p.m. in the evening. from 8:00 a.m. to 8:00 p.m. in between that time whenever he comes like he came at 2:17 so by 2:47 I will be starting thrombololis if he came at 5:00 in the evening I'll do by 5:30 if if I'm working in a bigger hospital where cath facility is available patient came at 5 heart attack occurred at morning then by 90 minutes that is by 6:30 I'll do the procedure so this is what I wanted to explain for 90 minutes 30 minutes and 12 hours the window period is calculated from symptom by window period is calculated from symptom whereas the door time is from the arrival into the hospital. So this is like some baseline information that I have mentioned. Now I think couple of guys were requesting for a break but actual exam is like uh long now like we started at uh 12 and it's only 2 hours whereas the exam is going to go for like 2 and 1/2 hours 2 3 and 1/2 hours and in fact you will be making an entry much more earlier. Yes Deepak that is okay. Transfer time we take 120 minutes. Uh uh I'll just modify Deepak what you said in rescue PCI in rescue PC no no Deepak it is not like this it is not like this uh there are two separate strategies that are being used one is the transport time right if the transport time is more than 2 hours then we don't do any transfer of the patient we do we we straight away are do going to do a thrombolyis in a patient right and if it is transfer time is less than 120 minutes then we take him to catalab that's a separate algorithm for if you're working in a non-cathlab hospital but suppose in a non-cathlab hospital there is no improvement occurring within 90 minutes you have to anyway shift to a cath lab hospital that decision making will be 90 minutes so yes I think your uh point is seen transfer time and 90 minutes okay fine fine deep your point is taken okay we are having a 20-year-old boy with skeletal muscle uh skeletal muscle weakness and grip myotonia he's having a chloride channel defect and which of the following is correct about this case uh guys this is not cystic fibrosis come on come on guys I know you're tired but that does not mean the topic is neurology right and this is not cystic fibrosis skeletal muscle weakness is not a feature of uh uh skeletal muscle weakness is not a feature of uh uh cystic fibrosis and uh it does not have a grip myotonia you know what is grip myotonia you will like hold the finger like you ask ask the patient to grab your finger so he can grab your finger he can't let it go like you grab it you let it go here you'll grab it and Keep it grabing right. So that is like grip myotonia. That is a slow relaxation of muscles. So this guys is a question that is trying to test your nerves. This is not cystic fibrosis. Cystic fibrosis will present with recurrent pneumonia episodes. Along with this there would be presence of malabsorption syndrome. There is no mention of any recurrent pneumonia or malabsorption syndrome. Becker's muscular distrophe and skeletal muscle distrophy. Becker's muscular and Dene muscular distrophe do not have grip myotonia and both of them are having a defect in distrophin gene. So some questions in the paper will be solved by exclusion. Not all questions are going to be a lollipop. This is an example of the same. The correct answer for this as now most guys are realizing would be given as option number B that is called as Becker's disease. Becker's disease is a channelopathy. Becker's disease is a channelopathy. If you listen to the NITP PG segment I have discussed channelopathies, hypocalemic periodic paralysis, hypercalemic periodic paralysis. I have described uh uh Anderson Tavi syndrome all those things. Right? So that is where I've said this statement chloride general defect in the skeletal muscle and having a grip myotonia. This is Becca's disease. So this question is like based on exclusion capability guys not every question is going to be like a lollipop right. So I had to make it like you know not every MCQ will be sag right. So let's attempt now the second one. Uh chanopath is okay doctor. We'll try to do that channelopathies otherwise like if you listen to rapid revision doctor that would be a much more better way to give justice to the topic because here I'll just give you maybe a pneumonic or a hack that would not be sufficient for that topic it's only 20 minutes you listen at 1.5x it will take you minute of your time sir that I am saying and you will get a better understanding believe me if you move on to the channelopathy topic minute it will make it easier for you know here I'll give you shortcut and a pneummonic that shortcuts do not work in an MCQ. So I think that more justice to the topic. Okay fine. Star of death blood in the basil systems. This would be subcon hemorrhage. The case scenario in this particular case would be 25 year old lady presenting with severe headache. Doc I have to address most of them. Uh 25y old lady presents with severe headache and multiple vomiting episodes and she's the headache started after missing a breakfast. So in the first two lines of the question initially you will think that this is migraine because migraine attacks can also and vomiting episodes can be starting after missing the breakfast. But then the key word in the question is present to uh do nucal rigidity and that would be like you know when you say the word nucal rigidity in a question. Nucal rigidity tells you either it will be menitis or it's going to be subordin hemorrhage in a patient. Even if they don't give you the CT scan in this case, your answer would be given as subreular hemorrhage on the basis of the combination of headache with nucal rigidity. If it was there's no fever in this case, so I can't say menitis. This is not migraine because there is no nuclear rigidity. Intraranial space occupying lesion will be having a long history and tension headache is always a diagnosis of exclusion. I mean you straight away cannot diagnose it as tension headache. It is always a diagnosis of exclusion. So this would be answered as subre hemorrhage. the worst headache of her life. The most common location of beranurism is anter communicating artery. But if he says what is the most common location prone to rupture. If he changes the question to what is the most common site that is prone to rupture then it is going to be posterior communicating artery. So there are two separate MCQs and the most common cranial nerve which will be involved in both a ruptured as well as the unruptured berry anorism is third nerve paly. It is going to contribute to development of tossis in this patient. Yes. top of the baselor artery. Yes, Dr. Shrea, you perfectly right. The investigational choice for suboral hemorrhage in this patient would be answered as a non-contracity scan. There would be two findings that would be given. One would be your down and out also. Uh there would be one presence of blood in the sylvian fissure and the second feature that can be given is the star of death. Then they've asked what is the next best investigation for this condition. You can comment in the ch chat box here. Uh sixth nerve will involve due to raise ICP but overall the most because usually the PCOM one will be adjacent to the third nerve only. So six nerve will involve if there is development of raise ICP. Okay. We will be doing CT andography. Okay. Before that better answer than CT andography. Before CT andography what is a better Okay. Very good. Invasive cerebral angography. Guys, I need to anyway put a endovvester coiling procedure in the patient. I have to put in a uh I have to ensure the fact that there is a platinum coil deployed inside the berry so that it can prevent a rupture. It can prevent uh development of rebleading in this patient. So on a comparison if I have to select between CT andography and invasive cereal angography my first answer would be given as invasive cerebal angography. uh normally I always talk about non-invasive investigation to be done but in this question I'm talking about a invasive investigation to be done because I need to in this particular case fix the problem by going in for in the same setting only know when the patient will be taken in the kath lab we can take a femoral access go up into the uh descending iota go up to arch of iota caroted artery from caroted artery into the brain blood vessel that is uh wherever the berry is located. So it is endovvascular coiling which can be done in the same setting for treatment of choice. So invasive cerebal angography will be a better answer over city angography in this particular case. Whenever the berry will burst the feeder vessel of that will tend to undergo spasm like this berry had actually popped off. So what will happen is that the feeder vessel related to this the feeder vessel related to this will exhibit a protective vasospasm and that will cause a cerebral eskeemia and that is it the drug of choice for this patient that would be done coiling coiling doctor not clipping not clipping it is foiling that would be answered the drug of choice for this patient would be answered as uh neoipin the drug of choice for this condition to prevent the vasop spasm from occurring yes a very good answer should you give anti-hypit hypotensive drugs to this patient then Dr. Sangeita my point is if I give anti-epotensive drugs I will worsen the brain perfusion. Let me just highlight that formula before you. Cerebral perfusion pressure is a difference of mean artiller pressure minus the intracurren pressure. So I think in the question the BP was given to be like 160 that is good 160 is a good value because if ICP will raise the raised systolic BP is a compensatory mechanism that is maintaining the peripheral profusion of this patient. So even if the BP of this patient is elevated I will not lower it. Obviously if the BP is more than 220 by 130 I will be lowering the blood pressure of this patient but otherwise in cases of raised ICP I can call it word like permissive hypertension that increase mean artal pressure will counterbalance the raised ICP of the patient and will maintain the brain perfusion of a patient. So lowering of blood pressure of this patient would not be advised unless and until the patient has gone into hypertensive crisis and majority of the cases where you have a berry anorism rupture it is because of the inherent weakness in the brain blood vessel. This lady is not hypertensive. She's only 25 years of age. She's non-hypertensive. Her BP is elevated because of the compensatory pushings reflex operating in this case. I repeat my statement. This is a 25 year old lady. The reason why her BP is elevated is primarily because of a compensatory pushings reflex mechanism that is operating and that is what is called as permissive hypertension in this patient. So nicardipin will be used in this patient if BP is elevated but otherwise a more specific drug neodyepin will be used to prevent this vasop spasm from occurring to prevent the worsening of the brain eskeemia. And if he says what is the most common cause of death in subural hemorrhage you guys can comment in the chat box leading cause of death in this patient. Yes guys, the leading cause of death in this patient having blood in the basil systems. The star of death. The worst headache of my life. Triclap headache. Waiting for your answers. Yes, guys. Without any. Okay. Vasogenic cerebral edema. Very good. Cerebral infection. That is one. Okay. Yes. Uh a more technical answer would be DCI. The most common cause of death is vasospasm. And to make it sound sophisticated in the MCQ, it is spasm only. Now that is spasm only. That spasm peaks by about 48 hours after the acute event of subre hemorrhage. The spasm worsens after 48 hours of the acute event. So therefore these patients can have a late neurological deterioration. There's a possibility that when she came her GCS was 10 on 15 or maybe 12 on 15 but after 48 hours her GCS will become less. Her relatives will fight with you and agree argue with you. Oh our patient is deteriorated under your care. You will try to explain to them that why the patient is deteriorating is because of the fact that there is a vasop spasm protective vospasm occurring because the brain is trying to prevent the chances of rebreeding. Nowadays these chances have become lesser because we do immediately coiling and if I will do coiling in this case like this then the chances of this vasospasm and all these things will become relatively lesser but still overall like lots of time these facilities may not be available then it is delayed cerebral eskeemia that would be required. There are two procedures that you can be doing in this patient as you can see one procedure we can be doing in this patient is clipping. The second procedure that you can be doing in this patient is the foiling part. In the textbook first coiling part is given and then the clipping part is given. So the coiling part because of faster I mean faster intervention no for clipping I'll have to send to neurosurgery department they have to take a transfer then they'll do a cranottomy then they'll do a clipping in a patient and endo interventional neuroraiology is gradually replacing the I mean the neurosurgery domain. So that is why DCI delayed cerebal eskeemia that is a more sophisticated word for vasospasm that is present for thunderclap headache which is a presentation for this condition. What do you mean by thunderclap headache? I mean headache increasing in how much duration? Like suppose I'm talking to you and suddenly I hold my head and I say oh I can't take this session again. If headache worsens within 5 minutes like 5 minutes ago I was okay but if within 5 minutes my headache becomes so severe that I just hold my head and I say oh sorry doctor I can't take it I don't know what is going on I'm having the worst headache of my life that is what you mean by the word thundercluff headache. So it is like yeah it's a range at least 60 seconds to 5 minutes. It starts within 1 minute peaks like you know I'm talking to you suddenly I hold mad and then like I I stop talking to you and after 5 minutes you are asking me what happened what happened and you are saying Right like that I'm I'm like no man just don't ask me anything just take me to the hospital like something like that right so it starts within 1 minute peaks by 5 minutes that is like the thunderclub headache uh sangeita nicardine is to be answered for hypertensive crisis like if I say patient is having hypertensive crisis the definition of crisis is with target organ damage like hemorrhagic stroke is stroke in hemorrhic stroke and iskeemic stroke the cutffs are different for hemorrhic 220 by 130 is when we intervene at Iske token is 185 by 110 that I'll discuss in my subsequent slides. Nicardipin is for hypertensive crisis and in subre hemorrhage it is neoin to be answered. I hope that solves the query. Okay, moving to the next question. This lady fell in the bathroom and she had a lucid interval. I mean she developed unconsciousness then she became conscious and you know consciousness between two periods of unconsciousness in a sense that this lady is now becoming forgetful drowsy and now waking not waking up after 7 days the non-contraity head is given in this case the answer in this case would be given as yes answer would be given as acute subdural hemorrhage on the right hand side in this case you can notice this is left and this is right and you can notice the concave or convex bleed which is present in this case. This would be an acute subdual hemorrhage in this patient. Let us compare this with the next image. Same question but in this particular case you are noticing that the area has become black. The area has become black. So the answer in this patient would be given as chronic subdural hemorrhage. Tell me the treatment of choice for chronic subdural hemorrhage. The area is appearing black. So we calling it chronic subdural lamage. Yeah. Bridging vein rupture. Tell me the treatment of choice for chronic subdural hemorrhage. You want me to give option. Cranotomy bhole surgery between the two. Yes. For chronic subdural hemorrhage. They have asked what will be the treatment that would be done. Your answer would be given as burl surgery would be done in this case for chronic subdural hemorrhage. In acute subdural hemorrhage we might require a cranottomy in a patient depending on the intracurren hemorrhage score in a patient. And then is the standard question. Yes. Very good. Very good. A 25year-old guy had a road traffic accident. His GCS is low. The non-contrast city head is shown. I'll zoom into the city head. You can see this punctuate bleeds. You can see this punctuate bleeds at the junction of the gray matter and the white matter. Yes. Okay. Options are traumatic external injury, diffuse external injury, cerebral contusion, extra dural hemorrhage. Select between one. Chromatic external injury, diffuse external injury, contusion and extra dural hemorrhage. Yes, the correct answer is diffuse exonal injury. If you are able to see four or more than four punctuate bleeds, If you are able to see four or more than four punctuate bleeds at the junction of the gray matter and the white matter, that's important. The bleeds are present at the gray and the white matter interface. Then you are going to be saying that this is diffused exal injury. uh there's a possibility that the CT scan in this patient can be normal also because if the bleeds are going to be very very small in size then your answer would be given as traumatic external injury any patient with road traffic accident who would be having yes normal city that is what I'm trying to say if the patient is having a normal CT scan then we'll call it a traumatic external injury if we can see the bleeds then it is a then it is going to be called as a diffused external injury if the bleeds are very small the CT will be normal which is why he will also ask you the investigation choice for traumatic external injury. You can tell me what type of MRI will be done here. Investigation choice for traumatic external injury. Okay. Diffusion weighted MRI. Yes. Susceptibility weighted MRI. SWMR. It would be S SWMR. Investigational choice for traumatic exone injury would be answered as susceptibility weighted MRI. Uh there are two possibilities in a question. One can be CTS can can be normal or they can be visible bleeds also present depending on the situation the answer would be given and the guy would be having a progressive deterioration and it is conservative management that would be done in this case. Next is the case of extra dural hemorrhage where you can see that bleed present very very classical uh diagnosis is anyway mentioned can you tell me the treatment of choice okay options in this case are bar hole then is a cranotomy yes waiting for answers cranottomy with lation of the bleeder. In emergency scenario, we can do a bar hole in this case. But the treatment of choice in this patient would be answered as cranotomy with legation of the bleeder. It would be a decompressive hemictomy that would be done along with lation of the bleeder would be done for management of this patient of EDH which is a very straightforward scenario where the bleed would be occurring from the middle maninja artery. Okay, very good. Very good. Uh, moving to the next one. A 55year-old lady with hypertension develops a sudden onset face and arm and leg weakness for past 3 hours. Uh, this is a pure motor stroke that I'm describing. In pure motor strokes, usually the area that is involved is also beginning with P. That is going to be a posterior limb of the internal capsule that would be involved. Yes guys the diagnosis in this condition would be given by you as intracerebral hemorrhage the case scenario that is given to you is ach it is a intra cerebral hemorrhage in this particular case it is in this patient that the BP of this patient would be elevated the person would have gone into hypertensive crisis in hypertensive crisis the BP can be as high as 220 by 120 mm of mercury along with this target organ damage would be present. There can be two questioners that can be asked to you. What is what is the target BP to be attained? Can you have quick comments in the chat box? What is what is going to be yeah the leading cause of this is hypertensive crisis. What is the target BP to be attained? The drug that will be used I think somebody asked me where will we use nicardipine. This is where we are using nicardipene in the patient. Yes. The target BP in this patient would be less than 140 by 90. This has been asked in inert as well as in the FMG exam. The target BP in patient who's having a intraable hemorrhage would be kept at less than 140 by 90. The drug that will be used in this patient would be Nicaripin so that I am able to control the blood pressure of this patient and this was a pure motor stroke where the posterior limb of the internal capsule that would be damaged. Usually what is the blood vessel that will be damaged here are the small blood vessels. If he says what is the blood vessel? No sir, it is not first hour. It is 24 hours. It is It is first 24 hours. It's not first hour. It is the penetrating branches. It is the penetrating branches. No, it Yeah. Yeah. You write lenticular key branches will be affected. So it is penetrating branches of the lenticular artery. I want to bring to your attention. It is not the artery that will burst. It is the ch branches of the artery that will burst. So it is the chart sort of penetrating branches of the lenticular straight artery that would be bursting in this case and the most common site for this would be like the putamin the usual blood vessel that is affected in this patient is the middle ceral artery circulation. So hypertensive crisis uh it is mainly going to be like uh the trigger for development of this scenario of intra ventricular intra cerebral hemorrhage in a patient along with this there can be some extension into the brain also. So intraventricular can occur but this bleed that has been shown is the typical intraarimal bleeding or intraerbal hemorrhage that is occurring in this patient. Absolutely. It's not the middle cereal artery as I'm clarifying it is the chota branches M1 segment of middle cerebal artery lenticular straight artery lenticular branches they are the ones which would be affected. Okay. So I had a good interesting question coming up here mention there is a possibility that he can mention atrial fibrillation patient is having warfare toxicity and that is causing a brain hemorrhage in a person. So what is the antidote for warfarein toxicity causing a brain hemorrhage? Yes it is same as hemorrhic stroke doctor. It is same as hemorrhic stroke. I mean hemorrhic stroke is a term that I'll be using for like uh uh to explain to a non-medical person. hemorrhage but the technical word is the sight of bleeding that would be intraible hemorrhage but your point is spot on I mean hemorrhagic stroke intraable hemorrhage MCQ okay yes yes yes yes it is warfarein toxicity with brain hemorrhage what we will be giving is a prothroine complex concentrate and along with this we'll be giving is vitamin K to the patient but we'll not be giving fresh frozen plasma it is pre prothroine complex concentrate then for aixab band toxicity with the intracal hemorrhage the antidote that you'll be given is yes thank you Dr. Rosema quick comments a pixab band toxicity yes and dictionixon at alpha so lots of time like he might trying to mix it up the data that he's giving you he can be mixing it up with a bit of pharmacology and uh the next one I'm saying verbally only like mapap that's used for dabigatran based toxicity so I mean they can test your pharmacology there and you guys are anyway aware of that okay fine moving ahead Okay. Yes. Ishkemic is Yes. Yes. Yes. Yes. Yes. Yes. Uh doctor in ishkeemic stroke no he will usually ask you regarding the cut off for starting thrombolysis that is 185 by uh like okay I'll just write it because AIS will come up subsequently. You see AIS you have to you use tenectas. You are now aware the tenetas is FDA approved now or we can be using LTAS. The usage of this is contraindicated. If the BP is more than 185 by 110 mm of mercury. So my immediate goal in iskeemic stroke question will be that I need to keep a BP less than this. I can get like 180 by 100. I can get like 170 by 100. In acute eskeemic stroke in immediate basis what you're supposed to do is ensure that your BP is less than this particular value. In a stroke earlier there was lot of concern regarding lowering of BP because they said it will worsen the brain infection. But now he says if you don't lower the BP there they will be rebaded. So now they decided okay decrease it over next 24 hours to less than 140 the target but in AIS we keep it to like because of the risk of rebuilding and hemorrhagic stroke less than 140. Here it is 185 that I would like to obtain. Okay. Uh this patient is having piogenic menitis. How do I know piogenic? Because there are neutrfils present with low sugar. And the empirical treatment for piogenic menitis is always septraxin with vancomy. The correct answer for this uh no no it will not be empellin because if it was like a alcoholic patient or if the question was mentioning regarding a child here like there's no age group given so we'll take it to be an adult patient and the standard treatment for piogenic menagitis is septtoxin with mangy and empin is only to be asked for lististeria cytogens and in which age group listia is present then lististeria is common in neon units it is present after 55 years of age. It is common in those patients where the immunity is less or he mentions alcoholic. In all MCQs of piogenic menitis if it is neonate age more than 55 cell metered immunity is lesser or alcoholic then it is lististeria. That is when aine comes in otherwise like for standard treatment it is mainly going to be answered as septuxin plus venkcomy. The next question is also very simple and is a repeat one. lymphocitic pleiocytosis with uh uh case of cryptocal menitis in cryptocal menitis one that you have to give I mean treatment at the moment and then you have to start antiretroviral therapy this antiretroviral therapy is to be started subsequently after like the CD4 count of this patient has tend to increase the CD4 count of the patient should be more than 100 like you you have to give prophylaxis in this patient and subsequently when the CD4 for count is more than 100 for at least more than in fact more than 150 for more than 3 months that is when we can be starting anti-retroviral therapy in this patient prior to that it is prophylaxis that would be given for this patient uh yes the main treatment for this patient would be liposomaal amphotarin B plus flu cytosine and then later we give fluconazole guys the answer is not C I mean I think this was the easy question it is first liposal amphotin B And then we give fluonazole for these patients and later on antiretroviral therapy should be given for these patients only when the CD4 count of the patient is elevated. So first we have to treat this patient and then subsequently why don't we because they don't cross the bloodb brain barrier doctor amoglycosytes have limited penetration into the bloodb brain barrier. So that is why we give septra which has a third generation sephalosphorus they have a good penetration into the bloodb brain barrier. If the CD count is less then we'll have to you know only later later after it is more than like this particular value then we we will have to intervene. Okay, quick inputs here with respect to the flowchart. Okay, pankage uh I think uh I have again addressed that in my rapid region. I'll try to do this in this video also. Okay, drug choice is not fluconazoo man drug choice is not fluconazoo. It is liposomaal amphottoin B with flu five flu cytosine and then for prevention subsequently this is given for 2 weeks and then subsequently for 8 weeks we'll be giving and anyway like because they ask about it no if patient is having TB and uh you have to start anti-retroviral therapy subsequently like TB with AIDS then uh in patient of tuberculosis with HIV first AT is anyway to be given and after 2 weeks it is anti retroviral therapy to be given but if he mentions the word HIV with tubercular menitis then we will have to start anti-retroviral therapy after a gap of 4 to 8 weeks yes the reverse can happen reverse can happen if it is tubercular menitis given in a question if it is tubercular menitis given in those circumstances the answer for starting the anti-retroviral therapy would be delayed in a patient. If the reversal is done, then it is obviously the risk of iris which has been asked multiple times. Immune reconstitution inflammatory syndrome yes upper limit of 8 weeks. Upper limit we have to answer. If suppose 4 weeks is also given and 8 weeks is also given then we will answer it at 8 weeks because I don't want to take a chance now symptoms tubercular menitis and anyway TB menitis is slow to respond to treatment also so if at least four weeks also given and 8 weeks also given then mark it as 8 weeks per say that is primarily to minimize the chances of minimize the chances of iris in a patient the final summary is decrease the risk of immune reconstitution inflammatory syndrome okay as far as findings of menitis are concerned in a patient. Normal cells would be anywhere between 0 to four 0 to 5 cells. Uh sugar would be 2/3 of the whatever is the blood sugar and the proteins would be in a range of 15 to 45 mg%. The opening pressure will be between 50 to 180 uh cm of water and if it is acute bactenitis then I'm going to be having neutrfils which are usually going to be like thousands to 10,000 neutrfils present. Uh the blood sugar in this patient will be less that is less than 0.6. Six proteins will be elevated, opening pressure will be elevated and the color of the CSA will be usually turbid. Never use color for diagnosis. Turbid or cloudy it does not matter. It is never useful for diagnosis. It is mainly the cells that would be used for polymorph nuclear cells. But in tubercul menitis you will mainly be having like mainly lymphocytes present. It is like lymphocytic piocytosis that would be seen in this case or he might give values also like he may say 80% lymphocytes 20% polymorphuclear cells whereas the situation would be reversed for the superior diagram in this particular case also sugar will be less but the only time the CSF sugar can be zero only time the CSF sugar can be zero can be acute bal menitis that is hypoglychia hypoglycoria so CSF sugar can be zero CSF sugar can be zero only in patients of acute viral menitis. The proteins in this case would be elevated anyway. They would be super elevated. So they can form a clot in the test tube that's what we call as a cop webagulum. The opening pressure would be elevated and the color in this particular case can either be strong or you can mention cloudy. As I've explained color is never to be useful for diagnosis of acute bacterial versus tubercular menitis. In viral menitis also we can be having 100 lymphocytes present. But in this particular case what you will notice is very characteristically thath it is the sugar in the CSF that would be normal but the proteins in this case would be elevated. The history would be short in this case and the color of the CSF in this particular case can be clear or it can still be like turbid in some cases it can be clear it can be turbid like I said color is never to be used for diagnosis. So in viral menitis it will always be a short history. In tubacular menitis it will usually be a malnourished individual. Usually you'll talk about a malnourished child and there would be a long-standing history given usually like the history will be over weeks or maybe over months as well. But in menitis the history will be always over a couple of days never like going into weeks altogether. But if we they give you a report in which everything is normal normal and only the proteins are elevated. If they give you a report where everything is normal normal and only the proteins are elevated then it would be gulen bar syndrome about which I'll talk about in the later part of the discussion where intravenous immigrins would be used. Bulan bar syndrome is usually asked with respect to the following situations. Either it is going to be like it happened in Pune. It can be compil as the risk factor or it can be E.oli or it can be hepatitis E virus or like it happened in Maharashtra that is Zika virus previously. So Gujarat sorry Zika virus compilacto jun e.oli coli hepatitis E virus or Zika virus are the triggers for developing the bulimar syndrome where we use brighten criteria for diagnosis and the discussion of that Brighton criteria would be like taken up subsequently then is subreact hemorrhage in subract hemorrhage you will notice RBC's in the CSF we don't have RBC's in the CSF in any other condition except for the condition that we're discussing at the moment the pressure can be elevated but uh yeah bloody CSF can be written here so as such nowadays we don't do lumbar puncture for diagnosis of subreant hemorrhage but just for the sake of completion in patients after 24 hours you might be having a yellow tinge to the CSF and this yellow tinge to the CSF is what is called as zanthromic CSF though for this is only for academic reasons because in subord hemorrhage it is straight away invasive cerebal angography that should be done in the patient subsequently okay then is the standard images one you can notice this cobweb coagulum and you can notice the green You can notice the bluish stain, bluish stain with the reddish bacteria that is the red baseli can be seen in the background. So I know that I'm dealing with a case of tubacular menitis where for management purposes I'll be using antitubercular treatment for 1 year and along with this we'll be using steroids that is dexona or dexamethasone will be given for 6 weeks. The reason why we give steroids is to reduce the cerebal edema component. But if you look at the right image you can notice uh uh I can say turbid CSF and then you can see in the gram stain in the gram stain you can see these blue blue dots these blue dots are two two right in in groups of two. So this is a diplocus this is a gram positive diplocus. So because it is a gram positive diplocus I can mention this as the answer is numocco focus but suppose these images were reddish if these images were not like uh I can say like on comparison mode I don't have a appropriate color for ground stain for gram negative so I'm using a red color but if it was gram negative and it was a diplocus then I would have thought in terms of niceria menitrais so I don't have appropriate colors of the ground stain so I'm just saying blue versus red but what I'm trying to emphasize before you is that if it is going to be bluish bluish appearance then it is pneumocus if it's going to be reddish it is nicer menitis both are diplopus and this would be a presentation with respect to piogenic menitis the leading cause of this anyway is numokus but if he mentions a rash if he mentions thrombocytoenia he talks about pika he talks about perpura then in those circumstances if pika and papura are given in a cost water fitton is given then again nera menita disc is which to be answered. Okay. Uh next is a question for you guys since you've been silent. Uh some guys are commenting but still like this is the pelvic crest. This is the pelvic this is the uh I mean the pelvis of the patient. So what I'm doing is that I'm using the peak of the iliac crest. This is the iliac crest and I'm drawing a line. I'm drawing a line so that I can reach L3 L4 space. Tell me the name of this line which is connecting the pelvic which is connecting the iliac crest of the patient. I mean you draw imaginary line like uh I'll just do do this activity once again. Uh you can see that this is the pelvis of the patient. I'm talking about iliac crest. So iliac crest is the reference. Iliac crest is the reference. And then I'm drawing a line which is connecting and is bicting L3 L4. So this line is the one that is called as two fears line. This line that I'm mentioning at the moment before you is called as Tofu's line. This Tufier's line would help you identify L3 L4. The interspace between L3 L4 below this is L4 L5. So to how to identify L3, L4 is the Tofier's line and that helps you basically determine the the location and then subsequently like you can do lumbar puncture. Uh the first needle that you can see here, you can comment in the chat box what is the name of the initial needle like this needle which is having a cutting edge which is more sharp right. This is called as quinkage needle. And the second one that you can see yes would be called as spot needle. That would be a traumatic needle. Using u these needles I can be managing the post lumbar puncture headache relatively. Please comment in the chat box. What is the drug of choice for post lumbar puncture headache? Post dural puncture headache. PDPH drug of choice for management of postdual puncture headache. Yes, IV caffeine. IV caffeine is the drug of choice for management of postdual puncture headache. Very good. Very good. Yeah, we we'll do conservative that's okay. But the drug of choice for this condition is caffeine basically and that can be given uh introvenously or it can be given orally also orally in the form of hot drinks etc. Though the last resort we can do in these patients is we can also give a blood patch where we will inject patient's own blood into the same inter uh into the same intervertebral space so as to seal the tear in the durometer of this patient. So low volume blood patch low volume blood patch can also be used in this patient as a last resort but the single best answer for this would be intravenous caffeine to be used. Then is that classical star sky appearance that you can see and you can also notice that rice grain calcification. This that you can see is the cystic circ. This is the rice grain calcification that is present. You can see the stis sky appearance multiple hypoense lesions with the eccentric white dot that is the skollex. You can see the skollex in the periphery where the arrow is present. Uh yeah this is not caused by eating pork. As you know the main route of transmission of this would be fural consumption. It is foral consumption. Fioral root of transmission. It is not pork that is responsible. It is fural that is mainly root of transmission. And yes cycosis salosis the larvae that will be hatching in this patient. Question in the paper said how would you differentiate whether it is tuberculoma or whether it is neuroscyosis lesions. So the test that can be done is magnetic resonance spectroscopy. A magnetic resonance spectroscopy shows a lipid peak. Then it goes in favor of diagnosis as a tuberculoma which is a differential diagnosis of neuroscystic curcosis. The investigation to be done is MR spectroscopy. If he says what is the first test to be done in a patient? The initial test to be done for identification of neuroscycosis. than the initial test in neuroscysteic cycosis we will be having a amino acid peak and in cases of tuberculoma there would be a lipid peak present the first test that we'll be doing in this patient is a CSF imolot for neuroscystic surfoses antigens that's the initial test that would be done if he says what is the imaging modality of choice for this condition then our answer would be given as gadolenium enhanced MRI yes amino acid peak and neuroscyis processes you are right doctor spot on then it is a gadolinium enhanced MRI that will be used and imaging to differentiate from a tuberculoma is magnetic resonance spectroscopy we'll do a fundus examination for subretinal cystic circa and to rule out papadema component in this patient in fact biopsy is an absolute criteria for diagnosis of this condition biopsy like if he says absolute criteria for diagnosis then it is mainly a biopsy or it is fund showing subretinal cyic circa like he can give you multiple correct options there. Biopsy is one or fund showing subretinal cystic circa or like absolute criteria for diagnosis of neurocytosis. They've also asked for management of this patient. So we will not start with elendazone. We'll start dexamethasone in these patients to decrease the vasogenic cerebral edema. After about 40 to 72 hours when the swelling in the brain will come down that is when this patient will be started on elendazone. It is albendazole that is the subsequent drug that would be started for management of this patient and uh subsequently like antipalyptic drugs would be started in these patients also that would be like sodium valperate and antiptic drugs may be continued in these patients for minimum 2 years so that we can handle these patients relatively better. uh that's to prevent the recurrence of seizures in these patients also. Yes. And subsequently dexamethasone would be used. So great guys neuroscysteicis was a good one. As far as acute eskeemic stroke is concerned I just want to bring to your attention that in acute eskeemic stroke you might be able to pick up this very classical finding. Please comment in the chat box. We have carbomasopene for focal seizures. Uh can you tell me the radological finding that is shown before you at the moment? This one that I'm showing that big clot that is present. Yes. Dense MCI. This is the initial finding that would be seen with acute schemic stroke. Then in the subsequent part what you will get is loss of gray matter and white matter differentiation like the gray and the white matter can be seen on a CT scan differently but then the differentiation part would be lost and subsequently in this patient there would be a development of yes I can pick up that hypo density in my screen also. Yes, here this is the hypodensity that would be developing though that hypodensity will be taking some time to occur. The hypodensity will take like approximately 6 hours to appear. So there's a possibility that the CT scan can be normal also. The clinical presentation in this case will be classical like diabetics patient uh patient diabetes and hypertension patient is having a sudden onset face deviation and arm weakness for the last 3 hours and a dense MCS sign is present. The investigational choice in this condition would be a non-contra city head but because CT head in the patient can be normal also. If the patient will come early the CT scan will be normal. So in those circumstances early detection of acute eskeemic stroke. Early detection of acute eskeemic stroke can be done with help of diffusion weighted MRI. The most common cause for acute eskeemic stroke is atrial fibrillation that is nonvalular atrial fibrillation. Very good. CT scan is done primarily because you want to rule out allergic stroke. The window period for management of stroke would be 6 hours. A large number of questions will be testing your knowledge with respect to acute stroke consultation. So always answer first for assessing of airway. It is ABC. It is airway BP and it is not breathing. It is airway blood pressure and clearly establish the time the last patient was seen normal because you want to establish the window period with respect to management. You want to establish the window period with respect to management guys. It is ABC it is airway then it is blood pressure checking because thrombolyis is contraindicated. If the systolic BP is more than 185 by 110. If the BP is higher than this, I'll try to lower it. Like in a stroke, the threshold was 220 by 130. Here the intervention would be at 185. And the NIHSS score value should be more than five. Then the person is eligible for endovvascular therapy or it is uh treatment with thrombolysis with IVPA or tactus any of the drugs can be used. LTSUS or tenactus can be used. The final summary is within 6 hours a patient will come. Though in the revised guidelines they are saying in all cases of large vessel stroke we should be going ahead with the endovvascular endovvascular therapy that is straight away remove the clot from the brain blood vessel but uh for the first 6 hours in a case of acute eskeemic strobe in TIA we do not thrombolize doctor in the TIA we do not do thrombolysis in the first 6 hours what we do in the patient is we have to thrombolize so in this patient like uh what the drug that can be used is like elaps or tactless as a molecule can be used. The objective is LTA place should be started within 6 hours. After giving LTA, CT andography can be repeated. CT andography can be done. The CT andography is to check for whether the patient is having a improvement or whether is not improving. So I mean CT andography can be done to confirm the resolution updated. It is city andography that should be done. It is so if it is yeah you can give I can use or can be used in a patient CT andography will help me in confir confirming the resolution in this particular case. A patient comes within 16 to 6 to 24 hours then it is throbectomy that would be done. The test to be done before this would be CT perfusion studies and if it shows perusion. If CT perfusion shows a adequate perfusion then it is mechanical throctomy that would be done in a patient. This throctomy can be written as EVT that is endovvascular therapy. In endovvascular therapy tima improvement occurs in 1 hour. TIA upper limit is 24 hours. TI resolution resolution usually starts. Transient is attack will not wait for 24 hours. Transient is attack is set to be transient. Upper limit is complete resolution occurs in 24 hours. It may take for 36 hours also. It is not a guarantee that 24 hours. It may take 36 hours. If I'm having weakness in my hand, I might it's not a guarantee now that only after 24 hours the weakness will completely resolve. I might say at 24 hours 80% improvement 36 I may say 100% improvement but resolution starts within 1 hour in a patient of stroke there will be no improvement it is always a progressive deterioration so TIA is a cut off for 24 hours that's an artificial value stroke improvement would have started within 1 hour Streptokinus is not used doctor for this and the cost difference is very huge. Streptokinus is used in myioardial inffection where here we don't use streptokinus. They're not FDA approved. There is only two eldas and tan plus for management of this patient. So what we need to do in this patient is mainly handle the treatment that is CT per profusion studies would be done and can we do a CT angography before in a patient then yeah we can be doing like suppose non-contrast CT scan of the patient is normal as a CT scan normal CT andography facility available I can be doing the CT angography before and after also no I can do a CT because CT andography will help me identify a large vessel occlusion LBU. So I can be doing a CTNography before if facility is available before giving Laplace and after giving LTA plus to the patient that is to see whether there is a success that as I have obtained or not. By success I mean that there would be a reperfusion that is occurring in this patient. So the message here is that CT andography can be done before doing a thrombolyis and after doing a thrombolyis to check for whether the patient has improved or not. contrast induced nephropathy contrast induced nephropathy to reversibleization even if I get a CIN and a contrast induced nephropathy I can still manage it right and I can use a lesser amount of dose that can be used in a patient so most of the time the EGFR of patient can be calculated and based on that the amount of dye that we can be giving to this patient can be relatively low. If the blockage is in the small branches then how can we do endovvascular therapy. Yeah. Yeah. Yeah. Exactly. If it is going to be endovvascular therapy will not work in cases of that is why no CT that is why I was saying a CTP to be done to demonstrate favorable perusion. If it is small vessel stroke, if it is a small vessel stroke and patient comes after 6 hours, then you cannot do a throbo throctomy with throbectomy is only possible for large vessel occlusion. That is why I mentioned that CT perfusion study would let me know whether it is beneficial to the patient or not. I would not like to waste my uh energy on doing a throctomy in a patient who is having clots in the smaller smaller total blood vessels then it will not be working. So Manish, I hope that resolves your query that throctomy is not going to work for small vessel stroke. But if I'm already done a CTA and CTP in a patient then I can see now whether I should be using the resource or not right the learning from this is when should you fire is based on the interpretations that I'm mentioning at the moment before you for within the first 6 hours and 6 to 24 hours for venus clot it is uh if it is venus clot then the finding will be different now then it is heperin that would be used to venus clot antifphospholipid antibbody syndrome mutation connect a question is given on connective tissue disorder antifphospholipid antibody syndrome SL patient factor 5 len mutation and he says patient subsequently CT scan to empty delta feature empty delta sign that is partical vein thrombosis in that cerebral vein thrombosis is ideally we should now be doing is a MR veinography in these patients. If it is empty delta sign in vertical vein thrombosis I should be doing a MR vein and uh MR magnetic resonance venography and then subsequently for management of these patients what we will be using is heperin or we can be using inoxiparin to a patient. So this is management of venus troa this that I mentioned is management of venus stroke where we will be doing a MR venography in a patient. So I think uh Dr. Bershiker your query is sorted. I mean this is a question in the paper where he mentioned a lady with bett disease I think and she has said because bettas arteries involvit they involve only the arteries but one vasculitis that involves arteries also and veins also is bett disease or it's going to be antifospholipid antibody syndrome that is where we will be using heperin for this patient. So I hope Dr. the query of yours is sorted. But this was an interesting discussion guys. I mean this is half a page only but we have concise the information into a very logical reasonable step that would be done. CT scan is normal. Next best investigation next to be done to intervention. If he says what is intervention to be done the intervention is obviously but he says what imaging can be done subsequently if CT scan is normal then I can do a CT angography to demonstrate the presence of large vessel occlusion in a patient. MIT it is like only treat aspirin and statin already suppose somebody in your relative is already had a heart attack and they say what can we keep at home it is chewable aspirin and it is a tova statin that can be kept at home that 80 milligram sata statin and aspirin that 325 mg and that can help you in managing the patient more effectively. It is aspirin in the pocket already. So it is advisable to give nitrates in the hospital only case to like I said don't give a device for nitrogen regularly or aspirin before as soon as the patient reaches the hospital Okay. You cannot explain the technical ifs and the buts there. Okay guys. Okay. Now we will study the contraindications for thrombolysis. Now we will study regarding contraindications to thrombolyis which are always asked in the exam. So how to remember them? You can practice with me. The pneumonic for this is storm. You can write this with me in case you are like you know at the moment in your room and you're listening to me at the moment. Right? Storm is the pneummonic right? So it would be sustained BP elevation despite treatment. Mark my words there. sustained BP elevation despite treatment. Guys, if the BP is more than 185 by 110 despite treatment, that is when you are going to be uh not doing thrombolyis in a patient and what you can do is like uh endovval therapy or a throctomy in that particular case. Then is bleeding diiathesis. If a person is having a tendency for bleeding, so T alphabet is for bleeding dithesis. A alphabet is for bleeding diiathesis guys. That's the important aspect to remember. O is for gastrointestinal bleeding. G O is for gastrointestinal bleeding like he had a peptic ulcer bleeding 21 days ago or within the previous 3 weeks if he's had a GI bleeding then I would not like to ensure like treatment GI bleeding will start again in the patient. Yes, this is INR. Very good pointer. INR more than 1.7 I I'm doing the practice of making it right writing it before you that is next point is like I don't think so anybody mistakes because recent head injury means bleeding or intracerable hemorrhage also means bleeding so that can be sold out and then can be recent myioardial infection also for recent major surgery however you need to remember 14 days for GI bleeding you need to remember this would be uh 21 days so try to remember at least one of them storm is a pneummonic that helps you rule out the contraindications for thrombolyis and lot of questions would be having these contra indications also that you need to remember so and this is a diagram that is showing regarding that evvascular therapy that I was talking about somebody was asking regarding ABCD2 score so we'll do that also in ABCD2 score guys we will be using it I mean why the question in any set was why do you use ABCD2 score so ABCD2 score is primarily used to basically evaluate the future risk or development of stroke in an individual. ABCD2 score is used to calculate percentage of chances. Very good. Very good. It is used to calculate the percentage of chances of stroke occurrence in a patient. Alphabet A would be standing for age more than 60 years. B is for blood pressure more than once 140 by 90. Then is clinical features of unilateral weakness which is given two points. Remember that duration D more than 60 minutes is two points. If it is lesser than that then the chances of resolution will be more and why we call it D2 is because duration is also there and diabetes valitis is also there. So age BP clinical feature duration and diabetes is the ABCD2 score that we use for evaluation of these patients and it is used to calculate the percentage of chances of stroke in a patient and in all cases of TIA what is the treatment that we'll be giving to the patient on a immediate basis it is aspirin and tova starting to inatient but based on ecoardigraphy report ecoardigraphy may person left atal appendage may clots in left atrial appendage there is clots present then any of the two treatments would be started that is a pixaban or warfarerin. If it is non-valvular atrial fibrillation then it is a pixaban. If it is valvular atrial fibrillation it is barferin that would be used. So these are like a that are used for management of transient eskeemic attack asprain aturvastin and a pixaban and depending on the situation you might have to answer this accordingly. The highest chances of transient eskeemic attack getting converted into stroke is 48 hours. Mark my words there. Usually improvement stroke improvement improvement first improvement improvement first start. If he says what is the cut off for transit HK attack it is 24 hours. And if he says chances of conversion into stroke are highest in then answer is 48 hours. Three values to be remembered. 1 hour, 24 hour and 48 hours. Spontaneous improvement begins within usually first hour. What is the cutff with which the symptoms will improve substantially? 24. It can be 26 also. It can be 28 also. I like suppose somebody had weakness in the hand. Then that weakness can improve by 90% in like 24 hours and maybe by 28 hours it will be 95% and maybe at 36 hours it can be 100%. So this is just a artificial cutff. Don't answer on the basis of whether if symptoms are worsening it is stroke. If symptoms are persisting it is it is it is stroke. If they're worsening they're persisting it is stroke. If they're improving it is transient. This was a FMG exam question. He said patients symptoms improved over 36 hours. 24 patient can improve not a stroke patient patient improved gradually over next 36 hours and what is the diagnosis of the patient most people answered it as cardioism or stroke no guys if improvement is occurring it has to be transit attack it is not a guarantee now improvement will occur at 24 hours It can be gradual gradual gradual and then subsequently the improvement will peak in a patient concept it is mainly TIA and stroke differentiation that are used. No. Okay. Fine. Fine. Uh mortality chances doctor in AIS the chances of mortality will be less. In hemorrhic stroke the mortality is higher that is mainly because of the fact that the blood pressure has not been controlled adequately and now like we are aggressively managing blood pressure. So chances of survival will very much be there. Venus stroke has excellent prognosis like in women with connective tissue disorder. Venus stroke excellent prognosis with complete functional recovery can be seen. Acute schemic stroke again improvement will occur. If you are going to do thrombolyis or mercy or throbectomy in a patient in the limited time frame. Hemorrhagic stroke has a bad prognosis especially if it is lower down. Cerebellum brain stem area bleed then bad prognosis. Low bar hemorrhage still chances of survival would be much more. uh 24 hours doctor in eskeemic stroke it is not initially like because we're doing thrombolyis now so initially after 24 hours like I think this was a question again when can you start aspirin in a patient of schemic stroke it is after 24 hours initially like because I've given thrombolyis so I would not like to give anticlants to the patient 530 session question easy question yes guys I want everybody to hit the comment box irrespective whatever is your status. Blood sugar mine is also low but I'll gradually bring it back exam. Yes guys time guys five would be too early I think 5:30. Okay. Caesars in a patient more than 5 minutes in a patient or JTCS. Yes guys quick answers random fast firing guys. What is the drug of choice in this particular case? Anika was the first one to hit the trigger. Yes, guys. Remaining people, I'm still waiting for the chat to come up. Yes. Yes. Anuman, I love the spirit. I love the spirit, man. Yes. Here the answer would be given as ivorazzipam because this is a case of GCSE. So we will not be answering it as valorate. It is ivorazzipam that would be given in this patient or we can give daopam also. For focal Caesars it is carbameopine ketone Caesars is sodium valporate. Keep commenting guys keep commenting. I want you to keep on hitting the comment button for all the drug drugs and type faster than writing that I am doing. Valporate is the common answer for for GTCS myoconic scissors atonic scissors and focal scissors is carbopine. For focal caesars I'll go into two. Okay. So I hope everybody has done the commenting till Valperate. What is the best drug for prevention of fibrillas? Options are oral daipom, rectal desapam. Quickly answer prevention, prevention is to be answered. What is the best drug? One is uh oral daipom. Second is rectal daipom to be given. Quick answers please. Okay. For prevention it is oral. It is not it is not rectile. It is oral daipop that is to be given. Ideally the answer would be given as oral globosm. In lot of pharmacology MCQs that oral globosome is not given then your answer would be given as oral daipopam. And if he says how do you treat the episode then it is rectal daisop but then rectal can be a little messy. So it is intraasal midazzylm. It is intraasal medazolum that would be used otherwise it is rectal daoparm that would be used. Yes. Yes. Rectal in episode. Absolutely. Absolutely. You guys are getting it right. Okay. Da choice for absent caesars would be answered as ethosimite especially considering that this would be seen in babies where the special EEG finding would be three per second spike and slowway pattern. Quick comments in the chat box. In which condition in the EEG do you get four to six Hz poly spike pattern? In which condition do you get periodic sharp wave complexes in the EEG? In which condition would you be getting? Keep on commenting. Keep on commenting guys. I'll I'll keep on giving the answers. Periodic lateralized epileptic form discharge blood periodic lateralized epileptic form discharges then is red maker complex waiting for answers grade. Four to six hertz is juvenile myoconic epilepsy which is also called as Jan syndrome where there can be future conversion to GTCS. Periodic sharp complexes would be seen with variant crutile jackup disease. Periodic lateralized epileptify form discharges would be seen with herpes simplex encphilitis where we use empirical asyclloe for management. Raid maker complex is used for raid maker. Okay. Sanscar was there to answer SSP that is subaccute sclerosing pan and sephilitis. I've just tried to summarize a couple of important EEG findings that can be present including the word triphysic waves. Yes guys, triphasic waves please. Conditions where you read triphysic waves in EEG wetting triphysic waves. Yes. Hippatic anphopathy. Second answer please. Apart from apatic encphilopathy, we also get it in variant fruits jackup disease. The last entry here is the most peculiar one where we get a grossly chaotic pattern which is called as hips arhythmia because traditionally the word arythmia rhymes with cardiology. But if I say the word hips arhythmia, I'll write that once again. If I say the word hips arhythmia then that would be for salam caesars that is also called as west syndrome in which we use act and we use vigrain for management of the patient. I had excellent responses from you guys. So just keep it up and keep the spirit up. I mean this is what I want quick answers for the common scenarios that we have uh quickly revised here for the epilepsy component. Uh we will look at Maestra Graves. I think everybody knows Amitab Bachan legend right Amitab Bachan in 1982 was shooting for that movie Kohi when he got hurt and he had required emergency surgery and he got infected blood transfusion and later on it was detected that he was having hepatitis B I mean the diagnosis was made when we had like he had 50% liver damage 50% liver damage so Amitab Bachan sir legend that he is bon he did not hide his hepatitis B status he let people be knowing it and that is why Amitab Bachan was made the global ambassador for uh goodwill ambassador for heperitis B foundation. So one Hammitab Bachan I mean he's like 85 plus I think at the moment and he's still recording still shooting I mean hats off to his dedication he does like shows you know for 3 and a half hours 4 hours stuff like that right but then Aab Bachan he had hepatitis B uh then he I mean his liver was damaged because of it and though I mean he hypotitis B is self-containing but it can cause liver damage and then uh even like masta gravis [Laughter] No, let's not uh let's not say that. I wish like legend to legend. Okay. G So Ma Gravis will be having uh all the D's coming up and the screening test for this condition would be answered as ice pack test anti ice pack test is the screening test for this condition. The investigation choice for this answer would be single fiber electromyioraphy. It is a SFMG. Apart from anti-acetylcoline receptor antibbody, it is anti- musk antibody elon muscula anti and then anti-lrp. Three antibodies that I would like you to remember for this condition. The most specific one is anti-acetylcoline receptor. The second is anti-muscle specific kynis antibody and the third antibbody is called as anti-RP antibbody. Lipoprotein receptor protein antibody LRP. Three antibbody is senior most specific one is antiotal receptor antibbody. Treatment of choice for this condition would be answered as thymectomy. Decremental response but is the answer for repetitive nerve stimulation. Repetitive nerve stimulation finding that is what is called as decremental response. The treatment that we do is obviously with pyostine and neostage main that I would not like to go into but for generalized variety thymectomy and then the same thing in the same spirit unit remember thymectomy is not required for or is contraindicated in ocular variety of mythographs there are fingers uh yeah lambertton syndrome incremental response repetitive nerve stimulation may incremental response is seen in which condition apart from lambert Button syndrome by comments in the chat box. Repetitive nerve stimulation incremental response is seen in lambertton syndrome which is seen with lung cancer where there is a prejunctional defect. Which other medical condition have you read where you get a incremental response on repetitive nerve stimulation? This person ate meat which was rotten. rotten meat and there was entry of some s'mores in the intestine which affect the neuromuscular junction and caused a decrease of acetylcoline production rotten meat rotten one that's not that's not variant crual jackup disease variant crual jackup disease tinted meat a baby a baby was given honey baby was given honey after birth and there was a prejunctional defect present. Very good. rotting rotten meat because defects paralysis one is like in a country like ours fresh nonveg food should always be fresh never like you know most of these restaurants etc they don't take good hygiene so be careful about your health because summers is going to be extreme in a country or exam like you have to be very particular about your gut health and stuff like that and anyway I got very good answers there and a word of caution non from a better place good place and not from like these local places yeah butter chicken fine last statement last slide that is for bull syndrome though spoken about it earlier that is uh that is fame fame is for remembering saying that this particular person would be having like uh infection initially in the form of food poisoning with compiler juni or eoli or it's going to be hepatitis E virus this is itself a question of a paper guys what is the extra hepatic manifestation of hepatitis E it is gulen bar syndrome what is the extra hepatic manifestation of hepatitis E it is genar syndrome then can be Zika virus which is responsible yeah Food preferences are like different for everybody depend. Okay. So in gulbur syndrome guys it is a flaccid weakness that would be present and there would this flaccid reflexes flaccid weakness would be associated with a reflexia and this a reflexia will always be having a ascending paralysis that is paralysis will start from the feet and then it will be going upwards and can cause diaphragmatic paralysis also. It would be monophysic illness. Monophysic would mean that the progression can be so fast that within 12 hours patient might be ventilator dependent or like weakness in first week would be in the legs then would be in the trunk then would be in the arms of the patient and then uh then a alphabet can also be used to remember albiminocytological dissociation that is uh that everything would be normal in the lumbar puncture but only the proteins would be elevated and uh I mean that fame pneummonic also helps you in identifying electrodiagnostic tests for this condition and the electrodiagnostic test would be demalination on a nerve conduction study. So the basically like yeah Pune we discussed had cases of uh GBS because the water supply was contaminated the water tanks were contaminated the government supply and electrodiagnostic studies and it is intravenous immunoglobins or plasma exchange that can be used the question in last time's paper was plasma exchange is done in refractory GBS that is not correct any of the two can be used guys the efficacy of the two is equal the efficacy of the two is equal the only thing is that we prefer intravenous similar globins because of the because of the ease of administration the MCQ said select the correct options all these options were there one option was that we use plasma feresis in refractory goullenber syndrome that is not a correct treatment because plasma plasma exchange is not a backup treatment it is also primary treatment if I'm working at a tertiary care I have facility available we can do plasma exchange also so that is like one government that you basically need to remember and I'll not let's not do that. Let's not do that. Right? I mean unnecessarily people will take snapshots of it and post and stuff like that. So why we doctors get into this? So my advice would be be careful because unnecessary controversies can occur. Okay? So let's keep stay. But I'm happy that you guys are aware. Doctors should be aware of politics. Doctors should be aware of everything that is going on. I'm totally with you. But then we should be careful regarding what we post especially as doctors there right so I think it's very very important so guys we're done for session one at the moment and uh we are done with the session number one guys uh I enjoyed working out with you guys 3 and a half hours of solid session that is what I want you to train up for and like in fact I want you to do multiple such sessions every single day so that you are mentally capable of handling everything that comes and they throw bricks at you in the paper and you say bye Right? I mean you I want you to be bricks of steel, right? I want your mental stamina to go up on an everyday basis. I know you guys are like very intelligent people. But then uh you know physical part also comes in in that in a sense that our ability to sit for three and a half hours has to be there and we have to continue with the same energy and the same enthusiasm in the first minute of the exam and the last minute of the exam. That would be my advice for you guys at this moment. So we'll see you in the evening guys. uh second session guys we'll reschedule for 5:30 because I think that all of us uh will need a little of a break. So instead of 5:00 guys it's it's going to be 5:30 that will be starting and my suggestion to you guys would be that uh the GT test is going to be live on very soon on prepad from 23rd to 37th April irrespective I mean it's not a question which is validam But then the more you give papers more you are able to attempt because every question you solve is one step closer to victory. We're sorted for this session guys. Thank you so much uh for joining with me for this long and uh uh not butter chicken it will be vegetarian. Take care. God bless you guys and see you again at uh 5:30 onwards. [Music] [Music]