SPEED 2026

00:00:06Speaker[Vedic chanting: opening salutation to the Guru, “Om Sri Gurubhyo Namah, Harih Om.”]

00:00:13[Vedic chanting: the Durga Suktam, beginning “Jatavedase sunavama somam”, invoking Agni and the Goddess Durga to carry the assembly safely across all difficulties, as a boat across the sea. The ASR rendering of the verses is unrecoverable and is not reproduced.]

00:01:43[Vedic chanting: the Durga Gayatri, “Katyayanaya vidmahe, Kanyakumari dhimahi, tanno Durgih prachodayat.”]

00:01:58Om Shanti, Shanti, Shantih.

00:00:03Speaker… the graduate, postgraduate and PhD courses, and then there are the medical institutions, and there is a mobile hospital. So the spirit of Bhagawan Baba is being celebrated at the most auspicious time. Today we celebrate Kalaratri, the Mata form of Kalaratri, and incidentally it also happens to be the day of Vidyarambham, what we call Akshara Abhyasa in Karnataka. That is, we start learning today; we begin our initiation into education today. Coincidentally, it happened to be the 17th of October. It was not planned that way, but today is the day we all started our learning, our Vidyarambham.

00:00:43Love in Action. Essentially, the Sathya Sai way has been humanising technology for more than [unclear] years, with more than [unclear] patient-years of health care. Puttaparthi used to be described as a stone's throw away from the Stone Age. From there, where there was absolutely nothing, almost 250 kilometres away, even now the nearest speciality hospital is more than 100 kilometres away. So health care has been brought to the level of human care.

00:01:12Why did Sir envisage SPEED? It was Sir's vision. We are now in the 11th year, the 12th edition, since there were two last year. There were more than 250 registrations, and we had two SPEEDs last year. The feedback was very good. The whole idea came from when we were students; the HOD has also been an alumna here. The idea is of converting this scalar into a vector. We all know speed is a scalar, but we need direction. Direction makes it a vector, so that velocity was given by Sir, essentially in living up to what is written up there: that health care and education should be provided free, just for the asking.

00:01:52We used to have, and still have, a lot of students who come here as observers. Sir has never put it as ‘our students’ and ‘outside students’; everybody is the same. There is no faculty member here who has not been at SPEED before, so it is family for us. Many of them are one phone call away, and they agreed at the very last moment, although they all have very busy schedules. The only thing we expect is that you should not come back here next year as a student, but very much, of course, as faculty if you wish to.

00:02:21This is our every-day morning at Whitefield and Prasanthigram. I don't know of too many institutes which have this on an everyday basis. It was made an absolute rigour that this should happen every single day, and it still goes on. Every case is discussed, every patient is thrashed out, every sign is discussed. There have been days when, answering Sir, I have said ‘atrial fibrillation with a tall a wave’. I have also been there, and there has been learning out of that.

00:02:53I think it is good to go for the exams with a lot of preparation. You can't go for the exams on the last day and think it is a one-day job; it doesn't work that way. I am sure all our teachers have taught us that. About the need for SPEED, which everybody feels: there are a lot of other courses and a lot of YouTube videos, but the point was problem-oriented discussion. We were all taught by our teachers, and by everybody here, that knowledge in the mind should find the correct expression on the tip of the tongue. At that point, if you are not able to substantiate your findings or your clinical sign, it becomes difficult to go ahead.

00:03:28Exposure is not the same in all institutes, so Sir thought that there should be a homogenisation of the whole thing. All of us are equal when we pass out of MD or DNB Medicine, and we should be the same as we pass out. So knowledge should be shared on such a platform. There has been a lot of representation; in fact, a lot of institutes from the north are participating, and some of those students are here today.

00:03:49This picture is put here to tell you that it is not going to be three examiners; it is going to be the whole panel asking you questions. Getting ten people to ask you questions is not very common in a lot of such programmes.

00:04:08Patients have come from across the country. Our real wealth is our faculty and our patients, and of course the whole team that works with us; that selfless work is really the wealth of this institute. But more than that, the patients, because many of them come with faith in Swami, in Baba, and they have allowed us to learn a lot from them. So I think they have been our biggest teachers also.

00:04:30So this is not just about speed; let us make it a transformation in action. I hope you really have a very good time at SPEED, because we have loved bringing it to you as much as we feel you should love learning from it. This is the basic pattern of an examination; we can discuss it later.

00:04:51We will now have our senior faculty invite our guests with a small floral bouquet. [Guest faculty are welcomed with bouquets; names omitted.]

00:05:12Thank you, sir, for being with us. Our first guest has been one of the most senior professors in the country, a former head of department, and my examiner; he gave me my DNB degree. [Introductions of the other visiting faculty, with their names and institutions, omitted.] Thank you all for joining us again.

00:05:44[A senior faculty member is welcomed; name omitted.] Thank you, ma'am. Other teachers will be joining us, and we will now have a short video about the hospital.

00:00:03CandidateA 50-year-old man from West Bengal, with no formal education, a farmer by occupation, belonging to the lower socioeconomic class. The informants are the patient himself and his son. He came with chief complaints of angina on exertion for 5 years, exertional palpitations for 3 years, exertional fatigue for 3 years, and dyspnea on exertion for one year. Coming to the history of presenting illness, sir…

00:00:33FacultyOne second, sorry to interrupt you. Don't use the word ‘angina’ here.

00:00:37CandidateYes, sir. Chest pain.

00:00:40FacultyYes. After that, whether it is anginal or non-anginal, cardiac or not, we will see. If you say angina, you are committing straight away. So it is better to use the words ‘chest pain’.

00:00:54So what were the chief complaints?

00:00:54CandidateChest pain for 5 years, sir; palpitations for 3 years; fatigue for 2 years; dyspnea for one year.

00:01:10FacultyOkay, go ahead.

00:01:14CandidateThe patient was apparently all right 5 years back. Then he developed chest pain, insidious in onset and progressive. Initially he was able to do all the heavy lifting activities in farming without difficulty, but it gradually progressed to the point that he could not lift that heavy equipment. Initially he was able to climb at least 3 flights of stairs without much difficulty; currently he is not able to climb even one floor without symptoms.

00:01:49The patient gives a history of visiting a local cardiologist within one year of developing these symptoms, where he was told that he needed to visit a higher centre for further management. He then visited here, where he was told that he needed open-heart surgery and was asked to come back within the next few months, but he could not come back for review because of financial constraints. He used to take one tablet per day, in the morning, and continued his activities locally. But his symptoms progressed to the point that he could not continue his daily farming activities, and he has stopped going to the farm for the last one year, sir.

00:02:35The patient also gives a history of chest pain at night, sir, which woke him from sleep and was associated with palpitations during those episodes. He said these episodes lasted at least 30 to 60 minutes, gradually subsided, and he used to go back to sleep.

00:02:58He gives a history of palpitations for 3 years, more during exertion and relieved on rest. They were regular in nature and not associated with syncope, and there is no history of post-palpitation diuresis, sir.

00:03:21He gives a history of exertional fatigue for 2 years. Initially he was able to climb 2 floors without much difficulty, but now he is not able to climb one floor without symptoms. He visited our hospital last month with these symptoms and is being evaluated here, sir.

00:03:44There is a history of dyspnea on exertion for one year, insidious in onset and gradually progressive, to the point that he is not able to climb even one flight of stairs without dyspnea. No history of PND or orthopnea; no history of syncope or loss of consciousness in the past. No history of recurrent sore throat in childhood, migratory joint pains, or monthly intramuscular injections in the past. No history of lower-limb edema, abdominal distension or reduced urine output.

00:04:36Can I come to the past history, sir?

00:04:39FacultyDo you want him to analyse the present history now, or shall we do it at the end?

00:04:44One second. I will just tell you that the history seems all right, but you are going back and forth. In the exam, the examiners may not have sufficient time to listen, so you must present in a quick, chronological order. It does not matter even if you just say he is in NYHA class 2 or 3; you don't have to describe it in detail, at least at the DM or DNB level. Unlike undergraduates or postgraduates, you don't have to describe everything. You can straight away act like a consultant and present as you would in the OPD. From here we have got so many symptoms and we have gone back and forth: chest pain, and dyspnea on exertion being the last symptom to appear.

00:05:34So, taking the clue from Sir, what do you think from the present illness? Okay, you finish; we won't disturb you till the past history.

00:05:42CandidatePast history, sir. The patient is not a known case of diabetes mellitus, hypertension, asthma or tuberculosis, and there is no history of CVA in the past.

00:06:03Coming to the family history, sir: the patient gives a history of sudden death of his grandfather at the age of 50 years, and of the death of his elder brother one year back, also at the age of 50 years. The brother was admitted locally with some cardiac disease and was declared dead within 24 hours in hospital. So, his grandfather and his elder brother.

00:06:35FacultyOkay.

00:06:37CandidatePersonal history, sir: diet is mixed, appetite normal, sleep disturbed by recurrent anginal symptoms at night, bowel and bladder regular; he denies addictions, sir.

00:06:51Treatment history: the patient is currently on one medication, which he takes once, in the morning only. He gives a history of undergoing a procedure in our hospital in the last month through the right hand, and was told that he has to see a surgeon for further management.

00:07:11FacultyOkay. Have you completed the history?

00:07:15CandidateCompleted, yes.

00:07:19FacultyWhat could you get from your history? What is your interpretation?

00:07:23CandidateThe patient has prolonged, progressive angina, with palpitations, [unclear] history, and dyspnea as the last symptom. Recently he was seen here and was told that he needs open-heart surgery. I was thinking of valvular heart disease as my first differential, sir, and within that, aortic stenosis.

00:07:45FacultyWait, just hold on. Before we go to the actual things, what do you deduce from the history, in terms of what is happening to his hemodynamics? What is happening to his heart?

00:08:02CandidateThe patient is giving a history of angina, sir…

00:08:06FacultyHow do you know it is angina? Nowadays the classification is only two, isn't it: typical angina or non-cardiac chest pain? There is no atypical angina in this; it has been removed, isn't it? So what category does this fall under?

00:08:23CandidateIt falls under typical angina, sir, because it is brought on by exertion and relieved by rest.

00:08:30FacultySo how do you suggest that this is angina or not angina? What parameters do you take? WHO has given some parameters; we go by that. It is called PQR, to which we also add S and T. Sometimes we say PQRST, just to make it sure. So what is P?

00:08:51CandidateP is the pressure kind of… precipitating factors.

00:08:57FacultyOkay. Q?

00:08:57CandidateQuality of the pain.

00:09:02FacultyYes. R?

00:09:02CandidateR is retrosternal?

00:09:02FacultyNo, R is relief: relieving factors. So: precipitating factors, quality of pain, relieving factors. What is S?

00:09:14CandidateSite, the site of the pain.

00:09:14FacultyAnd the most important one, T, which is not ‘stress’ but is called the temporal profile. What is the temporal profile? How long it lasts. So how long does typical angina last?

00:09:27CandidateSir, typical angina lasts less than 20 minutes and should be brought on by exertion. The location is retrosternal, a squeezing type of pain, or it comes on when the patient is in a cold environment.

00:09:39FacultySo applying these criteria, does it fit typical anginal pain or not?

00:09:47CandidateYes, sir. It is brought on by exertion and relieved with rest, and he describes it as more of a precordial, squeezing chest pain.

00:09:55FacultyHow long does it last?

00:10:00CandidateHe says for 5 years… The episodes were lasting less than 20 minutes only.

00:10:05FacultyYou also said he was getting chest pain at night.

00:10:08CandidateYes, ma'am. At night, and that too recently, for the last 2 years, he has had brief episodes of sudden chest pain which woke him from sleep, lasting less than 30 minutes only, ma'am.

00:10:22FacultyActually, typical angina lasts only 2 to 5 minutes. Less than 2 minutes is probably non-cardiac chest pain. Rarely it can go up to 10. Definitely, as you said, it will be less than 20 minutes, but actually it lasts only 2 to 5 minutes if it is typical anginal pain.

00:10:41Coming to the nocturnal part of it: what does this nocturnal chest pain fit into? Can it not be PND?

00:10:48CandidateNo, sir, he is not specifically describing PND.

00:10:51FacultyHow do you say that this is nocturnal chest pain?

00:10:54CandidateHe says it woke him from sleep, it was squeezing in type, it was associated with palpitations during those episodes, and sometimes he had sweating as well. It got relieved after he got up and waited for some time, and then he used to go back to sleep.

00:11:08FacultyHow sure are you that it is not PND?

00:11:22CandidateNo dyspnea, only chest pain.

00:11:22FacultySo what is the factor that distinguishes PND from nocturnal angina? How do you differentiate PND from nocturnal angina?

00:11:39CandidatePND will make him gasp for air; it will make him get up and go to the window, gasping, with difficulty in breathing, sir. But he says it is more of pain, chest pain only, which got relieved within a few minutes, and then he went back to sleep. PND might not let him go back to sleep, sir; if it is very severe, he might be awake the whole night.

00:12:01FacultyOkay. One small digression: what is linked angina?

00:12:06CandidateSir, linked angina is referred angina because of a vasovagal reflex. Sorry, because of epigastric reflux there will be vasovagal activity, leading to reduced coronary supply, which can produce an ischemic type of pain.

00:12:25FacultyLinked angina means it is linked to the gastric system, but it is not due to GERD or reflux. It is something else, like postprandial angina due to what? What is the culprit artery in linked angina? Is there any culprit artery? What about the superior mesenteric artery; does it form part of it? So it is something linked to the GI system; it is postprandial. As far as I know it is not equivalent to GERD, but yes, it is linked to the gastrointestinal system. Okay, fine.

00:13:16Then, coming to the next symptom, palpitations. How long should palpitations last before a patient gets syncope? You know very well that if it is ventricular, it will be immediate. But suppose it is atrial fibrillation?

00:13:35CandidateSir, atrial fibrillation can present during rest or exertion, and it is not…

00:13:38FacultyIf it is paroxysmal, how long should atrial fibrillation last before the patient gets syncope, or before cerebral blood flow is compromised? Of course it can vary from patient to patient and depends on the heart rate; if the rate is very fast there will be hemodynamic compromise. But generally speaking, have you any idea?

00:14:07CandidateNormally it should be 30 minutes; only then can the patient have compromise of the cerebral circulation.

00:14:12FacultyOkay. So these palpitations have progressed along with the anginal symptoms. What do you think is the cause of the palpitations?

00:14:27CandidateThe patient says they are regular palpitations, brought on by exertion and relieved with rest. Ma'am, I was thinking either that the forceful contraction of the LV is being felt as palpitation, or that the patient has an associated regurgitant lesion which is bringing on this symptom.

00:14:48FacultyNo. In this patient, are these palpitations due to a rhythm disturbance, or due to something else?

00:14:58CandidateI am suspecting associated lesions, like mitral regurgitation or aortic regurgitation: a volume-overload state leading to palpitations.

00:15:09FacultySo how can you distinguish whether palpitations due to a volume-overload state are due to mitral regurgitation or aortic regurgitation? What is the symptomatology that differentiates them?

00:15:27CandidateSir, in mitral regurgitation fatigue is the first symptom, followed by palpitations, sir.

00:15:40FacultySo fatigue is the distinguishing feature? Why the fatigue?

00:15:46CandidateReduced cardiac output during exertion leads to reduced supply to the peripheral musculature, resulting in fatigue.

00:16:00FacultyIs angina common with MR or with AR?

00:16:00CandidateAR. AR can cause it through the runoff phenomenon: the patient has reduced coronary filling and reduced coronary perfusion pressure, which can lead to anginal symptoms.

00:16:25Faculty[unclear] more in AR or MR? Is end-systolic wall stress more in AR or in MR?

00:16:43CandidateSir, the determinants of myocardial oxygen demand are heart rate, contractility… So wall stress… eccentric dilatation will have…

00:16:58FacultyWhat is wall stress?

00:17:02CandidateWall stress is the pressure on the muscle because of the overload state.

00:17:08FacultyThere is a formula for wall stress.

00:17:13CandidateYes, sir. Wall stress is equal to [inaudible] into the radius of the chamber, divided by the thickness of the wall.

00:17:27FacultyOkay: PR by 2T. Not twice; PR by 2T. So what does wall stress do to the LV?

00:17:38CandidateSir, when the patient has a volume-overload or pressure-overload state… In the pressure-overload state the LV becomes thickened to reduce the wall stress, sir, as in aortic stenosis. In regurgitant lesions the radius increases, sir, and hence wall stress increases more; the compensation is less than in stenotic lesions, with eccentric dilatation of the chambers.

00:18:12FacultyHow do you explain the fatigue here?

00:18:17CandidateBecause of the chronic nature of the disease, reduced cardiac output has resulted in fatigue in this patient, sir.

00:18:29FacultyHeart failure? You mean heart failure?

00:18:34CandidateYes, sir. The patient has also developed dyspnea recently, sir: heart failure.

00:18:40FacultyBut the patient can have reduced output because of regurgitation and also because of a stenotic pathology. Anything else? So from this you have to come to a diagnosis, a provisional diagnosis.

00:19:00CandidateFrom my history, the diagnosis, sir? The differential diagnosis, sir? Shall I tell you, sir?

00:19:09FacultyNo. From history, what do you diagnose?

00:19:16CandidateSir, congenital heart disease, bicuspid aortic valve.

00:19:20FacultyWhat is the NYHA class of symptoms?

00:19:40Now just tell us the pathology; then you can tell the etiology. Pathology, pathophysiology, then etiology. What is the pathological diagnosis?

00:19:49CandidateSir, congenital heart disease, bicuspid aortic valve, aortic stenosis with aortic regurgitation.

00:19:55FacultyHow do you say bicuspid aortic valve from the history?

00:20:01CandidateSir, he developed angina as the first symptom, followed by palpitations and fatigue, sir, and then dyspnea. In this order of sequence I was thinking of aortic stenosis as my first diagnosis, sir. But aortic stenosis is usually seen in elderly patients, and he was around 45 years of age when he developed these symptoms. So in a younger patient with this aortic stenotic pathology, I was thinking more of a bicuspid pathology, sir.

00:20:32FacultySo initially it was AS, and then it became AR? It started with AS?

00:20:36CandidateYes, sorry, yes. He had angina because of aortic stenosis.

00:20:40FacultyThen you add AR. How did AR come? Was there any endocarditis, or an intervention?

00:20:44CandidateNo, nothing associated.

00:20:52Faculty[unclear] In bicuspid aortic valve, stenosis develops and becomes severe. We are talking of the symptoms: angina, fatigability, palpitation. Aortic stenosis will not produce palpitations; volume overload is not a feature of aortic stenosis. Then how do you explain these things? How did severe AR come about? Look for a dilated aortic annulus. Because of the chronicity of the stenosis? What is the natural history of bicuspid aortic valve? How many develop AR, how many mixed disease?

00:21:29CandidateSir, in bicuspid aortic valve, AR is the predominant pathology that develops.

00:21:40FacultyIn bicuspid aortic valve, AR is the predominant lesion?

00:21:53Just remember: one-third, one-third, one-third.

00:22:02Would you like to consider any other form of disease?

00:22:02CandidateYes, sir. He has also given a history of cardiac death in his family members, sir, so I was thinking of HCM as one more differential, with mitral regurgitation.

00:22:17FacultyAt 45 years of age, in India, which disease would be the commonest?

00:22:26CandidateRheumatic disease is the commonest, not ischemic.

00:22:26FacultySuppose I say this is ischemic: ischemic MR. Coronary artery disease, severe triple-vessel disease, with ischemic MR causing palpitations and fatigue, with severe angina. Is that possible? Is CAD with ischemic MR possible in this case?

00:22:55CandidateYes, sir. He has developed dyspnea also, sir; if he has any LV dysfunction, that can result from ischemia.

00:23:05FacultyHow do you conclude LV dysfunction?

00:23:05CandidateThe history of dyspnea, sir, in the last one year.

00:23:15FacultyAnd he also has fatigue.

00:23:18CandidateSo, first, bicuspid aortic valve disease, sir…

00:23:24FacultyAR dominant? Then tell me: palpitation, resting palpitation, nocturnal angina; how do you explain them? [unclear] syncope? [unclear], could be more than that.

00:23:50So your pathology is aortic valve disease, which could now be AR dominant, or aortic valve disease with coronary disease, both.

00:24:02CandidateHe might have coronary artery disease, which might have [unclear] his aortic stenosis symptoms, sir.

00:24:10FacultyDoes he have any risk factors for heart attack or heart disease? Diabetes?

00:24:15CandidateHe doesn't have any risk factors, sir.

00:24:15FacultyHe said no risk factors, and the brother had sudden death. We don't know whether it was ischemic heart disease. Both individuals, the grandfather and the brother, had sudden death, so again we are not very sure whether it was ischemic heart disease. Angina starting at 45 years without any risk factors is possible; we see so many. But still, if there is a family history of sudden death, and angina, what do you think of first? [unclear: possibly ‘hypertrophic cardiomyopathy as the first diagnosis’]

00:24:54CandidateHe was not very sure about the deaths of the family members. When I asked, he told it like that, and I was thinking it might be an associated cardiomyopathy.

00:25:14FacultyThat means congenital, I mean familial, bicuspid disease? Does bicuspid valve run in families?

00:25:25CandidateYes, sir. In familial cases the associated gene is on chromosome 9, with NOTCH1 mutation. It is familial in up to 10%.

00:25:34FacultyNo, tell me: if there is a family history of sudden cardiac death in two members, and the patient now has symptoms of angina, fatigability and palpitation, what do you think? What is your first diagnosis? He has been told to go for surgery; that is different. People also do surgery for hypertrophic obstructive cardiomyopathy [unclear].

00:26:07So what is your final impression at the end of the history?

00:26:14CandidateValvular heart disease I was thinking, sir, with cardiomyopathy as the second diagnosis, and ischemic heart disease as the third differential, sir.

00:26:28FacultyWhat is it that you want to get from your history? There are certain components of your diagnosis, isn't it? You want the etiological diagnosis, the anatomical diagnosis, the complications, and the NYHA functional class. These are the final components of your diagnosis. What does history give you? Most importantly, it helps you identify the etiology; examination gives you the anatomical diagnosis. You combine the two, with the relevant questions you ask the patient. So from your history, what do you think is the etiology here? What pathological process is causing the disease in him?

00:27:24CandidateI am thinking bicuspid, so congenital. He has a problem that has been present for a long time, so congenital heart disease is a possibility in this case.

00:27:35FacultyDo you want to stop your differential diagnosis there, or widen your thinking and keep cardiomyopathy also in the differential? Which one would you consider?

00:27:46CandidateHypertrophic cardiomyopathy, sir.

00:27:46FacultyYou already said cardiomyopathy.

00:27:50Sir, I am asking about my own issue. Any patient who has, as mentioned, a bicuspid valve with severe AS would get angina pectoris. If you are taking isolated aortic valve disease, it has to be severe for angina pectoris. Then he developed palpitations and nocturnal angina, symptoms of [unclear]. How did that happen? Severe AS has now become AR, with all the symptoms of AR. How did that happen without endocarditis, without any fever or anything like that?

00:28:28CandidateI asked, sir. I asked for any history of hospital admission or fever; there was none.

00:28:33FacultyAs per your diagnosis, how do you justify it?

00:28:43Candidate[unclear] Maybe the valves have become calcified, leading to reduced coaptation, which can lead to regurgitation.

00:29:00FacultyIf the patient has aortic valve disease, and if it is very specific, what is the dominant pathology? You said that because the patient develops severe calcification, the [unclear] disease then develops. No, not possible. It must be just AR only; all the symptoms can be described by AR.

00:29:29Tell me one more thing. In the classical teaching of [inaudible], you have angina, syncope and dyspnea, three symptoms, and without treatment you know there is the 5, 3, 2 and all that. But in daily life, when you see patients with aortic valve disease, many complain of dyspnea as the predominant symptom. Why does it occur? Once dyspnea develops, they say longevity is limited; it is not like that, but you do see patients who have dyspnea as the predominant symptom. Why does it occur in AS?

00:30:02CandidateSir, because of increased LV end-diastolic pressure, leading to increased LA pressure, leading to PVH, which produces the dyspneic symptoms.

00:30:16FacultyPVH will occur in AS. Because of…?

00:30:24CandidateResistance to flow out of the LV has created the back-flow.

00:30:24FacultyAnd if there is increased LV end-diastolic pressure or volume in AR, it should get reflected straight away to the LA, and the patient should have PVH. But it doesn't occur; patients with AR do not develop dyspnea. Why? Is there associated mitral disease also?

00:30:44CandidateIt might progress…

00:30:44FacultyNo, without mitral valve disease.

00:30:44CandidateYes, sir.

00:30:48FacultyThere is increased LV end-diastolic pressure, but it doesn't get reflected to the LA unless there is failure of the LV. What prevents it from getting the LA involved?

00:31:03CandidateDecreasing the wall thickness?

00:31:03FacultyLet's say free AR is there. The end-diastolic pressure is very high, you know, 35, but the LA pressure doesn't go up that much, and PVH doesn't occur. What prevents it from going into the LA, the LA pressure going up?

00:31:24CandidateThe mitral valve?

00:31:27FacultySo what does AR do to prevent that pressure from going into the LA? You will see it on echo, many times. It lifts the anterior mitral leaflet into a semi-closed position. The free AR lifts the anterior mitral leaflet into a semi-closed position and thus prevents the LV pressure from getting transmitted to the LA, correct? That is why PVH is a late feature, or it will not occur. Okay, we will go forward to the examination.

00:32:06Can it be lone AR only, sir? Lone AR, with a very large regurgitant volume? Can you explain it? [unclear]

00:32:27All right. Fatigue is also a rare symptom, no? Yes, palpitation is the commonest presenting symptom.

00:32:35CandidateGeneral examination, sir. The patient is moderately built and moderately nourished, well oriented to time, place and person. Height 160 cm, weight 49 kg, BMI 19.1 kg/m². Pulse rate 76 beats per minute, regularly irregular, low volume, normal character.

00:32:52FacultyWait, just hold on. What are you saying, regularly irregular?

00:32:57CandidateYes, sir.

00:32:57FacultyOkay. What does it mean? Okay, go on.

00:32:57CandidateNo radio-radial delay, no radio-femoral delay. All peripheral pulses are felt, with a pulse deficit of less than 10 beats per minute, sir.

00:33:13Blood pressure, sir: right upper limb 108/80 mmHg, left upper limb 106/[unclear] mmHg, bilateral lower limbs 112 mmHg systolic. Respiratory rate 14 cycles per minute, thoracoabdominal type. Saturation 98% in all four limbs. No peripheral signs of infective endocarditis or aortic regurgitation noted, sir.

00:33:41FacultySo what is the interpretation of this finding of yours, ‘regularly irregular’?

00:33:47CandidateThe patient might be having premature ventricular contractions, because the pulse deficit is less than 10 beats per minute.

00:33:59FacultyWhy does it become regularly irregular: every second beat, every third beat? What is the nature of the irregularity? You said it is regularly irregular; for example, bigeminy?

00:34:18CandidateIt could be trigeminy or quadrigeminy. After at least 5 to 6 beats I was getting one extra beat, premature compared with the previous cycles.

00:34:30FacultySo you could feel the premature beat? Or did you feel a pause?

00:34:35CandidateNo, sir, I was feeling the premature beat; after that a little pause, and then it continued again.

00:34:44FacultySo, 5 to 6 beats?

00:34:44CandidateYes, sir, a premature beat, and then it continued. About 7 to 8 beats, not 5; 7 to 8, sir.

00:34:54FacultyIf you felt premature beats, you can just say that, because it is not that regular; you are saying 5, 6, 7, 8. Why don't you just describe the pulse as irregular and stop at that? What is the ‘regularity’ in this irregularity?

00:35:02CandidateOkay, sir. I will mention irregular, sir.

00:35:15The patient has pallor; no icterus, no cyanosis, no clubbing, no lymphadenopathy, no pedal edema.

00:35:24Jugular venous pressure, sir: it is visible 2 cm above the sternal angle at 45 degrees, with normal waveform, sir.

00:35:35FacultyAbove the sternal angle. What is the normal JVP measurement?

00:35:41CandidateIt will be less than 3 cm above the sternal angle, sir. It is less than 8 [unclear], sir, normally.

00:35:46FacultySo here it is 2 cm. And how did you see that?

00:35:54CandidateSir, I used two scales, sir, and a [unclear] light, at 45 degrees.

00:35:58FacultyAt 45 degrees, if the venous pulsation is seen above the clavicle, is that normal? Even at 45 degrees it generally is not seen above the clavicle. So then how did you see it? How did you measure it?

00:36:16CandidateUsing the scales, sir.

00:36:16FacultyNo, you must see it. Otherwise, unless you see the upper level of the column and the pulsation… In the sitting position, clearly it is abnormal; there is no question about it. But even at 45 degrees, if pulsations are seen above the clavicle, it is generally considered abnormal, and it will be more than 3 cm from the sternal angle. Anyway, you said 2. Can you go down to 30 degrees, or does it have to be 45 degrees? Can it be 60 degrees?

00:36:48CandidateNo, sir.

00:36:53FacultyAnd in what way does the measurement change?

00:36:53CandidateSir, if the patient is at 60 degrees, we cannot take 3 cm as the cut-off, sir; it should be lower, sir.

00:37:05FacultyBecause as the patient comes to 60 degrees you have a different normal value, at 30 degrees another, and at 45 degrees another? What are the values for these positions? See, how did you measure it? How did you put those two scales?

00:37:17CandidateOne scale I put perpendicular to the sternal angle, sir, and the other scale…

00:37:27FacultyThat is why I keep telling you: in the examination, do not describe the JVP at the 45-degree position at all, because it invites all these questions which Sir is asking. Just say, with the patient sitting upright by the side of the bed, whether the JVP is seen above the clavicle; then it is elevated, that is all. Then you describe the waveforms. That is much simpler than trying to measure exactly from the sternal angle, and then having to quote the CT study on what the centre is: what is the phlebostatic axis? Do you know what the phlebostatic axis is?

00:38:17Anybody in the audience? What is the phlebostatic axis, when they describe the JVP?

00:38:23Isn't it the centre of the mid right atrium, which corresponds to which area? The mid-axillary line; no, the fourth space in the mid-axillary line. That is the phlebostatic axis, where we keep the transducer in cardiac care, because that is where the pressure transducer will measure accurately from zero. So that is important. So just say that in the sitting position it is visible or not visible; that's enough.

00:38:55And of the two scales you put, one is placed horizontally at the upper level of the venous pulsation, and the second one perpendicular to that scale, perpendicular to the ground: basically horizontal and vertical. It is not perpendicular to the sternum. The sternum is at an angle; you can't put that scale perpendicular to the sternum, correct? That is the important thing to know: vertical height. You are measuring the vertical height of the column of blood, and that should be the same whether you measure at 30, 45 or 60 degrees, because it is the vertical height that you are measuring. Okay, go ahead.

00:39:37CandidateJVP: normal waveform, sir. Cardiovascular examination, sir: inspection and palpation. The chest is bilaterally symmetrical; the apex is located in the 5th intercostal space…

00:39:53FacultyOne small thing I will tell you; some examiners are a little finicky about this. You have told the blood pressure, the pulse, everything; that is also the cardiovascular system, and it gives a lot more information about the cardiovascular system. So you don't have to say separately ‘cardiovascular system: inspection and palpation’. The JVP and blood pressure are all part of the cardiovascular system examination; they are not part of the general examination. So remember that.

00:40:16CandidateOkay, sir.

00:40:25Faculty[unclear] Four headings. For the JVP you should describe four headings, 1, 2, 3, 4, like this.

00:40:39CandidateSir, one is the JVP pressure, and the waveform, and…

00:40:43FacultyHow is it, meaning respiratory variation. Respiratory variation, and something else: the hepatojugular, the abdominojugular reflux. [unclear] Do not mention those things [unclear].

00:41:12CandidateApex located in the 5th intercostal space at the mid-clavicular line, with medial retraction, heaving in type. A systolic thrill in the right intercostal space was noted. Suprasternal pulsation was present. No palpable P2; sorry, a palpable S4 was there. No palpable P2, no parasternal heave, no dilated veins over the precordium, no hepatojugular reflux.

00:41:41FacultyWhy have you brought the AJR here? You were doing palpation.

00:41:50CandidateYes, palpation; I have to return. Sorry, the JVP examination I have to complete there.

00:41:56FacultyWas the thrill present?

00:41:56CandidateYes, sir. A systolic thrill was present in the right second intercostal space, sir, and actually the thrill was getting accentuated after the ectopic beats.

00:42:12FacultyYou could appreciate that? Okay, good.

00:42:19The importance of the abdominojugular reflux was brought back in which trial, conducted in recent times? What was the name of the trial that brought back clinical examination findings like edema, two-pillow orthopnea and bendopnea [unclear]? Which trial is this? The ESCAPE trial: heart failure with the PA catheter [unclear].

00:42:50CandidatePercussion, sir: the left heart border corresponds to the apex; the right heart border is retrosternal; the left second intercostal space is resonant; hepatic dullness is percussed in the right 5th intercostal space in the mid-clavicular line; stomach tympany on the left side.

00:43:10Auscultation, sir.

00:43:10FacultyBefore we go to auscultation, what have we got? What are you going to expect now? What have we got so far? The patient has a low-volume pulse, with the blood pressure [unclear]. There are no signs of regurgitation. Then, the pulse character is normal… ectopics; the pulse character is not normal? The JVP is unremarkable. You have got a heaving apical impulse, a thrill in the right second intercostal space, no left parasternal heave, isn't it? So what are you going to expect now? What is the character of the apical impulse?

00:43:49CandidateHeaving apical impulse.

00:43:56FacultyThen you found the suprasternal pulsation also, which very importantly you have mentioned, and you could palpate the S4. Did you simultaneously palpate the…?

00:44:09CandidateI tried to check, sir, but I couldn't time it properly, sir.

00:44:13FacultyThis is one of the classical ones. Afterwards you can go and see it again; it is very easily appreciable. The apico-carotid delay is very clearly appreciable in this particular case; it doesn't take much time. The gap is quite long: the apico-carotid delay. What could be the pulse character? The pulse is also very low, slow rising. Based on the apico-carotid delay, what could be the pulse character? Pulsus parvus, that is, slow rising, late peaking.

00:44:49CandidateSlow-rising, late-peaking pulse, with low volume.

00:45:00FacultyBut we are getting the suprasternal pulsation there. Suprasternal pulsation: what do you say?

00:45:06CandidateMaybe a dilated aorta, or an associated regurgitant lesion, because the pulse volume and character are normal. Sir, I was expecting low volume with late peaking…

00:45:20FacultyNo, Sir is asking the cause of the suprasternal pulsation.

00:45:26CandidateOne is an associated regurgitant lesion, aortic regurgitation, or a dilated aorta.

00:45:35FacultyA dilated aorta; but the other things you have ruled out, isn't it, especially from the blood pressure and other measures?

00:45:42CandidateYes, sir.

00:45:42FacultyOkay. So now auscultation.

00:45:47CandidateAuscultation: S1 soft; S2 paradoxically split; LV S4; a harsh, high-pitched, late-peaking systolic ejection murmur, grade 4/6, best heard in the right second intercostal space.

00:45:58FacultyYou mentioned that S2 is paradoxically split, but did not mention the intensity: the intensity of aortic closure and pulmonary closure.

00:46:12CandidateS2 soft.

00:46:18FacultyS2 is soft, with paradoxical splitting?

00:46:18CandidateIt was soft.

00:46:18FacultyBoth are soft, but you are able to hear both sounds?

00:46:31CandidateInitially I was feeling that S2 was single, sir, because S2 was soft, but I made him expire more and checked again, sir, at that time.

00:46:44FacultySo if you have a paradoxical split, a theoretical question: how do you know which is A2 and which is P2? How are you sure which is the first sound? In paradoxical splitting it is P2, then A2. So how do you know which is P2, which is A2, and which is soft? In paradoxical splitting, how will you find out?

00:47:08Candidate[unclear] split means during inspiration we will hear one sound, and during expiration there will be the paradoxical split.

00:47:14FacultyI agree. But how do you know that this is P2 and not A2, and that is A2 and not P2? Right. The thing is that you must learn to inch your stethoscope. In fact, if you take the new Hurst, it always says start auscultating from the second right intercostal space, isn't it? Then go to the second left intercostal space and come down. Now at the apex, the sound which is heard is always A2, unless there is pulmonary artery hypertension. So if the first component of the second heart sound disappears at the apex, then that is P2, and the split is paradoxical. Similarly, if you want, you can recheck by inching backwards, and you will know which is P2 and which is A2. Fine. And please do not read the three types of paradoxical split mentioned in Abrams; you will get confused. Take only the classical paradoxical split, which you have explained.

00:48:28CandidateMurmur, sir: a harsh, high-pitched, late-peaking systolic ejection murmur, grade 4/6, heard in the right second intercostal space, radiating to both carotids, which was aggravated in intensity after an ectopic beat, sir.

00:48:40FacultyHarsh and high-pitched? The murmur is harsh. Is it high-pitched, low-pitched or medium-pitched? Medium-pitched, or mixed frequency.

00:49:05CandidateAnother, a decrescendo early diastolic murmur…

00:49:05FacultyYou mentioned some ectopics there. What is happening post-ectopic?

00:49:15CandidateIt is increasing in intensity, sir. Post-ectopic it is increasing, suggesting an increased gradient across the valve, hence severity of stenosis.

00:49:27FacultyIn which condition is that very useful?

00:49:33CandidateAortic stenosis versus mitral regurgitation, sir.

00:49:33FacultyThat is okay; that I agree. But which other condition? It will tell you the level of [unclear]. HCM, correct. Does it differentiate fixed obstruction from dynamic obstruction?

00:49:48CandidateYes, sir.

00:49:54Another decrescendo early diastolic murmur, grade 2/4, best heard in the left 3rd intercostal space. And a pansystolic murmur of…

00:50:11FacultyNo: what is the important component of the early diastolic murmur? You told the area, you told the timing of the murmur; then what else?

00:50:21Candidate[unclear] The length of the murmur. It was very short, sir; it was not going till S2, sir.

00:50:37UnclearNo, sir, the early diastolic murmur doesn't go up to S2.

00:50:42FacultyDid you mention that? [unclear]

00:50:53So is the length of the murmur important here? Is it important to assess severity?

00:51:01CandidateYes, ma'am. In MS…

00:51:01FacultyNo, here he is asking about the EDM.

00:51:06CandidateYes, ma'am. A prolonged early diastolic murmur is suggestive of a severe regurgitant lesion, ma'am: in aortic regurgitation, more than half of diastole.

00:51:16FacultyOf course; that's the reason [unclear], one of the most important things. So the longer the murmur, the more severe the regurgitation, isn't it? Except in acute AR, where it gets short. Okay.

00:51:34CandidateOne more murmur: a pansystolic murmur, grade 3/6, heard at the cardiac apex, radiating to the left axilla, best heard during expiration; post-ectopic, it was not getting aggravated.

00:51:56Other systems: respiratory system, bilateral air entry present, no added sounds. Per abdomen: soft, non-tender. CNS: [unclear]; no focal neurological deficit noted, sir.

00:52:08FacultyOkay. Did you look for anything? You said bicuspid aortic valve. Did you hear anything?

00:52:16CandidateI didn't hear any click.

00:52:22FacultyS1 was so soft. Why is S1 soft?

00:52:28CandidateOne is that I could hear a pansystolic murmur, ma'am, maybe associated mitral regurgitation; or calcification of the aortic leaflets.

00:52:36FacultyCalcification of the aortic leaflets causes a soft S1? Calcification of the aortic leaflets can cause a pansystolic murmur [unclear] and softening of S1?

00:52:50He said soft S1. I was asking why there is a soft S1, and he said calcified aortic valve. But tell me the mechanism: how does calcific aortic stenosis produce a soft S1? That is the question.

00:53:09CandidateIt cannot tense because of the calcification, so we cannot get that sound.

00:53:13FacultyS1 is the mitral valve, the mitral valve. S1 is soft because of the calcification? How?

00:53:21Nobody? If the calcification does something: it prolongs the PR interval. Long PR. And here there is [unclear]; see, there is LBBB there. In LBBB [unclear], LV activation is delayed [unclear]. So that can produce a soft S1. And MR is also there, but MR is not very significant here.

00:53:50You didn't get any signs of MR here? Any sign of MR other than this pansystolic murmur? Was there an S3?

00:54:00CandidateNo, sir.

00:54:00FacultyWas there an MDM?

00:54:00CandidateNo, sir, I didn't get it. I couldn't hear one.

00:54:05FacultyI'll ask you one question: what happens to S1 in pre-excitation? What happens to the intensity of the first heart sound in pre-excitation, when there is a short PR? Is it normal? Is it increased? Is it decreased?

00:54:32CandidateIf it is a long PR, S1 should be soft. If it is a short PR due to pre-excitation, the short PR will cause a loud S1.

00:54:41FacultyNot necessarily. Why? What is the mechanism? In a short PR, why is S1 loud? Just think about the mechanism.

00:54:51CandidateThere is a shorter time for the mitral valve to close [unclear], so…

00:54:56FacultyWhat you are saying is true, but remember, in WPW syndrome the QRS is not formed only by the pre-excited pathway. It can be fully pre-excited, but there is also the normal pathway; it is a fusion between the normal pathway and the bypass tract. So S1 tends to be normal; it doesn't tend to be that loud.

00:55:25CandidateCongenital heart disease: bicuspid aortic valve with severe aortic stenosis, with moderate aortic regurgitation, and mitral regurgitation.

00:55:49Faculty[Partly in Hindi; unclear] Multivalvular disease: the diagnosis could be rheumatic, or [unclear].

00:55:58Unclear[unclear] significant; AS is dominant. [unclear] LV diastolic dysfunction [unclear] or systolic dysfunction.

00:56:16FacultySo you've got a bicuspid aortic valve. Are you sure about that? Because to diagnose a bicuspid aortic valve clinically, at least you should have a… How did you decide on bicuspid? On history?

00:56:31CandidateBecause of the patient's history: he has aortic stenosis, and he has developed it at a younger age. So I was thinking more of a bicuspid etiology rather than rheumatic or any other etiology.

00:56:43FacultyBut you have got two other lesions. You said mitral regurgitation and aortic regurgitation along with aortic stenosis, so it can be rheumatic, isn't it? Okay, you have known the case. You have known the case; that's why we are talking like that.

00:57:05But with multivalvular disease, how do you diagnose bicuspid [unclear]? You may be right, but clinically, how can you give it as [unclear]?

00:57:22Even the history, as the other examiner pointed out, is more towards AR, and you are still focusing on aortic stenosis and bicuspid aortic valve, as if you have been biased. That's the impression that we get.

00:57:38If you are not sure of a bicuspid etiology, you should not mention it.

00:57:41CandidateOkay, sir.

00:57:41FacultyIn fact, when you come to the final diagnosis, be as non-specific as possible, because you should not give the impression that you know about the case. You may know it, that's all right, but still that impression should not be given.

00:57:57[unclear] Then I can say probably, okay: ECG, or whatever. What do you expect from this?

00:58:07CandidateLVH with strain pattern, and also LA enlargement.

00:58:19FacultyLeave the ectopics out. From the ECG, how will you know whether there is MR or AR?

00:58:25CandidateSir, both are volume-overload states. [unclear] leads with tall waves [unclear].

00:58:33FacultySir is asking how to differentiate MR from AR on the ECG, from, say, the precordial leads. More specific. Anybody?

00:58:50They all know the answers. Deep S waves in V1 and V2 would say that it is AR, correct. So if you get deep S waves in V1 and V2, you know it is more due to AR than to MR. Why does it occur? What is the reason for the deep S waves in V1 and V2?

00:59:12UnclearDeep S waves in V1 and V2 indicate LV forces. So that would be in AR, because there is eccentric dilatation; whereas in MR, because of left atrial enlargement, [unclear] gets activated.

00:59:24FacultyPerfect. That is the perfect answer: there is truncation of the S waves in MR. It does not occur in AR.

00:59:40Next, the echo. Or I can take the X-ray also.

00:59:49CandidateThis is [unclear]. This is a PA view chest X-ray, overexposed, with normal skeletal structures, with [unclear] CT ratio [unclear].

01:00:11FacultyFine. You can straight away say, at a consultant level you don't have to [unclear]; cardiomegaly is there. The cardiomegaly is of left ventricular type, very typical. You said MR; is there any left atrial enlargement?

01:00:33CandidateNo LA enlargement.

01:00:33FacultyYou can see the prominent, dilated ascending aorta. What is that due to?

01:00:42CandidateDilated aorta… [unclear] regurgitation.

01:00:51FacultyHow can it be post-stenotic? How will you get a dilated aorta? You said bicuspid aortic valve; what happens here?

01:00:59CandidateIt will have post-stenotic dilatation of the aorta.

01:00:59FacultyNot necessarily only post-stenotic. You have an aortopathy, if it is bicuspid.

01:01:20Okay, go to the echo. It almost looks like the Schmoo sign. Do you know what the Schmoo sign is? It doesn't matter; you don't have to know. It is classically described in bicuspid aortic valve AS.

01:01:50CandidateParasternal long-axis view showing the LA and LV, with the mitral valve opening, and the aortic valve. There is [unclear] septal myocardium, with not much [unclear].

01:02:11FacultyConcentric?

01:02:11CandidateConcentric, yes. This is showing concentric left ventricular hypertrophy, with [unclear] segments. Short-axis view at the papillary-muscle level showing LVH. This is at the apical level. This is the short-axis view at the aortic valve level, showing thickened aortic valve leaflets, and the pulmonary artery.

01:02:55FacultyThickened and calcific.

01:03:11What would you want to see to call it a bicuspid aortic valve in this view? To commit yourself to a case of bicuspid aortic valve, what is it that you specifically want to look for?

01:03:27CandidateClosure of the…

01:03:27FacultyYou want to see it in the closed position? Do you diagnose it in the closed position or the open position?

01:03:36CandidateHorizontal or vertical closure; the closed position.

01:03:40FacultyIn the closed position you can confuse it with a raphe; all three may be seen. What will be the shape of the aortic valve in a bicuspid aortic valve in systole? What does it look like with a tri-leaflet valve, and what does it look like with a bi-leaflet valve? Not again in the closed position. In the open position you see the triangular opening, and in a bicuspid aortic valve it is eye-shaped [unclear]. So it is the open position of the aortic valve which gives you the clue, or confirms your diagnosis.

01:04:25The open position is during systole. During systole you should see it [unclear], that's all.

01:04:34CandidateThe five-chamber view showing aortic regurgitation. This is the CW, the continuous-wave Doppler, taken at the [unclear] level, showing a maximum gradient of 83 and a mean gradient of 57, sir.

01:05:01FacultyWhat is the diagnosis? Tell me from the ECG, X-ray, clinical findings and echo.

01:05:06CandidateSir, calcific [unclear], with severe AS; mild to moderate AR, sir.

01:05:10FacultyModerate AR? Where is moderate AR? [unclear: possibly ‘mild’]

01:05:30And [unclear] LV function?

01:05:36CandidateLV function is good, sir. It looks good, sir.

01:05:36FacultyLV function is good. Then what is the L wave? Do you know what the L wave is? What does the L wave tell you about the LV?

01:05:54CandidateIncreased LV pressure, sir, in the diastolic period.

01:05:59FacultyIncreased LV pressure in diastole: it tells you that the LV is stiff, isn't it? Okay.

01:06:10For management, that's what you have to contemplate. Would you like to do a CT here? If so, what will you look for?

01:06:20CandidateAortic valve calcification, and the aorta…

01:06:20FacultyLook at the aorta now: the aortic size. Is the aorta dilated here? [unclear] And the coronaries [unclear], already done. No, you have to look at the aortic size, this being bicuspid [unclear].

01:06:45So what three measurements will you give to the surgeon when you are assessing this sort of case?

01:06:53CandidateThe aortic annulus, and the ascending aorta [unclear]; the dimensions at the sinus and the ST junction, along with [unclear].

01:07:09FacultyWhat do you want to do? Surgery? Why not TAVI? Why not?

01:07:19CandidateThe patient is young, and he doesn't have any comorbidities, sir.

01:07:19FacultyAll your statements are now getting rapidly reversed with advancements. Why don't you want to do a TAVI?

01:07:34CandidateSir, the patient does not have many comorbidities, and the surgical risk is less.

01:07:37FacultyWhat is the age at which you do TAVI?

01:07:42CandidateSir, he is a 49-year-old male.

01:07:45FacultyAt what age do you want to do a TAVI? What are the indications for doing a TAVI in India? What is it in the US, what is it in Europe, and what is it in India?

01:07:58In TAVI, which valve do they put: metallic or bioprosthetic?

01:08:05CandidateIn TAVI, sir, a bioprosthetic one.

01:08:05FacultyIt is bioprosthetic. Self-expanding or [unclear]? And of course there is patient preference. We have to discuss with the patient, even describe metallic versus bioprosthetic, TAVI versus surgery. If the patient says, ‘Do TAVI; I don't want my sternum split’… You can do minimally invasive surgery.

01:08:36But now you should suggest minimally invasive surgery, not just [unclear] surgery. Only if you understand minimally invasive aortic valve replacement. I think it is time to do that. Now what do you say? Nobody wants [unclear].

01:08:57The decision should be based on lifetime management, and not on just one thing. We should also know whether the surgeon is going to put a tissue valve or a mechanical valve at this age, 50 years. So what do you think, at 50 years of age?

01:09:09CandidateMetallic valve.

01:09:12FacultySo if a metallic valve is put, it is done for lifetime management. I can do it; I am ready to go for a valve-in-valve. It is patient preference; you have to discuss it with the patient. The patient may say, ‘Sir, next time I will go for valve-in-valve.’ I have a feeling this aorta is going to take only a 19 mm. It looks quite small, actually; it may take only a 19 mm, 20 mm. What was the annulus, 20 or 21?

01:09:41CandidateIt was small, sir: 20 or 21, sir.

01:09:45FacultyCan we just summarise the case, sir? We'll go to the next.

01:09:45Actually, you have presented quite well. Of course, you must be able to answer many of these questions which we ask; some will be straightforward, some will be a little tilted. But give the history short and nice, because many of these cases in the exam are not real long cases; they are short long cases. It must not be in telegraphic language, but at least in as precise language as possible, and don't go back and forth. Present the symptoms in chronological order. It doesn't matter if you have to say past history; everything can be presented as one history in our set-up. Otherwise it's good.

01:10:39Sir, one question to you. Suppose the patient wants a metallic valve; which valve will you put in? If you want a metallic valve, which valve will you put in? One that requires a very low INR.

01:10:58Anyone want to take that? If the patient has to be put on a metallic valve, which valve would you prefer?

01:11:00UnclearOn-X.

01:11:11FacultyThank you [name omitted]. Thank you, teachers. It was a wonderful case. It takes a lot of guts to stand and present. Thank you so much; give him a big hand. We all learn from such cases. I am sure we all learn from this; it is not just one person presenting.

00:00:00CandidateShall I start, sir?

00:00:00FacultyYes, please.

00:00:03CandidateThank you. This is a 23-year-old male patient who hails from Jharkhand. He studied till 12th standard.

00:00:08FacultyHow old?

00:00:08Candidate23 years old. He has studied till 12th standard, and he has not been working for the past 3 years due to his current condition. He is accompanied by his mother, who is giving the history along with the patient himself, and the history is reliable.

00:00:29His main complaints are dyspnea on exertion for the past 3 years, palpitations for the past 2 years, and hemoptysis, that is, coughing of blood, for the past 2 years.

00:00:43The patient was apparently normal 3 years ago, when he was involved in farm activities along with his father and was able to play with his friends. Later he started to have dyspnea on exertion, which is insidious in onset and gradually progressive in nature. Initially he used to have breathlessness after working in the field for one to two hours, but over a period of 2 years the symptoms have progressed. Now he is unable to work on the farm, and he cannot even go to the farm, which is about two and a half kilometres from his home. So now he stays at home and carries out his daily activities.

00:01:24There is no associated cough, no chronic fever and no breathlessness on lying down, and there is no loss of weight. He is in NYHA class 2, sir, having progressed from class 1 to class 2 over a period of 3 years.

00:01:39FacultyWhat is class 1?

00:01:44CandidateClass 1 is no limitation of physical activity, and having symptoms on exertion, sir.

00:01:51FacultyTry to get the exact wording. Say that again.

00:01:51CandidateThere is no limitation of physical activities, and having symptoms on doing exertional activities.

00:02:00FacultyAnybody? Class 1?

00:02:10AudienceKnown heart disease. Ordinary physical activity does not result in symptoms.

00:02:20FacultyWhat happens on more than ordinary physical activity is left unstated. That's one of the drawbacks. So to say that he has [symptoms on] more than that is not true [unclear]. Ordinary physical activity does not [cause symptoms]. Okay, so he's in class 2 now?

00:02:34CandidateYes, he is in class 2 now.

00:02:34FacultyDid you ask about PND?

00:02:38CandidateYes, sir, there is no history suggestive of it.

00:02:38FacultyWhat class does PND go to? If he has PND, then what class will he be?

00:02:50CandidatePND...

00:02:50FacultyYes. Orthopnea: what class is that?

00:02:50CandidateOrthopnea is class 3, class 3.

00:03:03FacultyDyspnea at rest? Dyspnea at rest?

00:03:08CandidateYes, sir, dyspnea on lying down, or at rest.

00:03:13FacultyIs that rest or not? Lying down is rest, isn't it?

00:03:13CandidateYes, sir. Class 4.

00:03:17FacultyClass 4. And PND? See how you slip up on the most [basic things]. I was even feeling bad to ask such questions; these are such basics. You know what NYHA class 1 is? These are all very basic questions. PND is which class?

00:03:34CandidatePND is not included in the [NYHA] classification.

00:03:38FacultyAnybody? No? Okay. Is PND included in the NYHA classification? You may be class 2, but you may still have PND, because the mechanism is entirely different. So orthopnea is included in the NYHA functional class, but PND isn't.

00:04:04So what are the other limitations of the NYHA classification? What are the components of functional class?

00:04:19CandidateSir, it tells at what level the person feels the symptoms.

00:04:22FacultyWhat are the components?

00:04:26CandidateIt's mainly used for chest pain, dyspnea, palpitations and fatigability, sir.

00:04:35FacultyWhat are the limitations of this functional class?

00:04:42CandidateIt does not include the duration of the symptom, sir. It is cross-sectional.

00:04:47FacultySo it can tell you about the functional class at that point of time. Yes. Next, duration is not included. Subjective or objective?

00:04:58CandidateYes, sir, symptoms are subjective, sir.

00:04:58FacultySubjective. With class 2, [unclear] also. Does it correlate properly with the level of disease?

00:05:13CandidateSince the symptoms are subjective, sir, it varies. Actually, it may not exactly tell the severity of the disease.

00:05:21FacultyDoes it factor in the effect of medical treatment?

00:05:26CandidateYes, sir, definitely. It is going to affect the management also, sir.

00:05:30FacultyExactly. A patient who is in class 4 today will, after diuretics, be in class 3 [unclear].

00:05:37CandidateYes, sir, after the treatment he may improve also.

00:05:40FacultyHe may improve after the treatment, but the valve lesion may be the same or may actually have worsened. It is a dynamic thing. It can vary with the treatment; it can vary with any precipitating conditions. Okay, continue.

00:05:56CandidateThere is history of palpitations for the past 2 years, which is also insidious in onset and gradually progressive. It is regular in nature, and it used to occur for a period of about 10 minutes [unclear]. It is relieved on taking rest and on bearing down. There is no associated syncope, sir.

00:06:15And there is history of hemoptysis, that is, coughing of blood, for the past 2 years. The patient has had about 4 to 5 episodes of coughing of blood over the past 2 years. Before coughing of blood he has 2 to 3 bouts of cough, followed by sputum with streaks of blood, which is fresh red in colour.

00:06:36FacultyMention some cardiac conditions where you get hemoptysis.

00:06:40CandidateMitral stenosis, sir.

00:06:40FacultyAnd why do you get it in mitral stenosis?

00:06:44CandidateSir, in mitral stenosis it is because of pulmonary hypertension, or it could be due to pulmonary apoplexy, or it could be due to an associated coagulopathy. Coagulopathy means the person is in AF and is taking medications, and if it is due to a raised INR [unclear].

00:06:59FacultyWhat are the others? Apart from medication, there are usually 4 causes mentioned. Okay, go ahead. So mitral stenosis is one.

00:07:07CandidateYes, mitral stenosis is one.

00:07:18FacultyAny other cardiac condition?

00:07:18CandidatePulmonary arterial hypertension, sir.

00:07:24FacultyPulmonary arterial hypertension: is it more common in the idiopathic variety of pulmonary hypertension or in Eisenmenger?

00:07:33CandidateIt is also common in idiopathic; it is more common in congenital heart disease–related PAH.

00:07:43FacultyWhy? The pathology? Why is it more common in Eisenmenger?

00:07:53CandidateThe pathology is the same, exactly the same pathology, because [unclear]; there is blood coagulation factor and platelet factor derangement.

00:08:12Sir, coming to other causes: in Eisenmenger also he will have PH; then it could be due to cyanotic conditions, or due to platelet dysfunction, or coagulopathy. They can have hemoptysis.

00:08:31FacultyWhy is there hemoptysis?

00:08:37CandidateBecause of the raised PA pressure, there will be rupture of the bronchial arteries, or bronchial erosion, causing the bleeding. The raised PA pressure is transmitted to the bronchial arteries, causing rupture and/or erosion of the bronchial arteries. Also, pulmonary infection.

00:09:10And hemoptysis can also occur in pulmonary embolism.

00:09:10FacultyOkay, continue.

00:09:15CandidateWith these complaints the patient consulted a local cardiologist in Jharkhand, where he was examined and told that there is a hole in the heart. He was further examined and underwent a groin procedure. Later he was told to continue the medications and not to undergo surgery immediately. So he was prescribed medication. After taking the medication, the symptoms have not completely subsided; there is persistence of the symptoms, sir, after which he has come here for further evaluation and management.

00:09:50There is no history of syncope, no chest pain, and no prolonged fever or rash. There is no history of swelling [unclear] or abdominal distension. There is no history suggestive of any seizure disorder or focal neurological deficit.

00:10:12There is a past history, sir. In early childhood, at the age of 3 years, the mother noticed the child was crying excessively, was irritable and was not gaining weight. With that complaint they showed him to the local doctor, where he was admitted for a period of one week and given IV antibiotics, and they were told he had pneumonia. After that he was told to follow up, and they were also told that it may subside over a period of time. Since the symptoms subsided over a period of 2 years and the child started to gain weight on his own, they didn't go to the doctor again. Until 3 years ago the patient was asymptomatic, so they did not consult a doctor; now, because of the symptoms, they have consulted again.

00:10:57Coming to the personal history: he has a mixed diet and normal appetite; bowel and bladder are normal. He is an ex-smoker; he stopped 3 years ago. The treatment history is of taking 2 medications. He is not able to name them, but he says he takes one medication 3 times daily. There is no history of similar complaints in the family members. The patient comes from a lower-middle-class family, where he lives with his mother, father and brother. The brother is fine and does not have a similar clinical history.

00:11:38FacultyDid you ask about consanguinity?

00:11:42CandidateYes, sir, it is a non-consanguineous marriage. The patient is accompanied by his mother, and she has told that it is a non-consanguineous marriage. The four of them live [unclear]; there are 4 rooms.

00:11:55FacultyWhy is consanguinity important?

00:11:55CandidateSir, consanguinity increases the risk of heart diseases, an increased risk of genetic disease also. There is a pooling of genes [unclear], and there is more chance of getting [them].

00:12:14FacultyThis is what I mean: inbred [unclear] can be more. Which kinds of diseases are a little more common when there is a history of consanguinity?

00:12:28CandidateAutosomal...

00:12:30FacultyRecessive or dominant?

00:12:30CandidateAutosomal recessive, autosomal dominant...

00:12:30FacultyRecessive. Why? Simple questions. For autosomal dominant you don't need consanguinity; without consanguinity you can pass it on. Recessive conditions: can you name one recessive condition in cardiology? We should know at least a few that are autosomal dominant and autosomal recessive. A few you must know.

00:13:00CandidateSir, in case of...

00:13:00FacultyAnybody? Autosomal recessive?

00:13:07AudiencePompe [unclear].

00:13:12Ellis–van Creveld.

00:13:12FacultyThis is what?

00:13:12CandidateYes, sir. Ellis–van Creveld syndrome, mainly also with peg-shaped teeth, sir.

00:13:17FacultyAutosomal dominant, or is it [unclear]? Okay, continue.

00:13:24CandidateOkay, sir, I would like to summarise the case. This is a 23-year-old male patient with insidious-onset, gradually progressive dyspnea on exertion, progressing from NYHA class 1 to NYHA class 2, associated with exertional palpitations and episodes of hemoptysis, for which the patient consulted a cardiologist. There he was examined and told he has a hole in the heart. He also underwent a groin procedure, after which he was told not to undergo the procedure and was advised medical management. There is also a childhood history of increased irritability and poor weight gain, with later improvement of the symptoms.

00:14:08FacultyThat is just one episode, right?

00:14:12CandidateYes, sir, that is only one episode. But the child used to have on-and-off infections, sir, not requiring hospitalisation or IV antibiotics.

00:14:22FacultyDiagnosis?

00:14:24CandidateSo my diagnosis would be acyanotic congenital heart disease with increased pulmonary blood flow, post-tricuspid shunt. So possibly it could be VSD with PAH, or PDA with PAH, or it could also be a partial or intermediate kind of AVCD with PAH. Yes, I am suspecting, sir...

00:14:54FacultyGrown-up congenital heart disease.

00:14:54CandidateYes, grown-up, and probably Eisenmenger physiology.

00:14:58FacultyWhich covers [it], yes. So he has been told that he is inoperable. So what do you think? Is it only Eisenmenger, or can it be anything else?

00:15:05CandidateSir, they have told that as of now it can't be operated; he needs medical management. He was given a course of medication, sir, so we may test the operability. Repeat operability can be tested, sir.

00:15:21FacultyAnything else you can think of other than Eisenmenger syndrome, if a cath procedure has been done and he is told that he is not operable? Any others apart from Eisenmenger syndrome?

00:15:36CandidateIt could be... If I exclude the hole in the heart, I may think of other things. Sir, if you include the hole in the heart as well, it could be Eisenmenger due to a small hole in the heart, like a small ASD; a small ASD with associated primary pulmonary hypertension...

00:15:54FacultySo you bring in 2 pathologies?

00:15:59CandidateIf I include only smaller, subtle defects associated with concurrent pulmonary hypertension, it may become...

00:16:07FacultyGenerally you do not bring in 2 pathologies when you're giving a diagnosis. But now that you have brought it in, tell me one condition where you get pulmonary hypertension and a hole in the heart, where the pulmonary hypertension may be out of proportion to the hole. In what condition? In what congenital condition can you get a defect and pulmonary hypertension which may not be entirely related to the cardiac condition? Anybody?

00:16:42CandidateAVCD, sir. They may be associated with pulmonary hypoplasia; AVCD in Down syndrome patients, sir. Down syndrome.

00:16:49FacultyYes, Down syndrome patients are known to have that.

00:16:53CandidateYes, sir, Down syndrome.

00:16:53FacultyOkay, but generally you don't bring in 2 pathologies, right? And don't say small ASD or small VSD, because that cannot produce Eisenmenger.

00:17:04Sorry, what was the question you had? How does he become inoperable even when he doesn't have Eisenmenger? Am I right?

00:17:09Yes. He doesn't have Eisenmenger, but he still becomes inoperable.

00:17:18CandidateSir, Eisenmenger is a late thing. Because of severe PH he may not be operable, sir.

00:17:23FacultyEisenmenger is a... You didn't understand the question. Try to understand the question. It is not Eisenmenger, but it is still inoperable.

00:17:36CandidateIt may be because of a single-ventricle physiology kind of thing; it may not be operable, sir.

00:17:40FacultySingle-ventricle physiology. Yes.

00:17:47CandidateComing to the examination, sir: the patient is well built but poorly nourished, conscious, cooperative and well oriented to time, place and person, with a height of [unclear] centimetres, a weight of 45 kg and a BMI of 14 kg/m². There is no [unclear]. Grade 3 clubbing is there, and the patient has central cyanosis. There is no lymphadenopathy and no edema, but severe conjunctival suffusion is present, sir. There are no signs of infective endocarditis [unclear] and no signs of [unclear] runoff.

00:18:24The heart rate is [unclear] beats per minute: normal volume, regular in rhythm, normal in character, with all peripheral pulses felt, no radio-radial delay and no radio-femoral delay. The blood pressure in the right upper limb is 100/70 and in the left upper limb 104/70, and in the lower limbs it is 115/[unclear] bilaterally, sir.

00:18:51The respiratory rate is 20 per minute, abdominothoracic type of respiration, sir. The saturation in all 4 limbs is about 89%.

00:19:03FacultyAt what level of saturation do you get cyanosis?

00:19:10CandidateGenerally less than 90%, 92%... less than 94% [unclear].

00:19:23FacultyDoes it correlate with the level of hemoglobin?

00:19:23CandidateYes, sir, definitely. About 5% [unclear] of deoxygenated hemoglobin causes cyanosis, sir.

00:19:32FacultyAt the same saturation [unclear], you may be cyanosed if you have a hemoglobin of 20, and you may [unclear] be cyanosed if you have a hemoglobin of 5.

00:19:41CandidateYes, sir.

00:19:44FacultySo the answer is not [simply] saturation [unclear]. Did the patient not notice that he is becoming blue?

00:19:52CandidateNo, sir. He's a bit dark also.

00:19:54FacultyDid you ask him positively at the end of your examination?

00:19:59CandidateYes, sir, I asked, actually, but he was not able to appreciate it. He is a bit dark in colour also, sir, so he's not able to appreciate it.

00:20:08Sir, the JVP was elevated when I examined him in the lying-down position with a pillow behind him.

00:20:16FacultyIn the lying-down position, when you say the JVP is elevated...

00:20:16CandidateNo, with one pillow, like that.

00:20:22FacultySo does that constitute... How do you say that the JVP is elevated?

00:20:29CandidateI make the person lie down at a 45-degree angle, sir. Then I will see...

00:20:34FacultyWhat was it, sir? Just make him sit up and see. Was it elevated in the sitting position?

00:20:38CandidateThe JVP was elevated, sir.

00:20:43FacultyThat's all. In the lying-down position the jugular venous pulsation will be seen normally also. In the sitting position, was it seen above the...?

00:20:51CandidateYes, it was seen, sir, and that's elevated.

00:20:55FacultyWhat was seen? The waves were seen, or the mean level was elevated?

00:20:57CandidateProminent a waves were seen, sir. Prominent a waves are seen, and it is about 5 centimetres from the sternal angle. So it is elevated, sir; there is elevation of the JVP, and there is normal respiratory variation.

00:21:14FacultyAnd a prominent a wave?

00:21:14CandidateProminent a wave, sir.

00:21:14FacultyOkay, fine. Since there is a prominent a wave, which lesion do you want to exclude here?

00:21:19CandidateSorry, sir?

00:21:22FacultyA prominent a wave with Eisenmenger physiology: which lesion do you want to exclude here? Which lesion can be excluded?

00:21:31CandidateSorry... Ebstein anomaly may not be involved.

00:21:42FacultySorry, which type of Eisenmenger physiology? If the patient has a very tall a wave, which do you want to exclude?

00:21:55CandidateEisenmenger [unclear]...

00:21:57FacultyEisenmenger can be excluded when you have a prominent [a wave]?

00:22:07CandidateUsually it will be caused by PH and severe RVH, sir. [unclear] level, sir; [unclear] level excluded.

00:22:18AudienceASD can be excluded with a prominent a wave.

00:22:33FacultyOkay.

00:22:36CandidateComing to inspection and palpation, sir: the chest is symmetrical and the trachea is central. The apical impulse is felt in the left 5th intercostal space, half an inch medial to the midclavicular line. It is diffuse in nature, with lateral retractions [unclear]. There is also a palpable P2. Sorry, palpable... P2 is felt in the left second intercostal space.

00:23:02FacultyHow do you know it is P2 and not A2?

00:23:02CandidateSorry: palpable second sound, sir.

00:23:07FacultyPalpable second sound. We don't know if it is A2 or P2. Just because it is palpable in the pulmonary area doesn't make it P2. [unclear]

00:23:17Her question is: can you get A2 in the pulmonary area?

00:23:22CandidateYes, sir, in TGA.

00:23:22FacultyCan you get A2 in the pulmonary area? Yes. [unclear] in CCTGA.

00:23:31CandidateThere are also visible pulsations in the left second intercostal space, and there is also a palpable second sound in the second intercostal space.

00:23:36FacultyAnd you can tell that depending on the company it keeps, based on the other history and examination findings [unclear]. Not now.

00:23:51CandidateSo there are pulsations in the second intercostal space, and a palpable S2, also visible [unclear].

00:24:01Coming to percussion, sir: the left heart border is along the apex, and the right heart border is retrosternal. The left second intercostal space is dull. The hepatic dullness is in the right 5th intercostal space, and stomach tympany is in the left [unclear] intercostal space. On auscultation, S1 is of normal intensity and S2 is loud. A single P2 is heard, sir, and it is loud. There is a single S2, a single sound, sir, and that is P2. A single, loud P2 is heard, sir.

00:24:39FacultyHow do you know it is P2 and not...?

00:24:51What happened to A2, then? You're saying there's only a pulmonary component; then what happened to the aortic component?

00:25:00CandidateSir, it would have become single, sir.

00:25:03FacultyPardon?

00:25:03CandidateIt has become single, sir.

00:25:07FacultyDo you say P2, or an isolated P2? You said single P2.

00:25:13CandidateThe single sound, yes, second sound.

00:25:13FacultyWhen you say P2 is loud, what are the defining criteria?

00:25:16CandidateIf I am able to hear P2 with the same intensity in the right second intercostal space, and I am able to hear it with good intensity at the apex also, sir, I take it as a loud P2.

00:25:29FacultyThat's all. At your apex, as well as the second intercostal space, at a similar intensity to A2 [unclear].

00:25:42CandidateAnd on auscultation, sir, S1 [unclear], S2 [unclear]. Loud at the apex, but there is no [unclear], due to pulmonary dilation, sir [unclear].

00:26:10FacultyASD is a condition where you can get a loud P2 at the apex but there is no PH. Why is P2 loud at the apex in ASD?

00:26:26CandidateThe RV is dominant, so all right ventricular events will be heard at the apex very well [unclear]. And P2 is loud [unclear]; pulmonary elasticity is increased, so pulmonary valve closure is very brisk even though there is no PH. It is because of increased flow, sir.

00:26:52And on auscultation there is also a high-intensity ejection click, a vascular ejection click, heard in the left second intercostal space, sir, and it is [unclear] phasic, non-phasic.

00:27:11FacultyWhere do you get a phasic click?

00:27:11CandidateA click is in valvular PS.

00:27:18FacultyWhat is phasic? She is asking.

00:27:18CandidateYes, sir. If the person is in deep inspiration, sir, the click will be reduced; that is [unclear]. If it is due to PH, there will be a more accentuated [click], sir.

00:27:34FacultyNo: phasic or non-phasic, she is asking.

00:27:37CandidateIt is non-phasic, sir. And there is also a harsh pansystolic murmur in the left lower [sternal border], in the left 4th intercostal space, which increases with respiration, with a grade of 3/6.

00:27:57It increases with inspiration, grade 3/6. And there is also a blowing early diastolic murmur of grade 2/4 heard in the left second intercostal space.

00:28:10FacultyYes, these murmurs I want to hear. What is blowing? What?

00:28:16CandidateEarly diastolic, blowing, in the left second intercostal space, sir. PR.

00:28:28So I would like to summarise. My diagnosis: situs solitus, levocardia, congenital heart disease with reduced Qp physiology as of now, with Eisenmenger, post-tricuspid, probably at the ventricular level, with severe PAH, no PVH, normal LV function and normal RV function, in normal sinus rhythm, with no signs of infective endocarditis and no signs of heart failure, in NYHA class 2, sir.

00:28:59FacultyYou said the JVP is elevated.

00:29:05CandidateYes, sir, the JVP is elevated, sir, but there is no heart failure.

00:29:10FacultyYou got an a wave?

00:29:10CandidateYes, a wave. The a wave is prominent, sir.

00:29:15FacultyNo, you said the JVP is elevated, not just the a wave. You said it's 5 centimetres.

00:29:15CandidateYes, sir.

00:29:15Faculty5 centimetres, that's elevated. Let me clarify: is the JVP elevated, or is it a prominent a wave?

00:29:24CandidateA prominent a wave, yes, sir. And I was able to see it up to 5 centimetres [unclear]. And also the a wave is prominent, sir; it could be due to PH.

00:29:39FacultyNo. Due to PH, without heart failure, how can you get [it]? No, then what's your concept of heart failure? PH without heart failure: can you get elevation of mean JVP? We are not talking about prominent a waves; we are talking about elevation of the mean JVP, which is what you presented.

00:30:00CandidateYes, sir, there will be elevation of the JVP in heart failure, sir.

00:30:03FacultyThen you will have to say it is incipient heart failure, or you will have to qualify it, but you can't say no heart failure. Heart failure is present. You have heart failure with preserved ejection fraction, reduced [ejection fraction]. What ultimately determines heart failure is elevated filling pressure.

00:30:22CandidateYes, right.

00:30:22FacultyFilling pressure is in the ventricle. If it's high, that's right.

00:30:37PH with reversal. And always present it like that. Don't present it as Eisenmenger; it is very difficult in Eisenmenger. If you read Paul Wood, he will say that it is very difficult to locate the level of the shunt, even with autopsies. Sometimes you have to take recourse [unclear]. So always present it as severe pulmonary hypertension. If there is [unclear], you can say [it]; if there is pulmonary regurgitation [unclear].

00:31:12One small question: what is the skin sign of an intermittent right-to-left shunt? What is the skin sign of an intermittent right-to-left shunt? What will be the skin sign, especially in a fair person?

00:31:34CandidateIt is a bluish hue.

00:31:34FacultyNo, it's called [unclear], in the fingers. It is supposed to be fine, especially lace-like [unclear].

00:31:49AudienceSir, [unclear]. I don't think that goes in favour of VSD.

00:32:06UnclearSingle-ventricle failure, sir [unclear].

00:32:10FacultySo you are considering Eisenmenger VSD, right?

00:32:10CandidateYes, sir.

00:32:13FacultySo what are the points in favour from your examination, and what are the points against that diagnosis of Eisenmenger VSD?

00:32:18CandidateThe points favouring Eisenmenger VSD: there is no cardiomegaly, that is, the heart is small, and there is an RV type of apex. Along with that, there is a single P2 sound, sir, and along with that PR is there, sir.

00:32:35FacultySo all Eisenmenger VSDs will have a single second heart sound?

00:32:35CandidateYes, sir.

00:32:40FacultyWhat happens with ASD?

00:32:40CandidateThere will be persistence of wide, fixed splitting of S2.

00:32:49FacultySo the presence of a single second heart sound can favour VSD [unclear], but its absence will not rule it out in most scenarios. Okay, so the PR murmur which you have here?

00:32:57CandidateYes, sir. They will have an associated narrowly split S2, sir. And along with that there will be a dilated aorta [unclear], and a more predominant PR is seen in [unclear].

00:33:12FacultyYes, absent pulmonary valve. In this case you are getting a clear murmur. Why not absent pulmonary valve? With absent pulmonary valve, why not?

00:33:17CandidateSir, if absent pulmonary valve were present, on examination there would be a to-and-fro murmur, sir. But in this case there is only an early diastolic murmur, sir. So I think [unclear]. And on history, there will also be recurrent respiratory tract infections, sir, but this patient is not having respiratory tract infections.

00:33:36FacultyNo, you can have [unclear].

00:33:41CandidateYes, sir.

00:33:41FacultyWhat apex do you get?

00:33:45CandidateIn both cases, an RV type of apex, sir: in absent pulmonary valve as well as [unclear], an RV type of apex.

00:33:58FacultyWhy do you get recurrent respiratory infections? You said that's a feature.

00:34:02CandidateYes, sir. Because there will be aneurysmal dilatation of the pulmonary arteries, which will cause obstruction of the bronchi, causing atelectasis and leading to infections.

00:34:14FacultyCould it be truncus?

00:34:14CandidateTruncus, sir: they usually present with cyanosis at birth only, sir; early onset of cyanosis will be there.

00:34:25FacultyNo, at birth it may be very minimal, minimal cyanosis may be there, and they develop Eisenmenger early [unclear].

00:34:33CandidateYes. Early age of cyanosis and early age of Eisenmenger is the picture of truncus, and prominent cyanosis.

00:34:47FacultyWhat are Eisenmenger syndrome and Eisenmenger complex? Is there any difference?

00:34:47CandidateYes. Eisenmenger complex is when the rise in RV pressure and PA pressure is more than the LV pressure, in the case of a VSD, sir, and there is shifting to a right-to-left shunt; in the case of VSD it is called Eisenmenger complex. Eisenmenger syndrome occurs due to defects apart from VSD, like PDA or ASD, or it could be due to an AP window.

00:35:21FacultyYes. Can multiple branch pulmonary stenoses behave as PH?

00:35:32CandidateYes, sir. In supravalvular PS, in Williams syndrome, there will be branch pulmonary stenosis [unclear]. Sorry, sir, what was the question?

00:35:43FacultyCan multiple branch pulmonary stenoses behave like PH, like PH at the ventricular level, not at the pulmonary [unclear]?

00:35:58Yes. What I was asking you, what I told you: no examiner wants one diagnosis. We don't want one diagnosis. You have to discuss. So why is it VSD, PDA? Why not ASD, the other diagnoses? [unclear] You will be in trouble. [unclear, partly in Hindi] So discuss.

00:36:30You also want to spend one hour, so we also need some discussion points. Otherwise, if you say VSD Eisenmenger, in 15 minutes we can get over. So we need some conversation points.

00:36:43Got it. What do you want, ECG or X-ray first?

00:36:43CandidateSir, I would go for X-ray, sir.

00:36:47FacultyWhy X-ray, if hypothetically there's only one investigation that we can get?

00:36:57CandidateI would go for X-ray, sir. On X-ray I am able to differentiate ASD, VSD or PDA. Along with that, I can differentiate the reason behind the increase [unclear]. In case of ASD, ma'am, there will be persistence of cardiomegaly; in case of VSD there won't be cardiomegaly; and in case of PDA...

00:37:24FacultyASD, ASD: what else? In VSD you get no cardiomegaly; what else do you get?

00:37:27CandidateAlong with that, in ASD there will be associated dilatation of the RA, sir, and an RV type of apex. In VSD there won't be cardiomegaly, and there will be a dilated MPA, and along with that peripheral pruning; LA enlargement may be there. And in PDA, sir, there will be associated enlargement of the aorta, and there is loss of the aortopulmonary window, radiological loss of the aortopulmonary window.

00:38:02Sir, this is a chest X-ray, PA view, with [unclear] exposure, showing no cardiomegaly, with a CT ratio of less than 0.5, and an RV type of apex. Along with that, there is a dilated MPA, and there is peripheral pruning of the vasculature, sir. There is also a dilated RPA, and there are multiple end-on vessels, more than 5 on both sides combined. So this is suggestive of PAH.

00:38:32FacultyNo, I just want an answer from you. Why not [unclear]? [unclear, partly in Hindi] What do you think?

00:39:10Why do you say it is pruned? Because [unclear], it is not so emphatically pruned, let me put it. And what will happen to the vascular markings in an overexposed X-ray? Is this overexposed or appropriately exposed?

00:39:24CandidateOverexposed.

00:39:24FacultyWhat will happen to the vascular markings?

00:39:27CandidateA bit more enhanced.

00:39:29FacultyMore enhanced? No. The lungs get blackened out, and they are actually less seen. So that's why it should be appropriately exposed.

00:39:41Can you trace the right descending pulmonary artery, the RDPA? Can you just show it? Why is it important?

00:39:51CandidateSir, in scimitar syndrome you can see a sword-like thing.

00:39:56FacultyScimitar syndrome there. What is scimitar syndrome?

00:40:00CandidateScimitar syndrome is a partial anomalous pulmonary venous connection, sir, associated with right lung hypoplasia, where the pulmonary veins from the right lower side make a confluence and drain into the IVC, sir. So it looks like a sword.

00:40:20FacultyA Turkish sword, yes. So you see that the right descending pulmonary artery is seen much lower. Have you seen the pictures of that? The textbooks have shown that. It is sometimes associated with sequestration of the lung.

00:40:39How would you radiologically say that there is pruning or no pruning?

00:40:43CandidateIf there is pruning, in the distal, peripheral one-third there will not be much vasculature.

00:40:52FacultyAbrupt reduction in the calibre of the vessel by more than 50%. Abrupt change in calibre.

00:41:09CandidateDescending pulmonary [unclear]. The ascending [unclear] is not enlarged.

00:41:13Faculty[unclear] means the descending pulmonary artery, the right pulmonary artery.

00:41:18CandidateYes, sir, the pulmonary artery is enlarged. The right pulmonary artery is enlarged, and the left main pulmonary artery is also enlarged. [unclear] it is underexposed [unclear].

00:41:32FacultyThis is the one sign on the X-ray which can tell you that a VSD is likely to be present. Not 'likely': 100% present. X-ray signs [unclear].

00:42:01CandidateIn VSD it is about 67% only, ma'am, but in TOF, right aortic arch [unclear].

00:42:08FacultyYou tell the diagnosis: right aortic arch with plethora, and right aortic arch with pulmonary oligemia. What are the diagnoses?

00:42:18CandidateYes, sir. For a right aortic arch with pulmonary oligemia, I will go for TOF physiology, sir; and for a right-sided aortic arch with plethora, VSD, sir, truncus.

00:42:38FacultyWant to see the ECG? We are running short of time.

00:42:49CandidateSir, the ECG shows a rate of 100 beats per minute, with right axis deviation of about plus [unclear] degrees, and there is prominence of the R wave compared to the S wave in V1, suggestive of RVH.

00:43:13FacultyThank you. Want to comment on right atrial and left atrial abnormality? Right atrial abnormality?

00:43:23CandidateThe initial force of the P wave in V1 is more than one small box, so I think of right atrial enlargement.

00:43:27FacultyThis is half standard. This is half standard. In V1 or V2, how tall should the initial positive vector be for right atrial enlargement?

00:43:44CandidateOne small box, sir.

00:43:44Faculty1.5, or the area; even that's mentioned.

00:43:53CandidateMore than one [unclear] small box.

00:43:56FacultyArea under the curve, just as you say for left atrial enlargement: the P terminal force. How will you diagnose left atrial enlargement based on the terminal vector in V1? What is the [unclear]?

00:44:12CandidateIf the terminal force of the P wave is more than one small box, call it left atrial enlargement.

00:44:17FacultyOne small box in which dimension?

00:44:25CandidateIt should be 0.04 in duration and one [unclear]...

00:44:29FacultyYes. So it is usually said more than 0.03 [unclear], in the old [unclear]. Similarly, that is the area subtended by it. Similarly, for the RA also it is there: 0.06, or 1.5 millimetres in height.

00:44:47Okay, what else is there? I think there's borderline left atrial enlargement based on this. The P terminal is actually more [unclear].

00:44:58CandidateBut there are no Q waves, sir, Q waves in the lateral leads.

00:45:02FacultyNo Q waves in the lateral leads. Why do you expect Q waves?

00:45:06CandidateNo, in [cases where] there is left ventricular enlargement, LV dilatation.

00:45:10FacultyWill we expect that in Eisenmenger VSD? Do you expect that?

00:45:13CandidateNo.

00:45:13FacultyPlease don't say it is not there because you are not expecting it in Eisenmenger VSD. Do you have LV dilatation? The first thing is to describe the findings correctly; then we look for an explanation. You can't say a finding is not there because you can't explain it. That's not the way it works.

00:45:32Do we have an echo? What's the Katz–Wachtel phenomenon?

00:45:35CandidateThe Katz–Wachtel phenomenon is in V2, V3, V4, sir: if the R wave plus the S wave is more than 50 millimetres, it indicates biventricular hypertrophy.

00:45:52So this is a PLAX view showing a large perimembranous VSD with muscular extension, with a bidirectional shunt: a non-restrictive VSD, sir.

00:46:07This is a short-axis view showing dilation of the RV and the RVOT.

00:46:19This is a short-axis view at the aortic level, showing the large non-restrictive VSD with a bidirectional shunt. And then also PR is there.

00:46:46FacultyWhat was the PR? Was it severe PR or non-severe?

00:47:03Unclear[unclear, in Hindi]

00:47:06CandidateSo it shows [unclear] PH.

00:47:19Here they are showing the mean PA pressure as 31.

00:47:23FacultyWhat is taken now?

00:47:23CandidateIt is showing a mean PA pressure of 30.

00:47:31FacultySo you have the right atrial pressure from your JVP, and you have the mean pulmonary artery [gradient] from the early PR gradient [unclear]. You have to be more objective and tell.

00:47:40CandidateSo it will come to 40, sir. [unclear] about 8, sir, approximately the RA pressure. So 31 means about [unclear], up to 40, sir.

00:47:53FacultyI feel the mean PA pressure is around 40. Is that consistent with the diagnosis of Eisenmenger?

00:48:02CandidateThe mean PA pressure should be more than 50, sir, actually, for severe PH, for Eisenmenger. More than severe PH will be there.

00:48:07FacultyHow do you define Eisenmenger? Do you know how Paul Wood described it? Anybody?

00:48:16CandidateSir, if severe PH causes a right-to-left shunt, resulting in cyanosis.

00:48:21FacultySo the PA pressure will be at what level?

00:48:21CandidateMore than 50, sir.

00:48:26FacultyIf his PA pressure is 50 and there's a non-restrictive VSD, what is the aortic pressure?

00:48:45CandidateThat's difficult.

00:48:45FacultyOkay. The PA pressure is 50. Okay? Let's say the systolic is 60 or something like that. What is the RV pressure?

00:48:55CandidateIt will be similar, sir.

00:48:55FacultyWhat is the LV pressure?

00:48:59CandidateSimilar, sir.

00:48:59FacultyWhat is the aortic pressure?

00:48:59CandidateSimilar.

00:49:04FacultyFor the aorta, there is no AS. So do you think that is 40? Unless there is pulmonary stenosis, can his [unclear] pressure be 100, and 30 or 40 [unclear]? Do you think that is possible? It is not consistent with your diagnosis at all. It has to be at systemic level.

00:49:33Good presentation. You can be a little slower; sometimes you go a little fast. Yes, good. More than anything else, I appreciate the fact that you had the courage to come up and present. This is what should really be appreciated, and all of you should do it. You are not here to impress me, or the other examiners, or anybody else, or your colleagues. You are here to pass the exam, that's all.

00:49:55When he makes a mistake, you may not remember it tomorrow. When you make a mistake, you'll remember each and every mistake, and you'll never do it again. So whatever your level of knowledge or ignorance, don't feel bad, and don't feel hesitant to come up, present and make mistakes. The more mistakes you make on stage, the more all of you will learn from it. So please take every opportunity, today and tomorrow, to come up and present.

00:50:27CandidateThank you, sir.

00:50:27FacultyYes, thank you. A comment on the previous case as well as this case. I think the JVP presentation needs to be sharper. The JVP is normally presented in 3 different parts: the mean JVP, the positive waves and the descents. You must include all 3 in the JVP. Even in the previous case it was a bit deficient, and even here you could have been sharper.

00:50:54The second thing is the X-ray description. Traditionally you start with the right heart border, the left heart border, and the peripheral pulmonary venous and pulmonary arterial [vasculature]. Please stick to that. Don't jump from one place to the other.

00:51:06The third thing is that eventually all exams are a series of questions, right? So you need to anticipate the series, and you should be able to quote one text for your answer. Loud S1: what is the definition? Soft S1: what is the definition? There will be huge interpersonal variations, but you should be able to speak by quoting just one text, whether you quote Hutchison, Paul Wood or Braunwald; you should be able to quote one. And I can assure you, the variations of heart sounds and murmurs cannot be more than 100-plus. But you need to anticipate these.

00:51:53And as the other examiner said (he's not here now), we are eventually here to discuss. We are here to identify whether you have understood the science behind it. Okay, all the best. Thank you.

00:00:04CandidateGood morning. My patient is a 33-year-old male, a resident of Odisha.

00:00:09FacultyOne minute. Be clear, and a little slow.

00:00:16CandidateThe patient is a 33-year-old male, a resident of Odisha, with formal education till 10th standard, currently unemployed, who presented with complaints of chest pain for the past 20 years. The patient was apparently asymptomatic until he developed chest pain on exertion, starting at around 13 years of age. He had typical chest pain; that is, he used to have chest pain while running, while bicycling and on walking around 2 kilometres, amounting to NYHA class 2. He did not have any shortness of breath, presyncope or syncope at that time. He consulted a heart specialist in Odisha.

00:00:55FacultySo you are done with chest pain? That is all you have said? See, angina is a clinical diagnosis. It is not a diagnosis you make on ECG, echo or a stress test, right? And if you get a history of typical angina, it has a very strong positive predictive value. So we expect you to say that it is the first symptom, and probably the only presenting complaint. You need to spend more time on the chest pain. What are all the things you will describe? The character of the pain?

00:01:31CandidateSir, the location was central, retrosternal, radiating to both shoulders. It increased on exertion and was relieved with rest. Usually, after exerting for 2 kilometres while walking or bicycling, he would have the pain.

00:01:46FacultyYou should also ask, though it is not always mentioned in books, how quickly does it reduce?

00:01:52CandidateWithin 5 to 10 minutes.

00:01:52FacultyUsually it lasts only 2 to 5 minutes. Sometimes patients say they get pain on exertion, maybe because they are doing something heavy with their hands, and it reduces after half an hour or one hour. That is not relief with rest. So please ask about that also: is it relieved within 5 minutes of taking rest?

00:02:11CandidateIt reduces.

00:02:11FacultyWhat else do you ask about when you describe the character of the pain?

00:02:19CandidateWe have the retrosternal location, the site of the pain.

00:02:23FacultyWhat is the character of the pain? What did he tell you?

00:02:23CandidateHe described it as a vague pain. He didn't describe any pricking or stabbing.

00:02:32FacultyDid you ask about the character? You must ask.

00:02:35CandidateHe said a vague pain, radiating to both shoulders.

00:02:35FacultyRadiation is one thing, character is another, so don't confuse the two, okay? And there is some confusion about this typical and atypical classification. That is based on the [year unclear] ACC/AHA guidelines, where they said they would like to discourage the use of it. Why? Because many of those with so-called atypical pain also tend to have ischemic heart disease. But if you look at the 2026 Braunwald, it is much broader. It says chest pain has three characteristics: retrosternal, what aggravates it, and what relieves it. And the latest Braunwald still says typical angina, atypical angina and non-anginal pain; that is there in the 2026 Braunwald.

00:03:31So I don't know whether we are ready to discard that. I personally like that classification, because I think it has huge value, as long as you realise that some patients with atypical or so-called non-anginal pain may still have coronary artery disease. But the guidelines say only...

00:03:52Yes, that was the 2021 [ACC/AHA, unclear] guidelines. The 2026 Braunwald is still mentioning it.

00:03:57UnclearBraunwald is quoting from the old reference.

00:03:57FacultyNo, 2026 has just come out. The most recent is probably acceptable. Okay, fine, it is acceptable.

00:04:13So all I am saying is that it is still a debatable point. I don't know whether we are ready to discard that classification as of now. The important thing is that in exams you need to have a reference, right? 'This book says this' or 'this guideline says this'; generally the examiner will then accept it. So be sure of your reference. But whatever it is, you should put it in the terms he described: the precipitating factor and the relieving factor. As I told you, keep that in mind always. Why only angina? For any pain: precipitating factor, relieving factor, all of that. Keep it.

00:04:55CandidateWith this complaint, he consulted a heart specialist in Odisha, and upon evaluation he was told he had a heart condition, for which he was referred to Bangalore, here at Sathya Sai. That was at the age of 15 years, 2 years after the onset of his symptoms. He was admitted here and underwent a balloon-based intervention via the right groin along with stenting, and he was started on one tablet, which he said was Ecosprin 75 mg once daily, which he continued.

00:05:24FacultySo at this point, what's your diagnosis?

00:05:27CandidateA balloon-based intervention at the age of 15 years, with stenting; he mentioned stenting, and he says he was started on Ecosprin 75. If stenting were not mentioned, one possibility would be balloon aortic valvotomy for aortic stenosis; then coarctation.

00:05:49FacultyIs that commonly done for aortic stenosis?

00:05:53CandidateBalloon aortic valvotomy, in children. Then balloon pulmonary valvotomy for PS.

00:05:53FacultyYes. Can that produce angina?

00:05:53CandidateIt can produce angina, with RVH.

00:06:00FacultyYes, it can.

00:06:06CandidateThen balloon mitral valvotomy for mitral stenosis.

00:06:10FacultyNo, but that will not present with chest pain. It is very clearly anginal chest pain; we are talking of anginal chest pain. Any other procedure? Okay, forget the procedure. A 13-year-old boy complains of anginal chest pain. What are the conditions you will think of?

00:06:33CandidateRVOT and LVOT obstructions are the main ones.

00:06:33FacultyAnything else?

00:06:38CandidateCoronary artery disease you have to consider.

00:06:41FacultyThird possibility? Louder.

00:06:45CandidateCoronary artery disease would be the third possibility.

00:06:45FacultyYou already mentioned that. Anything else? Any inflammatory disease involving the coronary arteries?

00:06:52CandidateInflammatory disease involving the coronary arteries that happened in the past. Younger patients can present with coronary artery involvement.

00:06:59FacultyAnything else?

00:07:03CandidateKawasaki. Can they present with aneurysms and stenosis?

00:07:03FacultyBefore 12, yes, but it could be the aftermath. It could be a late presentation. Though the most characteristic lesion is the aneurysm, stenosis is also described. What about coronary anomalies?

00:07:24CandidateCoronary anomalies can present. They can have an interarterial course, and on exertion they can develop symptoms, chest pain: a slit-like orifice with a long intramural course, and an interarterial course.

00:07:35FacultyWhy didn't you say it? [unclear] I get the marks, not you.

00:07:39CandidateBut for that, he would have been advised surgery.

00:07:42FacultyHere I am saying, if you discount the history of what he underwent, these are the possibilities you have to consider. So your primary thing is that he has coronary artery disease? That's your first diagnosis?

00:08:00CandidateNo, sir, LVOT. I am thinking of an LVOT obstruction with associated coarctation: LVOTO, bicuspid aortic valve with AS, which underwent balloon aortic valvotomy along with coarctation stenting; or pulmonary stenosis, peripheral pulmonary stenosis, for which they have done balloon angioplasty; or coronary artery disease.

00:08:20FacultyAt the age of 13 years, if there is familial hypercholesterolemia, they can present. Why can't that be one possibility? So after you take your history, you have so much time. There is one symptom. Sit and just think what questions the examiner might ask. There actually aren't that many; there are only a few. What are the conditions? Just sit and prepare. Spend a couple of minutes on that preparation, because ultimately for every question, 'can it be this, can it be that', the answer is just a matter of coming out with it. And if you come out with it, then you do well in the exam.

00:08:58If I have to ask you five questions to get that answer, you will go out saying that you gave all the right answers, but we won't be thinking so. I had to drag the answer out of you painfully; it should come easily from yourself. Continue.

00:09:16CandidatePost procedure, there was complete relief of his symptoms and he remained asymptomatic, that is NYHA functional class 1, for the next 10 years. In 2020 he again developed class 2 exertional chest pain of the same character, for which he underwent an angiogram in Odisha, again via the right groin, and he was then told to consult here again for open heart surgery. Currently he is admitted for the open heart surgery.

00:09:45He has no history of shortness of breath, presyncope or syncope; no history of claudication, palpitations or fatigue; no history of ankle edema; no history suggestive of systemic embolism or stroke; no history of joint pain, fever or monthly intramuscular injections; no history of prolonged fever requiring IV medications; and no history of bluish discoloration of the skin, recurrent LRTI or failure to thrive in childhood.

00:10:14Medication history: he has been prescribed Ecosprin 75 once daily, which he is still continuing. There are no hospitalizations other than these, and no other comorbidities. His development is normal. He was born of a non-consanguineous marriage. He has no siblings. His schooling was normal; he was formally educated till the age of 15 years, that is, he completed 10th standard. No family history of cardiac disease. He consumes a mixed diet; his appetite is normal.

00:10:57FacultyFamily history: you asked? There is nobody?

00:10:57CandidateNo, he is the only child; he has no siblings. In both parents, and even their first-degree relatives, there is no cardiac disease.

00:11:03FacultyYes, up to first-degree relatives: parents, siblings, and up to first cousins you can ask. Check with them.

00:11:14CandidatePersonal history: he consumes a mixed diet. His appetite is normal, sleep is not disturbed, and bowel and bladder habits are regular.

00:11:22FacultyAny history of hypertension there?

00:11:22CandidateNo, sir. He has not been diagnosed with hypertension.

00:11:25FacultyYou asked about hypertension?

00:11:25CandidateYes, I asked about hypertension. There is no history of hypertension, and he was prescribed only [unclear].

00:11:34FacultyRight, correct. Okay, so which conditions can cause coronary artery involvement in relation to LVOT obstruction?

00:11:45CandidateSupravalvar AS can present with coronary involvement. In supravalvar aortic stenosis they can have ostial lesions and skip lesions. Even familial hypercholesterolemia: they can present with valvular as well as supravalvar stenosis, and coronary artery disease.

00:12:06FacultyFamilial hypercholesterolemia, yes.

00:12:11CandidateAnd coarctation of aorta: coronary involvement, yes. Premature coronary disease occurs, in part because of systemic hypertension. Takayasu can present with aortic ostial lesions, skip lesions and coronary involvement.

00:12:30FacultyOkay, so LVOT obstruction can occur? [unclear] But again, there also you can get ostial involvement of the coronary artery, and regurgitation.

00:12:52CandidateA 33-year-old male with NYHA class 2 typical angina for the past 20 years, who underwent a balloon-based intervention with stenting via the right groin with complete relief of symptoms, currently on single antiplatelet therapy with aspirin, now again presenting with recurrence of angina of the same character for the past 6 years, and planned for open heart surgery.

00:13:16My first differential: congenital heart disease, LV outflow tract obstruction, likely a bicuspid aortic valve with coarctation of aorta, which underwent balloon valvotomy with coarctation stenting. Second differential: RV outflow tract obstruction, likely pulmonary stenosis, which underwent stenting for the same. Third differential: peripheral pulmonary stenosis, with stenting for the peripheral pulmonary stenosis.

00:13:45FacultyWhy do you mention stenting? Why do you mention it from the history?

00:13:50CandidateThe patient told me about a stent, sir. The patient said balloon with stent.

00:13:54FacultyHe is telling that, and he is on Ecosprin; all these three things.

00:14:01CandidateTypical angina, class 2, which was completely relieved after the procedure for 10 years, and then recurrence of symptoms.

00:14:12FacultyThe first procedure was at what age?

00:14:12CandidateAt the age of 15, sir.

00:14:16FacultyAt 13 he had angina; for 2 years he had symptoms; at 15 he underwent the procedure. How many years back?

00:14:20Candidate11 years back.

00:14:25FacultyHow many years back was the procedure done?

00:14:25Candidate17 years... 18 years back.

00:14:29FacultyHe is currently 33, so 18 years back.

00:14:36The third differential would be what? Any other details?

00:14:41CandidateFamilial hypercholesterolemia.

00:14:41FacultyOkay, what is against your first diagnosis? Could it be a case of aortic disease with pulmonary branch stenting done? Or was it part of the systemic circulation where stenting was done? [unclear]

00:14:56CandidateAt the age of 13 years, angina, which was relieved. Could it be pulmonary branch stenosis? I am thinking of balloon aortic valvotomy for aortic stenosis, which was severe and likely the cause of his complaints, and along with that he might have had a coarctation of aorta, for which they did coarctation stenting. Otherwise, the second differential is peripheral pulmonary stenosis presenting with angina, for which he underwent a stent.

00:15:17FacultyYes. Okay, so what is against your diagnosis of coarctation in this patient?

00:15:24CandidateHypertension. There is no hypertension.

00:15:24FacultyWhat are the causes of hypertension in coarctation?

00:15:33CandidateThere are three mechanisms, sir: mechanical, neural and renal. Mechanical is because of the obstruction causing the increase in pressures. In the neural mechanism, the baroreceptors get reset. And the renal mechanism is because of renal hypoperfusion: there can be RAAS activation, that is, activation of the renin-angiotensin-aldosterone axis because of renal hypoperfusion.

00:16:09FacultyIn what proportion of cases does hypertension persist after coarctation intervention? What are the predictors?

00:16:13CandidateSir, one is that if they present at an older age, they are likely to have persistent hypertension. If coarctoplasty or coarctation repair is done at a younger age, the hypertension may resolve. 30 to 50% of patients post coarctation repair will have persistent hypertension. If the gradient is more than 10 mmHg post coarctation intervention, the patient may develop [unclear] hypertension.

00:16:50FacultyWhat is the natural history of coarctation of aorta? How do these people present?

00:16:54CandidateOne presentation is hypertension, in which coarctation of aorta is incidentally detected.

00:17:03FacultyHow does a patient with coarctation present? When can they present?

00:17:07CandidateIn infancy they can present with heart failure; that is the infantile type. In the pediatric population they can present with hypertension or limb claudication. Adults also usually present with limb claudication. They can even present with subarachnoid hemorrhage because of berry aneurysm.

00:17:24FacultyWhat is the type of coarctation in the infantile type, and what is the presentation?

00:17:29CandidateDiffuse type. The arch will also be hypoplastic.

00:17:35FacultyHypoplastic, no. Is it preductal, postductal or juxtaductal, in the infantile type?

00:17:44CandidateThe preductal type is the commonest one in the infantile type.

00:17:50FacultyRight. And what is the presentation there? How do they present?

00:17:53CandidateSudden onset of breathlessness and heart failure that needs to be treated in the neonatal period; it can also present in children.

00:18:03FacultyAnd then in adulthood, you are thinking in terms of the adult type, the adolescent type of presentation. So what is the natural history of an adolescent who presents with coarctation?

00:18:15CandidateBP may persist in 30 to 50% of cases even after repair. The natural history without repair: one is systemic hypertension. They can have accelerated atherosclerosis because of that, and they can have coronary events and stroke. They can also have berry aneurysms, which can rupture and present with subarachnoid hemorrhage, vascular presentations.

00:18:35FacultyOkay, fine. There is a bimodal presentation [unclear].

00:18:43CandidateBimodal presentation of heart failure: heart failure in infants when the ductus closes [unclear]. Usually it doesn't happen before 40 years; beyond 40 years, patients develop heart failure. Other complications, as I told: hemorrhage from an aneurysm, aortic dissection can occur, AR, that is aortic incompetence, develops, premature coronary atherosclerosis, and infective endarteritis.

00:19:18FacultyYes. So these are the complications of coarctation. So what is the condition which presents with heart failure in the first year or very early infancy, in the presence of LV outflow obstruction? What is the condition which presents with heart failure in infancy or early childhood in patients with, say, aortic stenosis or coarctation of aorta?

00:19:43CandidateEarly... a unicuspid aortic valve will present.

00:19:49FacultyWhat happens in the left ventricle? It can happen even in adults with severe hypertension later on, and cause heart failure. Have you heard of it?

00:20:07CandidateSubendocardial fibroelastosis. Sir, there are two types: one is primary and the second is secondary. Secondary can occur due to coarctation of aorta.

00:20:17FacultyPrimary: initially it used to be an MCQ in all the entrance exams, where it was attributed to mumps virus [unclear]. But that is no longer true; it has not been found to be true that it is related to mumps virus infection. But there is primary subendocardial fibroelastosis and secondary subendocardial fibroelastosis.

00:20:42CandidateSo my differential diagnosis is either LVOT obstruction or RVOT obstruction, or coronary artery disease secondary to familial hypercholesterolemia, although he has not been prescribed high-intensity [statin]. He has not been prescribed a statin; that is why.

00:21:02FacultyOkay. Go ahead.

00:21:05CandidateThe patient is cooperative and oriented to time, place and person. Height 164 centimetres, weight 45 kg; BMI is 16.7, underweight. No pallor, icterus, cyanosis, clubbing, lymphadenopathy or pedal edema. Saturation on room air is 98%. There is no exertional desaturation. Temperature is normal. He had syndromic facial features in the form of a broad forehead, crowding of teeth and a large, wide mouth.

00:21:38Pulse rate 80 per minute, regular, low volume, late peaking; no radio-radial or radio-femoral delay. All the peripheral pulses are well felt. Bilaterally, the right radial and left radial are the same... The right radial pulse is a little more feeble than the left radial.

00:21:56FacultyI thought you just now said that all the peripheral pulses are the same?

00:22:01CandidateI said all peripheral pulses are felt, but there is a difference.

00:22:08FacultyAnd the carotid is not a peripheral pulse; it is a central pulse.

00:22:08CandidateThey are felt, sir. There is no loss of pulses.

00:22:12FacultyNo, you said all pulses are the same. Didn't you say that all peripheral pulses...?

00:22:20CandidateAll peripheral pulses are felt.

00:22:20FacultyThere is a very definite difference in the upper limb pulses versus the lower limb pulses.

00:22:27CandidateEspecially the right side. The right side is less compared to the left side.

00:22:30FacultyDid you feel the brachial? Is the brachial also weak?

00:22:34CandidateYes, the right brachial is also... It is feeble compared to the left side.

00:22:37FacultyYes, that's an important point, isn't it? Okay. Which pulse will you feel to see the character of the pulse?

00:22:46CandidateCarotids.

00:22:49FacultyDoes the radial give you any character? You can feel the radial and tell us what type of pulse?

00:22:54CandidateCollapsing pulse.

00:22:57FacultyYou feel that everywhere. But specifically, which pulse is better felt in the radial? What is that pulse?

00:23:09CandidatePulsus alternans.

00:23:09FacultySo pulsus alternans is one which is better felt in the radial; the others are better felt in the carotids. But this difference is there: yes, the right pulse is weaker.

00:23:20CandidatePulsus paradoxus also.

00:23:31FacultyParadoxus, yes. Where do you get pulsus alternans?

00:23:31CandidateLV dysfunction, severe LV dysfunction: alternating strong and weak beats.

00:23:42There is a bilateral carotid shudder with thrill.

00:23:42FacultyOkay, good.

00:23:50CandidateBlood pressure in the right upper limb is 96/80 and in the left upper limb 100/80. Lower limb systolic BP is 120.

00:24:03FacultyWhy is lower limb blood pressure higher than upper limb blood pressure in many patients, even normal ones?

00:24:08CandidateSphygmomanometric artefact, because of the bulk of the muscle.

00:24:14FacultyOkay, so supposing you use an adequately sized cuff, you still can sometimes get a higher pressure in the lower limbs.

00:24:25CandidateDirect continuation of the aorta. Also, the bulk of the muscle is more in the lower limb.

00:24:36If we measure intra-arterial BP, it will be the same.

00:24:45FacultyOkay.

00:24:45CandidateBut sometimes the femoral artery pulse waveform is different, from the summation of the reflected waves.

00:24:52FacultyI don't understand. [unclear]

00:24:58CandidateCentral BP is usually lower than the peripheral BP, because there is summation of the reflected waves, which can cause peripheral augmentation of BP.

00:25:06FacultyIf the peripheral pressure is higher, blood should flow from the periphery to the centre. Blood always flows down a gradient, right, like water. So why is it that if the lower limb pressure is higher than the upper limb, blood still flows from up here to down there?

00:25:30CandidateMean pressure.

00:25:30FacultyYes, the underlying mean pressure. So peripheral augmentation, summation of the tidal wave and so on. So you often get a higher pressure; even in the cath lab you can see it when you take a withdrawal from central to periphery. Yes, go ahead.

00:25:55CandidateJVP was not elevated, with normal waveforms, normal hepatojugular reflux and normal respiratory variation.

00:26:04FacultyIs it hepatojugular or abdominojugular?

00:26:08CandidateAbdominojugular is what is preferred now. Previously they described right upper quadrant pressure over the liver, but now it is replaced with the term abdominojugular, because even pressure over the abdomen, increasing the intra-abdominal pressure and compressing the IVC, can produce it.

00:26:24FacultyI think even the most recent Braunwald says abdominojugular reflux: pressure over the abdomen, but preferably the right hypochondrium. So that's not wrong; you can use both. Reflex or reflux? Reflux. All right, good. So if it is positive and there is not much RV involvement, what will the LA pressure be?

00:26:47CandidateThe LA pressure will be 15.

00:26:56There are no peripheral stigmata of infective endocarditis or acute rheumatic fever.

00:27:00FacultyWhat?

00:27:00CandidateNo peripheral stigmata of IE or acute rheumatic fever. Also, no features of familial [hypercholesterolemia]...

00:27:03FacultyTalk a little clearly, a little clearly, for us to understand. [unclear] Yes, you must give us that also.

00:27:15CandidateNo peripheral signs of familial hypercholesterolemia.

00:27:15FacultyWhat did you look for?

00:27:20CandidateArcus presenilis, xanthelasma, xanthomas: eruptive xanthomas, tendon xanthomas. And also the retina: if I can examine it, lipemia retinalis.

00:27:35FacultyLipemia retinalis. Where do you find lipemia retinalis and eruptive xanthomas?

00:27:39CandidateHypertriglyceridemia, familial hypertriglyceridemia.

00:27:41FacultyIf arcus is absent on one side, what is the diagnosis? The arcus is absent on one side: unilateral arcus.

00:27:57That means the carotid artery is occluded on that side. That's what it means. These are the googlies. Okay, continue.

00:28:07CandidateThe chest wall is symmetrical, with no visible scars, sinuses, dilated veins or pulsations. The apex is in the left 5th intercostal space in the midclavicular line; heaving apex. There was a palpable S4, and there was also an apico-carotid delay. No parasternal heave, no palpable S2, no thrill, no abnormal pulsations.

00:28:31FacultyVery definite thrill.

00:28:34CandidateAt the apex I was not sure whether it was there or not; it is an uncertain thrill.

00:28:39FacultyThere is a very definite thrill over the precordium. You want to go and check again?

00:28:42CandidateNo, sir. I looked for the thrill. I felt that at the apex there was a thrill, but I couldn't explain it.

00:28:49FacultySo just because you can't explain it, you don't change the finding. That is something you never do in the exam, because what we are trying to see is whether you have the skill, ability and knowledge to pick up the signs, right? The final diagnosis can be completely off; it doesn't matter. Can you pick up the findings? Can you interpret those findings logically? Even if you get the final diagnosis wrong, in many cases the cases are very complex. But don't alter your findings to suit what you think may be the diagnosis. That I don't think you should do.

00:29:22CandidateActually, I looked for a thrill on the right, where the murmur was, in the right second intercostal space. I didn't get it there. But at the apex I felt there is a... I thought it was a palpable heart sound, and at the apex it might be confusing.

00:29:35FacultyAt the apex, which palpable heart sound?

00:29:41CandidateS4.

00:29:41FacultyYou have come to auscultation now. Percussion? Okay, percussion is normal, right?

00:29:52CandidatePercussion is normal.

00:29:59FacultySo how much have we learned from the findings so far? Low volume pulses with late peaking...

00:30:10CandidateThere is no significant difference between upper limb and lower limb.

00:30:16FacultyOther than that, there is an asymmetry in the pulses. Asymmetry in the pulses: don't forget that. Blood pressure is only a little bit different; 96 versus 100 is almost the same. But on palpation, the right side [unclear].

00:30:33CandidateCarotid shudder and thrill are present; bilateral carotid shudder is present.

00:30:33FacultyYes.

00:30:38CandidateOn palpation, the apex is heaving, with a palpable S4 and a thrill at the apex.

00:30:47FacultyIs it at the apex?

00:30:50CandidateI find it.

00:30:58FacultyIn the exam, generally the examiners will not try to mislead you. So if they say, 'Why don't you go back and check?', that means you should be prepared to change your finding. Whereas otherwise, when you are in your hospital, we may constantly try to mislead you just to see how much you know. But not in the exam, right? Okay.

00:31:20CandidateS1 is loud. S2 is narrow... loud. A2 is loud. S2 is single: loud and single.

00:31:42FacultyOkay. Especially in congenital heart disease, the diagnosis really hinges on the second sound, just as arrhythmias hinge on the P wave. So before you say 'single second heart sound', be very careful. Look carefully, go more laterally sometimes or a little lower down, in inspiration and expiration, before you commit to a single second heart sound. I am not saying you are wrong. I am just saying that once you say it is single, you should be prepared for the next question, which will inevitably follow: what are the causes of a single second heart sound? And then you have to somehow work that into your diagnosis also.

00:32:29CandidateActually, I would like to commit to a narrowly split second heart sound.

00:32:33FacultyNarrow split? Now it has become a narrow split?

00:32:37CandidateBecause 'single' means it is not a true single...

00:32:41FacultyWhat do you mean, not a true single? Either it is single or it is split. No; see, again you are trying to change your finding to fit the diagnosis. Don't do that.

00:32:52Single. Actually, I also thought it was single; I couldn't hear a split. So don't change. Please don't change. Expect the question, be prepared with the answers; and then you may not be able to explain it, and it's okay. Never change your findings. If you are in doubt, go back and check those findings, and then decide whether those findings are more important than your diagnosis.

00:33:27CandidateI feel the issue is the overlapping of A2 and P2, the combination; so there is only a single heart sound.

00:33:35FacultyThen I am going to ask you that also: why is it single? You are saying A2 and P2 are fused; you have to explain that. Okay, continue.

00:33:44CandidateThere is a harsh, mixed-frequency, long crescendo-decrescendo murmur, mid-to-late peaking, grade 3/6, best heard in the right second intercostal space and conducted to both carotids. The same murmur is heard over the entire precordium, even over the back.

00:34:06FacultyAnd yet it is 3/6, when you have accepted that there is a thrill?

00:34:12CandidateI am still not sure, sir. I don't want to commit; I am not sure of this. If you say there is a thrill, I will commit: 3/6 becomes 4/6. So, no thrill.

00:34:23FacultyNo thrill? See how much you have changed. You said no thrill, then you said thrill, then no thrill. I asked you to go and check, and you said, 'No, it is there; the thrill is there.' That is what you told me. Don't change your findings. Okay.

00:34:42CandidateOther system examination: nothing significant.

00:34:46FacultyDid you look for a thrill or a murmur or a bruit anywhere else?

00:34:52CandidateI wanted to look. I did the renal areas, but I felt it is the same murmur, radiating. The renal areas were auscultated; there is a systolic sound.

00:35:01Faculty[unclear] for coarctation. What did you have? Coarctation. You brought in coarctation also, no?

00:35:06CandidateYes.

00:35:10FacultySo what will you look for? Upper limb and lower limb BP discrepancies: one thing that you did. Don't you look for a murmur at the back? Is the murmur heard over the back? Did you auscultate over the back?

00:35:23CandidateI didn't get a continuous murmur. It is extensively heard, soft, a little bit more on the left side, but it is there.

00:35:26FacultyIt is there; it is very well heard all over the back. Always, in such cases where you have a doubt, you must auscultate suprascapular, interscapular, infrascapular and lower down. That will distinguish between coarctation of aorta and [AS, unclear]: the [AS, unclear] murmur will be heard only up to the lower interscapular region and won't be heard below that, whereas the other will be heard right down the back. So that's an important thing you have to keep in mind.

00:35:59Yes, you've got a lot of... it is heard quite extensively. But keep in mind that a loud murmur, as even books have said, you can hear on the top of the head also; it can be widely heard. That's the interpretation of it: is it the same murmur which you hear in other places, or is there another murmur? That's another point altogether. But the point is, you should look for it. You made a diagnosis of coarctation; you should look for it.

00:36:28CandidateContinuous over...

00:36:33FacultyI didn't ask about continuous. Did you hear any murmur? It is there. Now you are changing again.

00:36:43CandidateSir, I didn't get that finding, but over the bilateral renal areas I felt it is the same murmur being conducted.

00:36:46FacultyIf you auscultate over the femorals... Should you? Should you not? You found an asymmetry in pulses; you found that the right radial and brachial are weaker. Then shouldn't you auscultate at least the femorals also? You can have some stenosis there. These are things you shouldn't [miss].

00:37:17Done? Anything additional? So now we come to the tough part. What's the diagnosis?

00:37:23CandidateSitus solitus, levocardia, congenital heart disease, severe valvar aortic stenosis, likely etiology bicuspid aortic valve.

00:37:33FacultyWhy did you say bicuspid?

00:37:39CandidateAortic stenosis in a young patient, and a history of likely coarctoplasty.

00:37:47FacultyCoarctoplasty is your assumption. We don't know that coarctoplasty has been done. All we know is that he says he had some stent put in. We don't know where it is.

00:37:58CandidateSounds: the second heart sound...

00:37:58FacultyThere's no hypertension, mind you. Coarctation without hypertension is a little unusual.

00:38:05CandidateOnce you treat the coarctation, the hypertension can persist in 30 to 50% of cases.

00:38:13FacultyYes, but not in all cases; it can persist for reasons I think we have discussed. Okay.

00:38:17CandidateLoud A2 and loud S1. The loud S1 would be because of the click, which is merging with S1, and the loud A2 because of the dilatation of the aorta. So these two. And a young patient with severe aortic stenosis who underwent a balloon-based procedure, balloon valvotomy, with all this.

00:38:40FacultySo your diagnosis again is coarctation and severe...

00:38:40CandidateSir, severe aortic stenosis, likely etiology bicuspid, status post [balloon valvotomy] and stenting at the age of 15 years; now NYHA functional class 2, no evidence of PVH, no evidence of pulmonary arterial hypertension, in sinus rhythm, no evidence of infective endocarditis.

00:39:01FacultyExplain the single second heart sound. I told you I am going to ask you.

00:39:04CandidateThe single second heart sound in this patient will be because of three reasons. The first one is overlapping of the A2 and P2 components, with a loud A2 component.

00:39:18FacultyOverlapping can happen in normal people also, but why is it single? Normally, during inspiration, A2 and P2 separate; they will separate by at least [unclear], so then you don't call it single. If it is single during expiration, you don't call it a single second heart sound. When you say single, you are hearing it single in inspiration and in expiration, correct?

00:39:41CandidateIn severe aortic stenosis, since A2 comes very late, it can split paradoxically.

00:39:46FacultyOkay. Other than that, what are the other possibilities?

00:39:54CandidateThe murmur obscuring... with paradoxical splitting, the murmur is obscuring the pulmonary component.

00:39:57FacultyThat with a grade 3 murmur? Not even a grade 4 murmur. Okay, what else?

00:40:08For some reason, one component is very soft. In AS, A2 can be soft; in PS, P2 can be soft. Sometimes you may not hear it. And in others, not in him, if you have COPD, emphysema, obesity or a thick chest wall, you may not hear it. My point is, whenever you say single second heart sound, don't make that statement so casually, because it has to fit in with the diagnosis, or you have to give an explanation for it, okay? Done? Any DD?

00:40:53So you have said aortic stenosis and post-coarctation. You haven't explained why the right-sided pulses are weaker, have you? You've got two or three findings here. Please bring them all together; try and give something. And sometimes the findings are such that it is difficult to explain them. Then say that you can't explain it, before I ask you about it.

00:41:28CandidateThe click was not there, sir, but there is a loud S1, and A2 is audible, preserved.

00:41:31FacultyYes. Why is there no click?

00:41:35CandidateIt could be merged with S1. The loud S1 could be because the click is merged with S1.

00:41:39FacultyNo, that happens in mitral stenosis. What happens in severe mitral stenosis doesn't happen in aortic stenosis. The aortic valve opens at 80 mmHg; there is a lot of time from S1 to the opening of the aortic valve.

00:41:53CandidateHe is 33 years old, so it could be calcified.

00:41:59FacultyYes, but A2 is [preserved]. Will you describe the aortic stenosis? Supravalvar or subvalvar?

00:42:04CandidateSupravalvar... no click.

00:42:08FacultySupravalvar: A2 is well preserved, understand, and there is no ejection click, so it can't be valvar. The point, again, is that the lesion is either below or above the valve. And if you are getting a disparity in both upper limb pulses, think of supravalvar aortic stenosis.

00:42:26CandidateSupravalvar aortic stenosis. I did not get [unclear] that the right upper limb pulse was not better felt; it is radiating to both carotids. The right side is weaker, but in the blood pressure there is no difference.

00:42:39FacultyBut there is no clinically definite difference? Clinically, the right-side pulses are definitely weak.

00:42:45CandidateMaybe it might have been done at that time. Maybe something.

00:42:50FacultyCould it be discrete subaortic stenosis?

00:42:54CandidateDiscrete subaortic stenosis, subvalvar aortic stenosis, is possible, but usually there will be associated aortic regurgitation. I did not get any AR murmur, so that is why I did not consider it.

00:43:10FacultyIn the majority of cases, and the presentation... I mean, the missing click. You can't tell that; you may be missing the click.

00:43:16CandidateNo click, no AR murmur.

00:43:22FacultyWhat about the carotids?

00:43:22CandidateBoth are the same. Even the thrill is present bilaterally, radiating to both.

00:43:36FacultyIf the radial pulse is very weak but the BP is the same on both sides, what are the other possibilities? Sometimes there can be a brachioradial delay in severe aortic stenosis; the radial pulse may be very weak. But brachioradial delay is very rare. But anyway, he has had some procedure. If he had some procedure, for example radial access...

00:43:55CandidateI asked him about that, sir, whether he underwent a procedure through the right radial during the angiogram, but he said both procedures were through the right groin. I asked him about that.

00:44:03FacultyOkay, but keep in mind that that's one of the causes: up to 4% of patients post radial intervention can have loss of the pulse. But then the brachial will be okay. Here even the brachial seems weaker. Okay, so that's something you have not explained. Any differential diagnosis you want to bring in here?

00:44:31Can it be aortoarteritis? Any chance?

00:44:34CandidateArteritis...

00:44:36FacultyCan that merit a stent?

00:44:42CandidateAortoarteritis, it is.

00:44:45FacultyWhich is the commonest vessel to be involved in aortoarteritis?

00:44:49CandidateTakayasu: subclavian.

00:44:49FacultySubclavian. In Indians, abdominal and renal involvement is more common; overall, subclavian. So maybe he underwent... or you think he underwent a renal intervention? But then there would have been hypertension, no? There's no history of hypertension at any point. So why can't it be that he underwent subclavian artery stenting?

00:45:07CandidateThere's no history of limb claudication.

00:45:10FacultyOh, that doesn't matter. Subclavian steal can have no symptoms.

00:45:13CandidateYes, but angina is the presenting complaint, which is not explained by an isolated subclavian lesion. There should have been associated coronary artery disease.

00:45:21FacultyOkay, so his main thing was angina. Yes, you're right. So what is acquired coarctation? Can that produce it? Anyway, this is coronary involvement. Coronary involvement can be there; hypertension itself can produce angina. But it is rather unusual: starting at 13 years, completely disappearing and then reappearing.

00:45:59Okay, there are definitely points which are difficult to understand, but as long as you are able to give some kind of explanation and you are able to discuss the findings, that's what we are really looking for. Whenever there is vascular involvement like this and you find something unequal, do a systematic vascular examination; that will help you to localise where it is. Start with the superficial temporal, which is a branch of the external carotid; then come down to both carotids, then the subclavian, then the brachial, then the radial. Similarly, don't forget the abdominal aorta and the iliacs, above Poupart's ligament; iliac, then femoral, then come down to the popliteal. And look for bruits over the femoral, over the carotid and over the back. All this will give you some clue to the diagnosis.

00:47:00Okay. Should you get the fundus examined? [unclear] Don't forget. Why?

00:47:07CandidateIn coarctation they can have retinal changes, in the form of [unclear] vessels.

00:47:11FacultyOkay, one is coarctation. Then in arteritis also they can have retinal changes. What are those?

00:47:18Candidate[unclear]

00:47:18FacultyWho described it?

00:47:18CandidateUyama and Asayama.

00:47:25FacultyIt was first described by Takayasu, who was an ophthalmologist. This is the classification given by [unclear]. Okay.

00:47:38Right. So can we go to the investigations? What do you want?

00:47:49CandidateECG, to look for LVH and [unclear].

00:47:52FacultyECG. Okay, good.

00:48:23Can you get it up? I can see it over here. Yes, come on.

00:48:32Candidate[Full, unclear] standardised ECG. Normal sinus rhythm, heart rate of around 80.

00:48:40FacultyYes, good.

00:48:40CandidateThe axis is around 60. Beyond 60; aVL is negative. There is LVH, with an LV strain pattern.

00:49:20FacultyLVH based on which criterion? Come on, it is obvious. Tell me.

00:49:26Candidate[unclear] V3... Cornell.

00:49:31FacultyWhich one?

00:49:36CandidateV3. Voltage criteria.

00:49:41FacultyVoltage criteria, okay. Why don't you just go with Sokolow-Lyon? It is half standardisation, because aVL is... yes, it is half standardisation. There is severe LVH; you don't even need to count it. So, severe LVH by Sokolow-Lyon. Tell me which strain pattern.

00:50:03CandidateT-wave inversion and downsloping ST depression in the lateral leads.

00:50:14FacultyWhat is deduced from the ECG?

00:50:20CandidateA diagnosis of LVH with LV strain.

00:50:30FacultyHow do you differentiate whether this is LVH with strain, or whether the T-wave inversions are because of ischemia? Is it because of ischemia, or because of LV pressure overload only?

00:50:47Okay, let's go to the X-ray.

00:50:55From the ECG, is it eccentric or concentric? [unclear] Eccentric? Now you have got heart failure. Eccentric with heart failure? [unclear]

00:52:00Explain the X-ray.

00:52:03CandidateNormal rotation and exposure. Cardiac silhouette [unclear]. [No] rib notching. [unclear] some stents.

00:52:37FacultySo you said coarctation was one diagnosis; that's why you look for rib notching. Where will you look for it?

00:52:43Candidate3rd to 8th ribs, lower border.

00:52:48FacultyPardon?

00:52:48Candidate3rd to 8th ribs, lower border.

00:52:52FacultyDon't bring one mic near another microphone. Lower border of the 3rd to 8th ribs. Okay, why lower border? Why 3rd to 8th?

00:52:59CandidateSir, lower border because of the posterior intercostal arteries; they run in the... The anastomosis happens between the anterior and the posterior intercostals...

00:53:09FacultyFinish your sentence: under the lower margins of the ribs.

00:53:16CandidateYes. The neurovascular bundle runs, and the anastomosis happens, along the lower edge of the rib. And the first and second ribs are not involved because the costocervical trunk gives the supreme, or superior, intercostal artery, which gives rise to the first two branches. So collateral anastomosis happens between the 3rd and the 8th. So rib notching is not there. And the post-stenotic segment is not dilated, so it is unlikely to be [coarctation, unclear].

00:53:47FacultySo, unlikely.

00:53:50CandidateI was looking at the aorta, but that is not there. With a bicuspid aortic valve they will have aortopathy; there is usually some dilatation of the ascending aorta.

00:54:01FacultyWhat else can you see in coarctation? The 3 sign can be there. What is the 3 sign? Can you explain the 3 sign?

00:54:06CandidatePre- and post-stenotic aortic dilatation.

00:54:13FacultyPre- and post-stenotic dilatation, is it?

00:54:13CandidateYes.

00:54:17FacultyIs there a pre-stenotic dilatation in coarctation? What is the segment before the coarctation called? No; first, the next question is: what is the segment before the coarctation called?

00:54:33CandidateIsthmus.

00:54:33FacultyThe isthmus is where the coarctation happens, the narrow portion. Above that is [unclear], and below that is the post-stenotic dilatation, isn't it? There are three segments of the coarctation. So what actually gives rise to this 3 sign?

00:54:50CandidateKnuckle; then there will be the stenotic segment; and then the distal portion will be...

00:54:52FacultyYou know, or you don't know?

00:54:59CandidatePre-stenotic dilatation.

00:54:59FacultyDilatation. The dilatation is not prominent. [unclear] The dip that you get in between is at the level of the ductus, or at the level of the coarctation, and below that is the post-stenotic dilatation. What is the reverse 3 sign?

00:55:26CandidateReverse 3 sign: on barium swallow you can get the E sign. If you perform a barium swallow, you will get the opposite of it.

00:55:30FacultyAnd there again it is the same; [unclear] subclavian, it is the same thing. Okay. Here, the pulmonary artery segment looks to be enlarged, no? MPA enlarged?

00:55:44CandidateNo.

00:55:48FacultyThe bay is a little filled out, no?

00:55:53CandidateActually, there are some stents in the [pulmonary arteries, unclear]: bilateral [unclear] stents.

00:56:02FacultyBilateral PA stents? This is in the right and the left?

00:56:16CandidateHere there are stents; they will be better seen here.

00:56:22FacultyBetter seen on your laptop? Is it the workstation?

00:56:24CandidateI thought stenting was not there. So when I looked for a stent, only these two.

00:56:34FacultyHere there is a stent, and here also there is a stent? At least from this, it is not clear. I don't know if it is clearer on your laptop.

00:56:51If you are saying on the right side, you are talking of peripheral pulmonary artery stenosis now. Is that what you mean?

00:57:05CandidateSir, here there is one stent, and here also there is one stent. This one, sir, is one stent, and here there is one stent. Two stents are there. This one, sir, on the left side.

00:57:15FacultyYes, it does look something like that. This is also there... that I can't make out.

00:57:29CandidateSir, this must be supravalvar aortic stenosis, because there is no [unclear], and if the PAs are stented, it must be supravalvar aortic stenosis. I have not heard the click also.

00:57:49Faculty[unclear] Now the others will take the cases. The left... is it the right? I still can't make it out. Okay, go ahead. Let's go to the next one.

00:58:45CandidateThis is the parasternal long-axis view, grayscale, showing severe concentric LVH and normal mitral valve opening. The [aortic valve, unclear] is not well visualised. There is an echogenic structure in the sinus.

00:59:11FacultyCan you comment on the aortic valve?

00:59:11CandidateThere is concentric LVH.

00:59:14FacultyWe don't know. Go to the previous parasternal long-axis view. Yes, see what's happened to the aorta.

00:59:28CandidateIt is not well visualised, sir, but there is an echogenic fixed structure seen here in the sinus. It looks thickened, and there is asymmetrical closure also, I think. Its closure is closer to the lower end rather than the upper end.

00:59:48FacultyColour: any turbulence seen?

00:59:51CandidateHere, actually, the colour flows are laminar.

01:00:02FacultyGo to the aortic valve; it can be better assessed in the short axis.

01:00:10CandidateParasternal short-axis view, grayscale, at the level of the mitral valve, showing normal mitral valve opening and concentric LVH.

01:00:21FacultyWhich one did you ask for? Apical?

01:00:25CandidateShort axis, aortic valve level. After that, there are some short-axis views, then this one.

01:00:42FacultyNot very clear. The aortic valve doesn't seem too thickened. Without colour.

01:00:58CandidateComplete obliteration of the LV cavity. The aortic valve opening is not well seen. At the supravalvar level there seems to be an obstruction.

01:01:36FacultyThe [unclear] cavity looks much better. Normal.

01:01:42CandidateNormal [unclear], with concentric LVH. Five-chamber view: normal aortic valve leaflets, and above that an echogenic thick structure can be seen causing narrowing.

01:02:05FacultyI would like to see colour Doppler.

01:02:05CandidateSir, this is the only view we got. It was a difficult echo to get, but we thought there was a narrowing.

01:02:13FacultyCan you just show that there was a narrowing at the supravalvar level?

01:02:22CandidateNo valvular regurgitation.

01:02:31AudienceCT is done, sir. In fact, sir, the case was kept for discussion for that reason, because the CT diagnosed it as query aortoarteritis, [unclear]. But there are very large coronaries on the CT, because they are exposed to much higher pressure, and there is an ostial stenosis of the left common carotid.

01:02:53Regarding what was said about why there is a discrepancy in the pulses: there is no clear indication why that was happening. There are a couple of discrepancies; we wanted to discuss this case, that's the only thing. It was an interesting case. It was clearly supravalvar AS, no doubt about that. The coronaries were quite enlarged, the aortic valve was normal and the left carotid has a stenosis.

01:03:16UnclearThat will give [unclear] aortic stenosis.

01:03:16AudienceYes, sir. But for the upper limb pulses, sir, actually the left was better than the right; I think that was also mentioned by the candidate. For the left pulse, there is no Coanda; I mean, it is like a reverse Coanda. Maybe, we thought, because the brachial is also weak...

01:03:33FacultySo why would there... It could be the innominate. [unclear] Or an additional stenosis in the right subclavian, the right subclavian independently, probably a little beyond the aortic origin, maybe a little distal also, which we commonly see in Takayasu also.

01:03:53AudienceYes.

01:03:53FacultySo what we know for sure is that there is supravalvar stenosis and peripheral pulmonary [stenosis]. What about the abdomen? Everything else is okay?

01:04:04AudienceNo, sir. Actually, the suprasternal view [unclear].

01:04:09FacultyLeft. Yes, that's the right carotid, isn't it? Or was that... which seems narrowed? Yes, coming from the aorta. The left: it is the left carotid, and next to it is the innominate. Yes, left. What about the left subclavian? Narrow?

01:04:35AudienceNo... right, sir. We are not seeing distally.

01:04:38FacultyThere seems to be something beyond the vertebral. Anyway, somewhere there it looks a little suspicious. Reconstruction is not there?

01:04:58AudienceNo, we don't have it.

01:05:02FacultyAnyway, I think you need to evaluate this more.

01:05:08AudienceI don't think they've done it yet. It was done just 2 days back, sir. We'll get it reconstructed.

01:05:12FacultySo you have supravalvar aortic stenosis; put on the light. You have left carotid stenosis, peripheral pulmonary stenosis, and possibly, clinically, something in the right subclavian. So why can't the whole thing be [aortoarteritis, unclear]? Because you have pulmonary artery involvement, and you have aortic involvement beyond the aortic valve; the supravalvar lesion can be just beyond the valve. With a supravalvar lesion you may get [unclear] of the subclavian artery, and you may get [unclear]. And in addition, the pulmonary vessels were involved.

01:06:01The first time, was his angina due to the peripheral pulmonary stenosis?

01:06:05AudienceNo: supravalvar aortic stenosis, severe LVH.

01:06:05FacultyBut the angina was relieved thereafter. He underwent angioplasty, and the typical angina was relieved for 10 years. Balloon angioplasty of the supravalvar segment, maybe, plus stenting of the [pulmonary arteries]?

01:06:22AudienceNo, not here; it was done somewhere else.

01:06:22FacultyOkay. So at that time only the peripheral [pulmonary arteries were treated]. That is at 13 years... at the age of 15 years, 18 years ago.

01:06:44Supravalvar aortic stenosis with bilateral branch pulmonary artery stenosis: LPA and RPA stenosis.

01:06:52AudienceSo, sir, if you tackle the pulmonary arteries, then [unclear].

01:06:58FacultySo after that... We can't do this case right now; let him come.

01:07:01AudienceHe didn't come for follow-up. He has been following up elsewhere, sir; this time this case was sent here, actually, for discussion.

01:07:14FacultyAnyway, the pulmonary artery [pressure, unclear] is 50 or something?

01:07:18AudienceThat is too much; that is the RVSP. Sir, the [PA mean pressure, unclear] is around 30.

01:07:24FacultyNot much, then. So they have to operate; they only have to do aortoplasty, the whole ascending aortoplasty. Difficult.

01:07:37So, in conclusion: there is controversy about the Coanda effect. Do you know what the controversy is? The Coanda effect says that the pressures are higher on the right side than on the left side. Actually, that may not be true; the pressures on the left side may be lower than those on the right side.

01:07:53UnclearSo, sir, you can explain that there could be an associated right innominate [stenosis].

01:07:53FacultyYes, that is true. That can be.

01:08:01What is the reason for Coanda? Why does Coanda happen?

01:08:11Not in him; I mean generally, why does Coanda happen? Generally, the Coanda effect is supposed to give higher pressures on the right side, but that may not always be true. It could be because of lower pressures on the left side rather than higher pressures on the right side. Yes, I am asking you why. What is the mechanism of Coanda?

01:08:31CandidateA wall-hugging jet will be there: a high-velocity jet directed to the right.

01:08:44FacultySo basically, you have a case where it is very difficult to get the diagnosis. So again I am coming back to the point: please don't fit your findings to whatever diagnosis you think it may be.

01:08:56CandidateNo, sir. After seeing the X-ray, with the examiner asking me, and there is no click and no ascending aortic dilatation, sir, I have to [revise, unclear].

01:09:04FacultyYou have to tell yourself [unclear]. You are not hearing a click, and right, there is no ascending aortic dilatation. It cannot be valvar.

01:09:24Yes, the presentation was good, except that this is a very difficult case. The more difficult the case, the easier it is to pass an exam. That is always true, because everybody discusses it, so they will give the benefit to the candidate. But what he said, you have to keep in mind: don't go back on your findings. Stick to your findings completely. Your presentation was quite good, but go a little slower. Your communication should be such that the people sitting in front of you understand what you are talking about. So be a little slow and clear in your communication.

00:00:03FacultyWe will start from one corner. Give the mic to the first person. Don't identify yourself; only your voice.

00:00:17When you describe a spotter, don't jump directly into the diagnosis. Most of the time it will be wrong, and you will lose all the marks. So start with 'This is an angiogram, this is such-and-such view', like that, and you will get some points. If you suddenly say 'This is TAPVC' and it is wrong, it is gone. So that is the first point.

00:00:47Can you describe what you are seeing?

00:00:57CandidateCine image showing a post-cardiac-surgery patient.

00:01:05FacultyVery good, that is how you should say it. Even if you don't tell the final diagnosis, you said this is post cardiac surgery because of the sternal wires, and you have some prosthetic material inside.

00:01:17CandidateYes, there is a prosthetic valve and a ring also.

00:01:22FacultyHow many prosthetic materials are there?

00:01:24CandidateTwo are there.

00:01:24FacultyWhat are they?

00:01:30CandidateOne is a ring, sir, and the other one is a valve, which is showing rocking.

00:01:35FacultyAn annular ring, very good. And there is also a prosthetic valve, a bileaflet valve; you can see the two leaflets. And what is happening to that valve?

00:01:50CandidateThere is rocking.

00:01:50FacultyRocking means what? Why does rocking happen?

00:01:58CandidateWhen the stitches which are holding the valve give way, the rocking happens.

00:02:03FacultyOkay, so most likely it happens due to what?

00:02:06CandidateInfective endocarditis.

00:02:06FacultySo this patient must be having infective endocarditis; this is rocking of the valve. The other one is the ring; the positions and all we will discuss later. Very good. Next person. So start like this: describe what you are seeing, and don't jump to the diagnosis.

00:02:27This is an intervention done for the condition which is seen in the ECG. This particular finding will not be obvious in an Indian patient; that is why the image of a very obviously white-skinned person is given. So identify the disease, identify the intervention, and what it was done for.

00:02:51CandidateIt shows an ECG with ventricular fibrillation.

00:02:54FacultyAnd initially what is there? It is not ventricular fibrillation to start with, no?

00:03:00CandidateYes, sir, there are VPCs with an R-on-T kind of phenomenon followed by ventricular fibrillation, and a facial picture of a woman with a malar rash. Maybe this is a patient with an infiltrative disease like sarcoidosis, and she might have undergone ICD implantation for this fibrillation.

00:03:32FacultyOkay, that is not it. What are you seeing? Is a malar rash usually on one side or both sides?

00:03:44CandidateUsually both sides.

00:03:44FacultyBoth sides. But what is happening here? Is it on one side or both sides? And what is happening to the face in the close-up which is shown?

00:03:57CandidateRight side.

00:04:01FacultyWhere is the hyperhidrosis? The hyperhidrosis is on the right side. So what is the procedure done?

00:04:13CandidateSympathectomy.

00:04:15FacultyIt is a cardiac sympathectomy, a left cardiac sympathetic denervation, done for what is actually an alternating bundle branch block pattern, an alternating VT going into VF. After that you get some side effects, in around 95% of the patients: ptosis, then unilateral facial flush, hyperhidrosis, etcetera. This is LCSD.

00:04:44It is a bidirectional tachycardia. You want to see the ECG again? It is a bidirectional tachycardia going into VF. So it was a good guess; I appreciate that he noticed the malar flush, but it was not the correct answer. It was a good guess, though, and you will get some points. You will not fail because of it.

00:05:21You can speak a little louder. Can you give him another mic?

00:05:28CandidateThere are two cine images, sir. On the right side, this image is taken in the LAO view, and—

00:05:32FacultyOkay, the view doesn't matter here. It is shown mostly in the AP view or slightly tilted views. What is there?

00:05:51CandidateLeads are there.

00:05:51FacultyLeads are there, okay. But nobody will show you normal leads, so there is something abnormal. What is that? What is the thing which is focused?

00:06:17CandidateThe diaphragm is focused.

00:06:17FacultySo what is happening to the diaphragm?

00:06:22CandidateThe diaphragm is contracting at the pacing rate.

00:06:27FacultyThis is on the right side. What is happening to the left side? You are seeing the left side; is it happening like that on the left side? It is not; only the right side is. Diaphragmatic pacing is happening only on the right side. So it is right diaphragmatic pacing. But the lead is also coming differently: the lead is coming from a left SVC. That is another issue. Okay, it is diaphragmatic pacing.

00:07:12UnclearI will come back, sir. It must be, sir, because of the left side.

00:07:28FacultyThe left side is not pacing; that is why I wanted to show it. Okay, next person. Phrenic nerve stimulation usually happens in—what is it?—CRT. That is where it usually happens. Okay, next one.

00:07:51This patient underwent an interventional therapeutic procedure a few months back and is now presenting with this symptom a few weeks or two months later. She had a TIA two times.

00:08:13TIA, transient ischaemic attack, two times, and she underwent the procedure.

00:08:27Can you speak a little louder? Can you give the other mic? I think there is some problem with this one.

00:08:47CandidateThe image is showing hairy patches over the right side of the abdomen.

00:08:52FacultyKeep the mic a little closer. The right side of the abdomen, okay. The side doesn't matter; you can say some rash is there.

00:09:09CandidateI cannot tell, sir. You answer it.

00:09:13FacultyOkay. I am going to name this an OSCE rule: the distance between the mic and the mouth is inversely proportional to how well you know the answer. Correct? Exactly, somebody said it. So anybody can guess.

00:09:39It is not amiodarone-related; it is device-related, very common in the West but not very common here. What do the devices contain? For example, this patient had a TIA, so what device?

00:09:55AudiencePFO.

00:09:55FacultyWhat does a PFO device contain?

00:09:58AudienceNickel.

00:09:58FacultyIt is a nickel allergy. It is very rare here but very common in the Western world. So this is a severe allergic dermatitis. It is usually self-limiting. The use of nickel ornaments is very common in the West, probably; that is why they get sensitised. We don't use nickel; we use gold, probably, and gold is very non-allergic. That is why we don't get it. Okay, next person.

00:10:59Go on describing.

00:11:02CandidateThis is an attempted left ventricular angiogram, probably in the RAO view.

00:11:05FacultyUsually, which view will you do a left ventricular angiogram in?

00:11:13CandidateRAO 30-degree view.

00:11:13FacultyOkay. It is an attempt at a left ventricular angiogram. Usually angiograms are done with side-hole catheters, and usually we do it with a pigtail. But what other catheter can you use? Actually, a diagnostic catheter.

00:11:33CandidateTiger catheter.

00:11:33FacultyWhat is the spelling of Tiger? Not only the person holding the mic; other people can also tell the spelling of Tiger. Speak louder. Anybody sitting in that row can answer it. What is the spelling of the Tiger catheter?

00:12:02Audience[unclear spelling offered]

00:12:02FacultyThat is not it. Okay. So a Tiger catheter can also be used for doing an LV angiogram. Why? Does it have side holes? It has side holes, so you can use it for LV angiography. But here, probably a Tiger catheter was used, and what is happening? It is hitting the left ventricular wall and has perforated the LV, and the contrast is filling the pericardium. So it is producing an effusion, and maybe the patient had tamponade [unclear]. I don't know what happened to the patient; it is not our case. I got it from somewhere.

00:12:53AudienceIt must have been a machine, a pressure injection. I think a hand injection will not do this.

00:13:03FacultyYes, but these Tiger injections are usually hand injections, which most of us do. Okay, next person, the next row behind. You will get your chance, don't worry. We have, I think, one more session today, so everybody will get a chance.

00:13:35Which view of the echocardiogram?

00:13:35CandidateSubcostal.

00:13:35FacultySubcostal view. What are you seeing? Very good. You can speak a little louder.

00:13:45CandidateIVC to RA, one mobile mass.

00:13:49FacultyOkay, very good. What are the situations where you get such a thing?

00:14:00CandidateCarcinoma, sir.

00:14:00FacultyRenal cell carcinoma is one of the commonest conditions. Otherwise, a large thrombus from the IVC can also, very rarely, do this, but the most common condition is renal cell carcinoma. Okay, good. Next one.

00:14:18You can tell the findings; you probably cannot tell the diagnosis, and that is not required. Post-surgery. Speak louder and clearly. Anyway, I am not seeing you; I don't think anybody else is seeing you. You can tell whatever you think it is.

00:14:40When you see an X-ray, especially when the heart is on the other side and all, you have to start by telling the situs. So is the situs clear in this?

00:14:51CandidateSitus solitus, but dextrocardia.

00:14:51FacultyDextrocardia, okay. Then what else are you seeing? Is it a postoperative patient? You are seeing the sternal wires. What else? You are seeing something else here. What is it most likely?

00:15:08CandidatePDA clip.

00:15:08FacultyOkay. Then what about the vascularity? Is it the same on both sides? There is differential vascularity: the vascularity is reduced on the right side, and there is a vascular shadow. Actually, this was a BDG done on the left side, which has become dilated. So the diagnosis is some complex congenital heart disease: pulmonary atresia, post-BDG. Okay, next person.

00:15:45I don't think it is very clear here, but it is clear on the other monitors.

00:15:50CandidateChest X-ray, PA view.

00:15:55FacultyHow will you differentiate between a PA and an AP view?

00:15:59CandidatePA and AP view you can differentiate by the level of the scapula. The scapulae will be wide apart in the PA view, and the clavicles will be horizontal in the PA view.

00:16:15FacultyOkay, anybody can make it better? Okay, go ahead. What are all the things you are seeing?

00:16:39CandidateThere is cardiomegaly, sir, with an LV type of apex.

00:16:50FacultyWhat are all the chambers enlarged? You said the LV is enlarged.

00:16:53CandidateThe LV is enlarged; the LA is enlarged.

00:16:53FacultyWhat are the signs of LA enlargement on an X-ray?

00:16:59CandidateThere is splaying of the carina, sir, more than 90 degrees, and there is a double shadow, and then there is straightening of the left heart border or a bulge below the pulmonary bay. There is also right atrial enlargement.

00:17:13FacultyRight atrial enlargement, and the criteria you should know; I think everybody knows them.

00:17:17CandidateAnd there is pulmonary venous congestion; you can see some cephalisation.

00:17:21FacultyVery good. You should know the stages of pulmonary venous hypertension, what is equalisation, what is cephalisation, all those things, and the reasons why they occur.

00:17:31CandidateThere are two valve shadows; two mechanical valves are seen. One looks like a ball-and-cage valve, sir.

00:17:38FacultyOkay. The ball-and-cage valve is in which position?

00:17:38CandidateIn the mitral position.

00:17:42FacultyWhy do you say it is in the mitral position? Two reasons.

00:17:47CandidateIf you draw a line from the right cardiophrenic angle to the hilum, if the valve lies above that level it is the aortic valve; if it lies below that it is the mitral valve, sir.

00:18:01FacultyFrom the cardiophrenic angle to the opposite-side hilum. If you draw a line from here to here, if the valve lies above it, it is the aortic valve; below it, it is the mitral valve. Okay. And one more reason why it is a mitral ball-and-cage valve?

00:18:20CandidateThe orientation: it is facing downwards, from the LA to the LV, the way the blood should go.

00:18:25FacultyAnd one more reason: how many struts are there? Four struts. A mitral valve will usually have four struts and an aortic valve will usually have three struts, except the very large ones. Okay. The other one, in the aortic position most likely, is a tilting-disc valve. Okay. And what is the pathology? Which valve is most likely abnormal?

00:18:54CandidateThe aortic valve, sir, because the LV is enlarged.

00:18:58FacultyNo. Why should there be LA enlargement in an aortic valve pathology? That occurs only in the late stage, no? So most likely it is a mitral valve pathology, because you have LA enlargement. And the LV enlargement could also be due to a paravalvular leak; most likely a paravalvular leak. Okay, next. Good.

00:19:25CandidateChest X-ray PA view. Pacemaker.

00:19:40FacultyWhere is it pacing?

00:19:45CandidatePerforated.

00:19:45FacultyVery good. Where is it now? What pacemaker is it? Is it a single-chamber pacemaker, a dual-chamber pacemaker or some other thing?

00:19:59CandidateSingle chamber.

00:20:06FacultyNow, what is thickened? Something is thickened here and here. What is it?

00:20:10CandidateShock coil.

00:20:10FacultyShock coils, so it is an ICD. So the ICD lead is perforated and it is in the abdominal cavity. Okay, perforated ICD lead. Next person.

00:20:29Just some fun. But don't tell the diagnosis, please; everybody will get a chance. Link these and diagnose: 'cherry on top' first, then the Popeye sign, and the last one is raccoon eyes. So what is the diagnosis?

00:20:56CandidateCardiac amyloidosis.

00:20:56FacultyOkay. So this is the Popeye sign; can you see it in the video? It is a bulge because of the tendon rupture; the biceps comes up like the cartoon character. Then 'cherry on top', and the raccoon eyes. Okay, next person.

00:21:28Who is having the mic?

00:21:31CandidateThese are angiograms of the left coronary artery.

00:21:35FacultyWhich view is it?

00:21:35CandidateRAO caudal view.

00:21:35FacultyVery good, RAO caudal view. You should know how the RAO and LAO views look depending on the position of the spine and the diaphragm and all. It is very basic; I think everybody knows it.

00:21:50CandidateIt shows the left main having aneurysmal dilatation.

00:21:53FacultyAneurysmal dilatation. So what is ectasia and what is an aneurysm? You all know: when the diameter is more than 1.5 times the normal diameter, it is called ectasia. When it is localised, it is called an aneurysm. Is it a saccular or a fusiform aneurysm?

00:22:14CandidateSaccular.

00:22:14FacultyIt is saccular, because the transverse diameter is more than the longitudinal diameter; then it is called saccular. If it is the other way, it is called fusiform. So what do you do for this? Will you do something, or what are the problems with this aneurysm? What happens to the blood flow in the aneurysm?

00:22:41CandidateThere can be stasis, and it can produce thrombus, and it can embolise.

00:22:47FacultySo what can you do for it?

00:22:52CandidateWe can do a covered stent, or we can do clipping [unclear] and do CABG.

00:22:56FacultyOkay, that is one option. Any percutaneous option, if the patient is not willing for surgery? You have a little margin before the bifurcation, probably a millimetre of margin. Difficult, but intervention-wise, can you do something?

00:23:18CandidateCovered stent.

00:23:18FacultyCovered stent. But I don't know whether a covered stent would be feasible in this patient. This patient was actually on follow-up for many years. The patient was not willing for anything, and on a 10-year follow-up nothing has happened to this patient. Okay, next person.

00:23:43Sorry, somehow it is not playing. One second.

00:24:02Tell me, the angiogram is in which view?

00:24:02CandidateRAO view, sir.

00:24:02FacultyRAO view, okay. How much volume will you give in a normal RV or LV angiogram? What are the settings? That you should know. Somebody may ask you what the settings are, what PSI you will keep and how much volume.

00:24:32CandidateUsually around 20 to 25 ml, around 14 to 16 ml per second, and a PSI of 750.

00:24:36FacultyHow much? 750. What is PSI?

00:24:41CandidatePressure per square inch; pascals per square inch.

00:24:41FacultyPounds per square inch. That is homework; go and find out. Okay. What is happening to this? Go on speaking.

00:25:05CandidateRestrictive VSD.

00:25:05FacultyRestrictive VSD? Okay, but to see a VSD on LV angiography, which chamber should fill? The RV should fill. Is the RV filling here?

00:25:20CandidateIt can be a Gerbode defect, from the LV to the RA.

00:25:30FacultyMore obvious things, no. For a Gerbode, the RA should fill and then the RV should fill. Here no right-sided chambers are filling; only the left-sided chambers are filling.

00:25:42CandidateSir, LV apical aneurysm.

00:25:47FacultySo what are the segments you identify in the RAO view of an LV angiogram? That you should know; that is commonly asked. Let me take the pointer there. See here: anterobasal, anterolateral, apical, diaphragmatic and posterobasal. Those are the segments, okay? So here, what is happening? Which segment is aneurysmal?

00:26:18CandidateThe posterobasal segment is aneurysmal.

00:26:18FacultyWhat are the two conditions where you get a posterobasal aneurysm like this? Which coronary involvement can do it?

00:26:33CandidateRCA, inferior MI with RV infarction.

00:26:38FacultyInferior MI can produce this. What other condition, which is common in the tropics, can develop like this? Submitral aneurysm; that is one cause. This patient actually had a submitral aneurysm producing a large aneurysm. And what other haemodynamic abnormalities are there in this angiogram?

00:27:02CandidateA posterobasal aneurysm is there. The rest of the LV is contracting normally; the other segments are contracting normally.

00:27:06FacultyWhat is happening to the blood from the LV? Where is it going? What is the chamber filling here?

00:27:19CandidateThere is severe mitral regurgitation.

00:27:19FacultyWhy do you say it is severe mitral regurgitation? Because the LA is almost as dense as the LV. And two other things are also filling here. What are they? Let me show with the pointer. Here is the LA appendage, and the pulmonary veins will fill. These are the two things you have to see. Somehow it is not replaying continuously. Here you can see the LA appendage filling, and the pulmonary veins also fill in the case of severe MR, and the density of the contrast is the same in the LV and in the LA. So what grading of MR does that indicate? Sellers grade [unclear].

00:28:15Okay, next: a 28-year-old male with dyspnea on exertion. What is the finding? Next person who is having the mic.

00:28:29CandidatePigtail catheter.

00:28:29FacultyVery good, a pigtail catheter in the LV, in which view? Where is the spine; which part of the screen? You were seeing RAO views; now it is seen in the LAO view. Okay, LAO view, and in the LAO view you should know the segments: this is the septal segment and this is the lateral segment.

00:29:00So here the patient is a 22-year-old male with dyspnea on exertion. You should have in mind the conditions which are possible. What are they? LV function is normal, so it is not coronary artery disease or anything. What is happening? It is a hypercontractile LV. Okay. And what is happening here? Some white things are seen here. Just see here carefully.

00:29:27CandidateSubvalvular—

00:29:30FacultyMore commonly? It is not a congenital heart disease. You are seeing the mitral valve; this is SAM. You can see the white things. Now look carefully: can you see the white mitral curtain going and hitting the septum? That is the SAM. You should know the mechanisms of LVOT obstruction in HCM. Stop.

00:30:04We will continue after this in the afternoon session. We will take one more. Again, who is having the mic?

00:30:17These are three findings; I think everybody should know these. What is the most common cardiac lesion associated with these three findings in this patient? You can describe what you are seeing.

00:30:34CandidateThe image is showing polydactyly.

00:30:37FacultyOkay, very good. What type of polydactyly? There are two types of polydactyly: post-axial and pre-axial. This is post-axial polydactyly. Okay, then?

00:30:55CandidateTeeth malformation.

00:30:55FacultyTeeth malformation, okay. And what is there in the ECG? The patient is having a wide split second heart sound, etcetera, but the ECG is like this.

00:31:12CandidateThe ECG shows left axis deviation.

00:31:12FacultySo what is the condition? This is a syndrome.

00:31:23CandidateEllis-van Creveld syndrome.

00:31:23FacultyAnd the most likely associated lesion is common atrium. Okay, common atrium; that is very common. We will stop here and continue later. Thank you.

00:31:31SpeakerThank you so much, sir, and thank you for accepting the invitation to this wonderful programme.

00:31:38FacultyEvery year I get the invitation, but my family doesn't get invited. Family never gets invited.

00:31:41SpeakerThank you so much, sir. We now break for lunch, but when...

00:00:08CandidateA female patient presenting with chest pain, dyspnea and syncope.

00:00:13FacultyChest pain, you forgot. Yes, not pulmonary embolism; something pulmonary. What about pulmonary hypertension?

00:00:23CandidateSo, primary pulmonary hypertension: a lady presenting with syncope and dyspnea. Family history [of] sudden cardiac death is another mode. That can also be thought of.

00:00:39FacultyDo you want to report it?

00:00:39CandidateYes. Her saturation is 98% on room air, with a pressure of 100/60, pulse 82 per minute, and BMI 22. The second sound is normally split; nothing significant in the [unclear].

00:01:05Probably HCM only. We will rule out severe AS, and PH also, idiopathic PH. If we are considering pulmonary hypertension, S2 is normally split, there is no loud S2, so I would focus more on HCM only.

00:01:23FacultyBefore the ECG of the patient, will you do any other thing to bring out the hemodynamic abnormality?

00:01:33CandidateI would like to see the JVP also.

00:01:33FacultyNo, you said HCM. In HCM, will you do something dynamic at this stage?

00:01:38CandidateDynamic auscultation will help. Yes, I should have said that.

00:01:48FacultyWhat dynamic maneuver will you do for the murmur? What is the simplest? People will say Valsalva maneuver; [unclear] difficult. What is the simplest thing you can do at the bedside for evaluating the murmur? What is the simplest thing you can do for dynamic auscultation at the bedside?

00:02:10CandidateHandgrip. Handgrip will decrease the murmur.

00:02:13FacultyJust remember this: stand, squat, stand. That's all you have to do. You will be changing preload, you will be changing afterload, and maybe the murmur will come out at that time. If you want, you can combine it with handgrip, but actually it is stand, squat, stand. And you also have to do the same thing: you have to stand with the patient, squat with the patient, and stand up with the patient.

00:02:39CandidateThis is at normal standardization. Rhythm is regular, rate around 80. The P wave shows right atrial enlargement, and biatrial enlargement is there. And the axis is...

00:02:58FacultyFrom the...?

00:03:00CandidateYes, 30. There is LVH in the QRS, and in the lateral leads there is T-wave inversion of concentric hypertrophy, but the typical T waves of HCM are not there [unclear]. There are no VPCs; sinus rhythm is there; the AV interval is normal.

00:03:36Faculty[unclear] atrial enlargement?

00:03:44CandidateBecause of LV dysfunction: an increase in LVEDP, pressure, because of pulmonary venous hypertension, causing [it].

00:03:56FacultyCan hypertrophy affect the right side?

00:04:00CandidateYes.

00:04:06FacultyThe RA has to contract over time. The RA has to be shared by both the chambers [unclear].

00:04:30CandidateThe first image shows a parasternal long-axis view, transthoracic echo. There is obvious LA enlargement; the aorta is of normal size. There is concentric LVH, and [unclear]. On colour, there is turbulence across the LVOT in systole, and there is MR, posterior. In the M-mode of the same, in systole there is grade 1 anterior [motion]: SAM grade 1 is there.

00:05:06FacultyAnd how do you explain the mild [unclear]? How do you explain that? Where is it? How do you explain that? Is it physiological or is it pathological? [unclear] Is there any clue why AR is happening?

00:05:48CandidateMR is there.

00:05:53FacultyWhat?

00:06:08Unclear[inaudible]

00:06:45CandidateSir, the hypertrophy looks as if there is some subaortic membrane, no?

00:06:59Faculty[unclear] enlargement causing it. This happens sometimes even in multivalvular disease. You know, if there is AR and MR, you correct the MR and the AR will disappear totally. Actually, [unclear] they have reported AR in about 7% [unclear].

00:07:27CandidateLVOT findings: as seen in the last pages, grade 1 SAM is there, and the chamber dimension is slightly decreased. On Doppler of the LVOT you can see a dagger shape, with increased gradient in mid-to-late systole; the peak pressure gradient is around 70.

00:08:01FacultyWhat is the mechanism? What is the mechanism?

00:08:11CandidateSAM. Mid-systolic [unclear].

00:08:22Unclear[inaudible]

00:08:45CandidateApical four-chamber view [unclear]: there is LA dilation with MR, a posterior jet MR, and the anterior leaflet tip... No, it is not posteriorly directed; it is centrally directed.

00:09:04FacultySo the MR is not exclusively due to SAM; something else is there.

00:09:04CandidateLA [dilation]: atrial functional MR, sir. Because of LA dilation there is dilation of the annulus, causing atrial functional [MR], unless it is prolapse.

00:09:23FacultyWhat are the mitral abnormalities in HCM?

00:09:29CandidateElongation of the anterior mitral leaflet, and [unclear].

00:09:36FacultyWhat about the attachment of the papillary muscles?

00:09:39CandidateSupernumerary papillary muscles. Chordal abnormalities. This can be part of the [unclear], and an increased number of papillary muscles can [unclear] the closure.

00:09:54And in the five-chamber view there is some regurgitation jet, mild [unclear] regurgitation jet also. And in the RV-focused apical four-chamber view there is no significant [unclear].

00:10:24FacultyWhat about the interatrial septum?

00:10:24CandidateIt is aneurysmal and bulging towards the right side.

00:10:30FacultyYes. More like a dome shape. That causes the Bernheim effect, sometimes referred to as atrial Bernheim [unclear].

00:10:48So this is the [unclear] of the patient. We will comment as it goes. Can you come out with a differential? What is the differential of this? How do you sum this up?

00:11:02CandidateHCM, ASH subtype, with an obstructive gradient: obstructive HCM.

00:11:16FacultyThat tells [us] obstruction [unclear] gradient. We saw [unclear], and incidentally we got a respiratory variation also, which was [unclear]. There is quite a bit of variation to see in terms of both [unclear].

00:11:43CandidateYes, E waves. No, this is not because of the [unclear]; because the LVOT obstruction is dynamic, it can vary with the [unclear].

00:11:57Unclear[unclear] because of the dynamic variation. Yes.

00:12:35CandidateOnly in the central part there is some decreased strain, but there is increased [unclear] along the rest of the area: hypercontractile LV. Also, fitting into the [differential of] amyloidosis, strain [unclear] is decreased only on the septal side. So the septal movement is grossly diminished.

00:13:06FacultyMostly [unclear]. In which condition is it reversed? In which condition is it reversed?

00:13:13Candidate[unclear]

00:13:18FacultyAny other cardiomyopathy [unclear]? Is there a particular Doppler [unclear]?

00:13:47Candidate[unclear] there is no reversal.

00:13:55FacultyIs the patient in failure?

00:13:58CandidateThe IVC is dilated, 2 centimetres, and collapsing 50%.

00:14:06FacultyWhat will be the estimated RA pressure in this patient?

00:14:14Candidate[unclear] RA pressure will be 10.

00:14:21FacultyCollapsing 50%, 2 centimetres. Okay. What do you expect of MRI?

00:14:27CandidateOne is to quantify the scar burden, which is important for primary prevention of sudden cardiac death. Secondly, to rule out RCM; other physiology can be ruled out by MRI. The pericardium also can be evaluated, and the dynamic obstruction can also be further evaluated.

00:14:51FacultyBasically, CMR is for two things: one is diagnosis, second is prognosis, risk. What are HCM mimics? HCM mimics? Other causes of hypertrophy. What are the conditions?

00:15:16CandidateFabry disease, hypertension, AS, severe AS.

00:15:21FacultyOkay.

00:15:21CandidateNoonan syndrome.

00:15:28FacultyThis slide: how does this slide [look]? It shows a very particular characteristic. If you see, on the right side, there is nulling of the myocardium before the [unclear]; the reverse of the [unclear]. That means you still have myocardium [unclear] before the [unclear]. [unclear] that's what is described in the literature. So, the patient presented to us 4 months back. But on this MRI, you can see that the blood pool [unclear], the myocardium was dark, and [unclear] still had no contrast. [unclear]

00:16:44What about the...?

00:17:10CandidateScintigraphy. Bone scintigraphy.

00:17:23UnclearBoth.

00:17:44FacultyIn hemochromatosis, what type of scanning will you use? MR scanning; what is that called?

00:17:52CandidateT2 star.

00:17:52FacultyNow, which other organ will be black?

00:17:52CandidateLiver.

00:17:55FacultyLiver and heart will be black. Okay. Are they amyloid now?

00:18:09UnclearI think...

00:18:11FacultyManagement?

00:18:24CandidateTafamidis is not available in India. Or you have silencers [unclear].

00:18:42FacultyYou have to also differentiate whether it is wild type or genetic. Thank you. Thank you so much.

00:19:00We'll go ahead with the case presentation and then we'll...

00:00:03CandidateThe informant is the patient herself; she is reliable. Chief complaints: dyspnea on exertion for the past 4 years, increased over the past 3 months; palpitations for the past 3 months; pedal edema for the past 2 months. Since the past history is significant, I would like to describe it first.

00:00:19FacultyNo, tell me the symptoms again, please.

00:00:23CandidateShortness of breath for 4 years, more since 3 months; palpitations for 3 months; pedal edema for 2 months. The past history of the patient is significant, and I would like to describe it first. At 35 years of age, the patient was admitted with...

00:00:42FacultyYou are going back to the past history?

00:00:45CandidateYes, sir.

00:00:48FacultyYou don't have to go from past to present like that. You can start from the beginning, what she had, and continue till the present time. That also can be done.

00:00:52CandidateAt 35 years of age, the patient was admitted with dyspnea and underwent a balloon dilatation procedure [unclear]. She later underwent two more such procedures over a span of 6 years; the last procedure was in 2013. After this she was asymptomatic, but was advised to take an intramuscular injection every 21 days, which she took for 4 years. Later, due to local site pain, it was switched over to oral medication. She was followed up for 5 years after the procedure and was later lost to follow-up.

00:01:27For the past 4 years she has complained of dyspnea. Initially she was able to do all household activities but became dyspneic on exertion. For the past 3 months she has been dyspneic during household activities and on climbing one flight of stairs, progressing from NYHA class I to class III. The dyspnea increases on lying down and is associated with cough. She also complains of palpitations for the past 2 months, which occur during exertion and are not associated with giddiness, blurring of vision or loss of consciousness. The palpitations are regular in nature.

00:02:07She also complains of pedal edema, which decreased with medication. For the above complaints she visited an outside hospital 2 months ago, where she was evaluated, told that she would need surgery, and referred to this institute. There is no history of chest pain, loss of consciousness, abdominal distension, hemoptysis or any focal neurological deficit. There is no history of sore throat or joint pain in childhood.

00:02:36Obstetric history: P2 L1. She has a 22-year-old daughter; her 18-year-old son died 4 years ago in an accident. Both pregnancies were full-term normal vaginal deliveries, and the pregnancy and postpartum periods were uneventful. Family history is not significant. Summarising the case of a [unclear]-year-old...

00:02:58FacultyHold on, hold on. See, good, you started from the beginning, but before the balloon dilatation we want to know what symptoms she had at the time they opted for balloon dilatation, because that will give us an idea. You can even start with whether there was any rheumatic fever; you said there is no rheumatic fever. That is the way you can present in the exam, because in the exam you won't have time, especially if you are the fourth candidate presenting. So start with what happened before the balloon dilatation, then come to the balloon dilatation and whatever came after, because these are all related.

00:03:41I think it is not a separate history. I specifically asked how many years she had the disease process. It probably started as mitral stenosis and she underwent balloon valvotomy; from whatever you described there is no other possibility in this. So it is a continuum. As sir said, start from the initial symptom before the balloon and present from there. That will be better.

00:04:07CandidateShe had only dyspnea, sir.

00:04:07FacultyBut for how many years did she have dyspnea before the procedure?

00:04:11CandidateShe is not able to recall, sir, and she is not able to recall the exact year of the procedures either. She speaks Tamil and there was some language difficulty, sir.

00:04:19FacultyWere both done here?

00:04:19CandidateYes, previously done here only.

00:04:27FacultyThere was no PND history?

00:04:27CandidateNo, sir. Orthopnea is there, on lying down. No PND.

00:04:32FacultyWhat is the importance of having orthopnea? Which is the worse symptom?

00:04:37CandidateOrthopnea is worse. Immediately on becoming recumbent there is increased preload from the venous system, which cannot be accommodated by the heart. So orthopnea is more severe than PND.

00:04:53FacultyWith the palpitations you mentioned some associated history. What all did you say?

00:04:56CandidateI said there is no history of giddiness, blurring of vision or loss of consciousness.

00:05:04FacultyAny other history you will ask? Post-palpitation diuresis: in which condition will you get it? In supraventricular tachycardia?

00:05:13CandidateIn SVT the patient can have diuresis because of release of ANP from the atria. There can be diuresis after SVT, sir.

00:05:21FacultyOkay. Can you tell me the hemodynamic sequence? What is she currently having?

00:05:27CandidateShe has increased pulmonary capillary pressure...

00:05:33FacultyFor the last 4 years. The history is the problem.

00:05:33CandidateYes. She has predominantly increased LA pressure, and dyspnea because of increased LA pressure and pulmonary capillary pressure. Along with this she has palpitations, which are exertional. It looks like volume overload, so I am suspecting an additional regurgitant lesion which can cause this palpitation in MS. Even in MS, AF can be a cause of palpitation, but the palpitation she described is regular and on exertion. So I would like to keep a regurgitant lesion, aortic regurgitation, as one of my possibilities. My first differential would be MS with MR or AR, and the second would be pure MS with AF. For the palpitations, I asked her to tap them out; she was not able to, but she said they are regular.

00:06:25FacultySo which is more likely, MR or AR?

00:06:31CandidateMore likely MR, sir.

00:06:31FacultyIf after the BMV she was totally asymptomatic, why are you considering MR in this?

00:06:40CandidateIt could have progressed after BMV. She could have had grade 1 or grade 2 MR, which would have progressed over the years.

00:06:49FacultyAnd is that likely? Severe MS was opened up, with no MR at that point. More likely it can be aortic regurgitation.

00:06:52CandidateYes.

00:07:02FacultyWas there fatigue?

00:07:02CandidateShe describes dyspnea and fatigue together, sir. The pedal edema is because of RV failure, because of pulmonary hypertension.

00:07:16FacultyMS causing pulmonary hypertension, followed by pedal edema. Can it persist due to right-sided valve disease like TR?

00:07:22CandidateYes, sir, TR. If it is rheumatic, TS and TR can be there, which can cause pedal edema.

00:07:32FacultyWhen there is TS [unclear], dyspnea will not be there.

00:07:34CandidateYes, dyspnea will decrease.

00:07:41FacultyBut once TS sets in, right heart failure features will go up, but the output from the right side will decrease. Dyspnea will decrease, but fatigue will [unclear] with organic tricuspid disease. They purchase relief of dyspnea at the price of fatigue. That's what it is: breathlessness reduces, fatigue increases, right heart failure features go up.

00:08:15Okay, so with this history, what are the likely possibilities?

00:08:18CandidateLikely she has acquired valvular heart disease, rheumatic multivalvular disease. Initially she had RHD with MS and BMV was done. Now she is having mitral restenosis and AR.

00:08:34FacultyShe underwent BMV three times.

00:08:41CandidateSo I am saying it is mitral restenosis and AR, with PH and TR.

00:08:46FacultySo which one will you consider as the first possibility?

00:08:51CandidateThe first possibility is restenosis, sir: severe mitral disease with AR.

00:08:57FacultyBut you said MR was one of the first possibilities you thought of initially.

00:09:01CandidateI reconsidered when you said that post-BMV, in the acute phase, you may have MR, but it won't progress after that. In the multiple case series also, the MR did not progress over long-term follow-up.

00:09:16FacultySuppose the last BMV produced MR, and it was, say, moderate or mild. Can it progress?

00:09:26CandidateLess likely, sir.

00:09:29FacultyIt is unlikely, but if the patient [unclear: possibly 'is not on secondary prophylaxis'], the level of MR can go up, it can go on to the right heart, and as you say she can develop pedal edema. It can happen that way.

00:09:45What are the mechanisms of pulmonary hypertension in mitral stenosis?

00:09:51CandidateFirst, because of increased LA pressure: backward, passive pressure transmission. Second, reactive pulmonary vasoconstriction; over time there can be pulmonary vascular obliteration, and PVOD also can develop. Third, structural changes. These are the three reasons.

00:10:13FacultyWhen you do a BMV for severe MS with severe PH, among these mechanisms producing PH, what all will come down, and over what time period? What happens on table, after the procedure?

00:10:27CandidateThe LA pressure and pulmonary capillary pressure will decrease, sir. The LA-to-LV gradient also will decrease, the area will increase, and over time the PVR will eventually come down.

00:10:40FacultyYou said there are three components. The passive component will come down immediately, if it is a good BMV and there is no MR.

00:10:44CandidateYes, sir.

00:10:48FacultyThen what happens to the reactive component?

00:10:50CandidateThe reactive component also will come down over time.

00:10:52FacultySome will come down immediately, but it will take some time; people say it will come down further up to 6 months or one year. What happens to the structural damage that has already occurred? That will persist, or may actually progress. It will relatively persist and will not come down.

00:11:06What is the transpulmonary gradient?

00:11:12CandidateThe transpulmonary gradient is the difference between the mean pulmonary artery pressure and the left atrial pressure.

00:11:19FacultyHow much is normal?

00:11:19Unclear[Numbers unclear.] The mean transpulmonary gradient, not the diastolic gradient...

00:11:34FacultySo what happens in post-capillary, pre-capillary and combined PH? How do you know it is post-capillary PH?

00:11:39CandidateBy the pulmonary capillary wedge pressure and by measuring pulmonary vascular resistance, you can find out whether it is pre-capillary or post-capillary. In pre-capillary PH there will be an increase in the transpulmonary gradient and in the pulmonary vascular resistance; in pre-capillary the transpulmonary gradient will remain high, ma'am, and in post-capillary it will decrease.

00:12:07In post-capillary PH there is a rise in LA pressure and pulmonary capillary wedge pressure, so the transpulmonary gradient will be the same, normal. In pre-capillary the transpulmonary gradient will increase. In post-capillary the diastolic gradient increases, but the transpulmonary gradient remains almost the same.

00:12:34Unclear[unclear] Sir is not asking about after the procedure, but normally: how to differentiate pre-capillary from post-capillary PH?

00:12:42CandidateIn pre-capillary PH, the mean transpulmonary gradient will be increased.

00:12:47FacultyIn pre-capillary, correct. The transpulmonary gradient will be increased. Something else?

00:12:58What is 'second stenosis'?

00:12:58CandidateBecause of reactive pulmonary vasoconstriction there will be an increase in pulmonary hypertension.

00:13:06FacultyWhat happens? What pathology happens?

00:13:12CandidatePulmonary reactive constriction: pulmonary artery constriction.

00:13:19FacultyMain pulmonary artery, [unclear], or what? At which level?

00:13:27UnclearAt the level of the arterioles, the pre-arterioles.

00:13:35FacultyWhat is the hypothesis?

00:13:41CandidateWood's hypothesis.

00:13:41FacultyWhat is the [unclear] of Wood's hypothesis? It is one of the mechanisms described: the 'second stenosis'. What is second stenosis?

00:14:08CandidateExamination: a [unclear]-year-old female, oriented to time, place and person. Height 158 cm, weight 62 kg, BMI 24.8. Pulse 84 beats per minute, regular, normal volume, normal character; no radio-radial or radio-femoral delay; all peripheral pulses felt.

00:14:26FacultyWhat is the pulse rate?

00:14:26Candidate84, sir. Regular.

00:14:33Blood pressure: right upper limb 130/60 mmHg, left upper limb 132/64; lower limb systolic blood pressure 140. Saturation 99% in all four limbs. Afebrile. JVP is 2 cm above the sternal angle, with normal waveforms and normal respiratory variation.

00:14:56Faculty2 cm above the sternal angle?

00:14:56CandidateNo, sir, total 5 plus 2, 7 cm.

00:15:04FacultyYou saw the JVP in the sitting position or in which position?

00:15:08CandidateAt 45 degrees, sir. In the sitting position the JVP was not visible.

00:15:14FacultySo it is normal, not elevated. 2 is normal, up to 3. Revise the JVP. Tell the JVP again.

00:15:19CandidateYes, sir, JVP is 2 cm above the sternal angle.

00:15:25FacultyJVP elevated or not elevated?

00:15:25CandidateNot elevated, sir.

00:15:28FacultyOkay. In the sitting position it is not visible, so the JVP mean pressure is not elevated: in the sitting position you are not seeing it above the clavicle.

00:15:39How do you measure the JVP if the wave is above, near the angle of the mandible?

00:15:44CandidateIf it goes above the angle of the mandible in the sitting position, you can raise the hand. What is it called...

00:15:54FacultyWhose manoeuvre is it called? Okay, no need of the name.

00:15:54UnclearGaertner's.

00:16:00CandidateIdentify a basilic vein or some vein in the arm, lift the arm, and then measure the vertical distance.

00:16:07FacultyCan you make the patient stand, or sit with the legs dangling, if you are not seeing the upper level?

00:16:11CandidateYes.

00:16:14FacultyYou can do that. But this is enough: patient in the sitting position, not visible above the clavicle, so the JVP is normal. That's what it is. So what do you think is the mean venous pressure in this patient?

00:16:29Candidate7 cm of water. So it will be equal to around...

00:16:32FacultyWhy do you want water? How do you say 7 cm? You didn't see anything above the clavicle. Then how are you calculating?

00:16:39CandidateAt [unclear] degrees it was 2 cm from the sternal angle, so 2 plus 5 is 7, just adding the RA-to-sternal-angle distance.

00:16:48FacultyOh, at 45 degrees you used it. How did you measure RA to the sternal angle as 5 cm?

00:16:52CandidateAssuming.

00:16:54FacultyRA to sternal angle is 5 cm, which is not true in everyone, but assuming it to be fixed, from there it is 2 cm, so a total of 7 cm...

00:17:02Candidate...of water, which will be equal to 5 to 6.

00:17:05FacultyWhy do you want to bring water here? Where did you get water from?

00:17:09CandidateWater for blood, sir. Blood.

00:17:14FacultyThere is a conversion factor for that also. What I am saying is, in the exam, don't get caught on the JVP like this by quoting the sternal angle. Just say that in the sitting position I could not see the JVP, so the mean pressure is normal.

00:17:31CandidateIn that case, do the waveforms have to be seen or not?

00:17:34FacultyYes. You can say that at 45 degrees you saw the waveforms. The mean JVP is not elevated, which you have already mentioned, and then the waveforms. You can't say 'I have not seen the waveform in the sitting position.' You will have to put the patient down, make it appear in the neck and observe the waveform. You have to put the patient at an appropriate angle so that it becomes manifest in the neck.

00:17:58Also the abdominojugular reflux. How will you elicit it?

00:18:05CandidateWe should ask the patient to breathe normally...

00:18:05FacultyIn what position will you put the patient?

00:18:09CandidateSupine position at 45 degrees.

00:18:12FacultySupine position, correct?

00:18:12CandidateSupine, with the neck elevated at 45 degrees: lying down, neck at 45 degrees. Relax the abdomen; you can fold the legs to relax the rectus abdominis.

00:18:21FacultyIs the supine position correct or not? First, why do you want to fold the legs? What will happen?

00:18:27CandidateThe rectus abdominis will relax, so that when you press, they won't voluntarily guard.

00:18:30FacultyYou will increase the preload. No.

00:18:35Let me make it clear to everybody. Don't put the patient in the supine position while you are trying to do the abdominojugular test. Put the patient at an angle where the upper level is just seen. As you keep on decreasing the angle, at one particular point you will be able to see the upper level of the JVP, the mean pressure. Keep the patient at that particular point and then give the compression of the abdomen. There is a particular angle at which you have to keep the patient to make the upper level of the JVP appear.

00:19:04Where will you give the pressure?

00:19:08CandidateRight upper quadrant or centre; it can be given over the entire abdomen, sir. If the patient has a tender hypochondrium we avoid it; otherwise it can be given over the right hypochondrium or the centre of the abdomen.

00:19:20FacultyOur idea is to increase the abdominal pressure. You can give it anywhere; anywhere is fine. Okay, now how long will you give it, and what is the result?

00:19:28CandidateResponse: 30 seconds [unclear]. Any elevation, if it persists for less than 3 seconds, is normal.

00:19:33Faculty3 seconds?

00:19:38Candidate3 cycles.

00:19:38Faculty3 cycles of what?

00:19:42CandidateCardiac cycles.

00:19:42FacultyWhat is the length of each cardiac cycle?

00:19:45Candidate800 milliseconds, depending on the heart rate.

00:19:45FacultyNo, that's why: it depends on the compression you give, not on the cardiac cycle. Which book are you referring to? What's your reference for this? This question will always be asked in the examination. Speak from the books. Don't say 'my teacher taught'; he will not come to your rescue there. 'Told in our clinics' counts for nothing. You always have to quote from books. So which book is your reference?

00:20:16CandidateJonathan Abrams. [unclear] three cycles, he said.

00:20:26FacultyNow, what is the physiological basis of this abdominojugular reflux on compression?

00:20:28CandidateOn compression of the abdomen there is increased venous return to the right ventricle. A normal ventricle will be able to handle the increase in volume. If there is [unclear] in the ventricle or any impending RV failure, the ventricle won't be able to accommodate the extra volume, and this will manifest as a rise in the JVP.

00:20:46FacultyThat is the point. The extra volume coming to the RA will not be handled by the system, so the mean pressure will go up. That is the mechanism. Okay, go ahead.

00:20:59CandidateNo pallor, icterus, cyanosis, clubbing or lymphadenopathy. No peripheral signs of acute rheumatic fever. Pistol-shot sound over the femoral artery and Duroziez's murmur are present; these are peripheral signs of AR. The diastolic pressure was around 60.

00:21:13FacultyBut you said the pulse is normal, of normal character, and then you got a pistol-shot sound?

00:21:23CandidateWith the pulse, yes sir, normal character.

00:21:25FacultyYour volume is normal, but your BP is 130/60. The pulse pressure is 70; the pulse pressure is wide. And one more discrepancy: your lower limb blood pressure is only 140.

00:21:40Candidate140 approximately. Severe MS could mask the Hill sign. The discrepancy could be masked by the [unclear] stenosis, underestimating [unclear].

00:21:56FacultyWhen you have a combined lesion, it depends upon the severity. If the pulse pressure is more than 40 and the diastolic pressure is less than 60, then AR is not masked; AR is likely to be dominant. If the pulse pressure is less than 40 and the diastolic pressure is more than 60, it is likely that MS is masking it.

00:22:16Candidate[unclear] 64, sir. BP [unclear] 64, sir. I thought I was speaking into the mic.

00:22:29FacultySo that is 64 [unclear]. Okay, pulses, okay.

00:22:46Cardiovascular system: inspection and palpation. [unclear] You can't have pistol-shot sounds and Duroziez's murmur with [unclear] normal. They are among the sensitive signs. These are the only three signs of AR. What are the three signs?

00:23:06UnclearPeripheral signs: [unclear], and pistol-shot sound, or Traube's sign.

00:23:06FacultyThat's all it is. The others are all just for the sake of enumerating.

00:23:27What BP apparatus are you using?

00:23:33CandidateMercury sphygmomanometer.

00:23:38FacultyBut currently we don't have mercury manometers; now they are banned.

00:23:43UnclearIt was there here.

00:23:43FacultyNo, it is not available in most places. So muffling and so on, we are not able to make out. Okay, what is the mechanism of the usual Omron? How do they assess the blood pressure? What is the method called?

00:24:12CandidateOscillometric.

00:24:12FacultyHow do they derive the pressures?

00:24:16CandidateOnly the mean pressure can be derived, sir; the rest is calculated.

00:24:19FacultyThe mean is derived, and from that the systolic and diastolic are derived. Okay, so that is the problem. Okay.

00:24:28CandidateInspection and palpation: no visible pulsations over the precordium. The apex is localised to the 5th intercostal space in the midclavicular line; it is tapping type.

00:24:37FacultyIn the midclavicular line and tapping type? You are not feeling the apex at all?

00:24:49CandidateIt's best felt there. The apex is of normal character, sorry. Normal apex.

00:24:59FacultyNormal apex? No. What is the duration? What is it here? In your patient, is it a normal apical character, or tapping?

00:25:09CandidateNormal, sir: not hyperdynamic or heaving. It is normal. No cardiomegaly, no abnormal [unclear], with respect to both site and character of the apex.

00:25:26FacultyI think we need a little clarification here. What is a normal apical impulse and what is a tapping apical impulse? Are they both the same?

00:25:37UnclearYes. No.

00:25:40FacultyBoth are the same? Tapping and this one are both the same? No. Anyone? What is a normal apical impulse?

00:25:53UnclearThe lowermost, outermost, perpendicular thrust, confined to one intercostal space, medial to the midclavicular line.

00:25:58FacultySo these are the various components: it should be a perpendicular thrust, and it should last less than one-third of systole, less than 50% of systole. This is normal. Do you really get the lift in a tapping apical impulse in mitral stenosis? The LV has gone down.

00:26:20CandidateSir, only the palpable S1. The first heart sound is perceived as the apical impulse.

00:26:24FacultyYou can localise the sound and say that the apex could be here. So you don't get that perpendicular thrust, because the LV has gone down and the RV is in front.

00:26:35CandidateThat should be corrected, sir.

00:26:35FacultyCorrect. There is a difference between a tapping type of apical impulse and a normal one. This is one of the commonest mistakes I am seeing students of today make, because they are not exposed to many cases of mitral stenosis now. But this is a very common case. Go through all this very clearly, in detail; know about the various studies of rheumatic fever and the basics of mitral stenosis.

00:27:02Okay, so you got a normal or tapping apex. Hemodynamically, which among the lesions is ruled out?

00:27:12CandidateSevere AR is out. MS is the most dominant lesion here. AR might be associated, but MS is more dominant.

00:27:16FacultyDue to two reasons. What are the two reasons?

00:27:20CandidateThere is no cardiomegaly, and the apex is of [normal] character.

00:27:24FacultyOkay, go ahead.

00:27:26CandidatePalpable second heart sound; systolic thrill in the right second intercostal space.

00:27:34FacultySystolic, right second intercostal space? Okay.

00:27:43CandidatePercussion: the left second intercostal space is dull, the right heart border is retrosternal, and the left heart border corresponds to the apex. Auscultation: S1 is loud; S2 is narrowly split with a loud P2; no additional sounds; three murmurs.

00:28:06FacultyNo, wait. Just summarise the findings so far.

00:28:11CandidateLoud S1, narrowly split S2 with loud P2...

00:28:11FacultyNo, starting from the blood pressure.

00:28:13CandidateJVP is not elevated. Sinus rhythm. Wide pulse pressure with negative Hill sign [unclear]. No cardiomegaly; the apex is in the normal position, with a normal apical impulse. There is a palpable P2 and a thrill in the right second intercostal space. S1 is loud and S2 is narrowly split with a loud P2.

00:28:37FacultyFrom this, what is your possibility? You said thrill in the right second intercostal space: is it systolic or diastolic?

00:28:51CandidateSystolic thrill.

00:28:51FacultyOkay. From this, what do you suppose, before going to the murmurs?

00:28:56CandidateSignificant MS is there, sir, causing the loud P2, with a normal apex and normal cardiac size. And AR is there, with a flow murmur causing the thrill.

00:29:10FacultyCan a flow murmur cause a thrill in the aortic area? Even severe AR can cause a thrill, but you said severe AR is not there. But a thrill is there. Which thrill is it?

00:29:19CandidateThrill in the aortic area, sir, probably because of AS.

00:29:25FacultyHe has committed with the systolic thrill: probably because of AS.

00:29:34CandidateSince AR is only moderate, I am thinking there will be associated AS also in this case. That's why I want to keep AS and AR with severe MS as my diagnosis at this point.

00:29:49FacultySo AR and AS are also there. So what is the severity?

00:29:49CandidateAS is moderate, sir; AS and AR both are moderate, because the apex is not heaving type, the pulse [unclear] is not there, and the systolic BP is 130, so there is no decapitation. If AR were there with severe AS, there would have been systolic decapitation; that also is not there. But the thrill is there, so there is a functional obstruction to aortic outflow. So moderate AS, moderate AR and severe MS is what I would keep at this point.

00:30:24FacultyOkay, now go to the murmurs. Is the murmur conducted to the carotids?

00:30:24CandidateYes, sir. Coming to the murmurs.

00:30:35A grade 2/4 low-frequency, rough, rumbling mid-diastolic murmur heard shortly after A2...

00:30:41I told: S1 loud, S2 narrowly split with loud P2, no additional sounds.

00:31:05FacultyS1 is loud, you said. So what do you expect?

00:31:09CandidateS1 loud means the MS is more significant, and the valve is pliable, not calcified. The opening snap is not there.

00:31:24FacultyYou were expecting an opening snap?

00:31:24CandidateMaybe it is absent because of the post-PMV status.

00:31:28FacultyWhat happens to the opening snap in this, with AR?

00:31:28CandidateBecause of the increase in LVEDP, the opening snap can be decreased in intensity and can be absent also. The A2-OS interval can decrease.

00:31:47FacultyWill the A2-OS interval decrease, or...? The LVEDP increases, so the opening will be [unclear: possibly 'delayed'].

00:32:04CandidateMurmurs: a grade 2/4, low-frequency, rough, rumbling mid-diastolic murmur, heard shortly after A2 and of long duration, best heard with the bell of the stethoscope in the left lateral position with breath held in expiration, with presystolic accentuation.

00:32:21A grade 3/6 high-frequency, blowing, decrescendo early diastolic murmur, heard in less than 50% of diastole, best heard in the left second intercostal space with the patient bending forward and breath held in expiration. A harsh, rough, grade 4/6 crescendo-decrescendo ejection systolic murmur with early systolic peaking, heard in the right second intercostal space and radiating to both carotids and the apex. Three murmurs are there.

00:32:59There is no murmur of MR. Only the AS murmur is conducted to the apex, sir.

00:33:12Final diagnosis: acquired valvular heart disease of rheumatic etiology, with severe MS, moderate AR and moderate AS, with evidence of moderate pulmonary venous hypertension. No signs of infective endocarditis.

00:33:32FacultyWhat is the evidence of PVH in this patient?

00:33:39CandidateIn the history, she has recurrent dyspnea, and P2 is loud. These are the two main things. No signs of active acute rheumatic fever, with normal LV function, in sinus rhythm, and currently in NYHA class II.

00:34:03FacultyOkay, why do you say normal LV function?

00:34:03CandidateThe apex is normal. MS won't cause LV dysfunction so early. If AS and AR caused LV dysfunction, there would be a sustained apex, and the blood pressure is 130.

00:34:19FacultyCorrect. Okay, you say severe MS. How much LA pressure do you think there is here?

00:34:27CandidateArbitrarily, sir, above 20. Above 20 it is severe MS.

00:34:31FacultyAbove 20? Then are you hearing any crepitations?

00:34:39CandidateBut it will get adapted. In long-standing MS the pulmonary venous lymphatics will improve, and the patient is in the hospital, so diuretics will have been administered. That will mask it.

00:34:50FacultyOkay. No TR?

00:34:57CandidateNo TR.

00:35:01FacultyOr was it there, with the pedal edema she had complained of?

00:35:01CandidateThere is no pedal edema now, sir. She said it was there up to the mid-knee.

00:35:09FacultyWhich manoeuvre will you do to bring out TR, if any?

00:35:14CandidateInspiration can increase it; or leg raising, passive leg raising, can bring out TR.

00:35:23FacultyWhat is that sign called?

00:35:26CandidateCarvallo's sign, with inspiration, sir: it increases with inspiration.

00:35:31FacultyOkay. So: rheumatic heart disease, severe MS, moderate AR, moderate AS, moderate PH, normal LV function, not in heart failure.

00:35:49Okay, just one point I wanted to...

00:35:49CandidateNo, sir, the BP is 130. That's why moderate AR, not severe.

00:35:58FacultyJust one clarification for everybody; all the students are here. While describing a murmur, should we speak of pitch or should we speak of frequency? In the books it is low-pitched, medium-pitched and high-pitched, but you kept on saying frequency. Pitch is what you are hearing; frequency is what you are recording and assessing on an instrument. So confine yourself to the standard. What is the relation between pitch and the murmur normally?

00:36:35CandidateBlowing will be high pitch, harsh will be medium pitch, and low, rough will be low pitch.

00:36:45FacultyWhat about flow? Which will be low?

00:36:45CandidateIncreased flow means lower frequency, sir; increased gradient means higher. Gradient is directly proportional, and flow is inversely proportional, to the frequency or pitch.

00:36:56FacultyAortic stenosis?

00:37:01CandidateThe gradient is high, but, as in AR, the flow also is high. So it comes under medium.

00:37:09FacultyBut you say harsh. Do you mean high pitch or low pitch?

00:37:12CandidateIt is mixed; medium pitch.

00:37:14FacultyHarsh is mixed. What is low pitch, medium pitch and high pitch, frequency-wise?

00:37:26CandidateIt is given in [unclear]: less than 150, [unclear figures], 125 to 300, above 300.

00:37:37FacultySo you can remember it as: less than 150, 150 to 300, and above 300.

00:37:44The diastolic murmur of MS: you said frequency. What will its frequency be? Is it easy to record or difficult to record?

00:37:51CandidateLow frequency, sir. It is difficult to record.

00:37:54FacultyDifficult to record. Nowadays there is one [digital stethoscope, name unclear]. Have you seen that advertisement? You put it on and you get the ECG and the phono both at the same time. You will not get an MDM. You will get every other murmur except the MDM, because it is low frequency, low pitch. Okay, you proceed further.

00:38:22CandidateShe is symptomatic, functional class II right now, and she has palpitations. So I would like to confirm the palpitations and rule out paroxysmal AF in her, and go ahead with an ECG, echo and X-ray to characterise the lesions properly. In this case, if the mitral valve is still pliable and BMV is anatomically feasible, then, if the AS and AR are moderate, only BMV. If either the AS or the AR needs intervention, or BMV is not feasible, then she will have to go for DVR.

00:39:05FacultyThat we will discuss when you come to management. Okay.

00:39:13So what do you expect on the ECG?

00:39:13CandidateOn the ECG I would expect the MS findings to predominate. The rhythm will be sinus, because it is regular, and I would expect LA enlargement.

00:39:25FacultyAnd what about the axis?

00:39:31CandidateThe axis would be...

00:39:34FacultyThere are two reasons why the axis should be in a particular direction.

00:39:34CandidateSince AS and AR are both there, with both concentric and eccentric hypertrophy, I would say left axis deviation.

00:39:40FacultyYou said the dominant lesion is mitral stenosis, with PH. Mitral stenosis causing RVH and PH gives right axis deviation. That will determine which is the dominant lesion.

00:39:55Do we expect LVH in this patient?

00:39:55CandidateNo, sir, less likely, because MS is more predominant.

00:40:05FacultyWhat is the earliest ECG sign of MS?

00:40:14CandidateLA enlargement.

00:40:16FacultyCorrect. But before that? What about the P-wave axis?

00:40:24UnclearThe P-wave axis should be less than [unclear] deviation of P; P inverted in lead III. That is the earliest sign.

00:40:38FacultyOkay, take up the investigations.

00:40:43CandidateWe'll go to the investigations, sir.

00:40:47FacultyYou have exceeded the time, is it? Okay. Show the ECG.

00:41:30So you said you will go ahead with BMV if the aortic valve lesions are not that significant. Will there be a problem in doing the BMV?

00:41:42CandidateAfter BMV the output will increase. The MS might be masking both the AS and the AR. So we should be careful in assessing; we can't use the normal methods.

00:42:00FacultyHow do you assess AS severity in the presence of severe MS?

00:42:09CandidateThe valve area: the aortic valve area by planimetry, and the continuity equation would be better in this case. Other estimates, the Doppler gradients, will be affected by the severe MS and the low-flow condition. If there is a discrepancy between the flow and the area, then we have to approach it like low-flow, low-gradient AS.

00:42:36FacultyYou have done BMV, or assisted? How do you know from the LA pressure tracing whether your BMV is going to be successful or not?

00:42:47CandidateFrom the LA tracing, whether the results will be good or not, after...

00:42:53FacultyBefore. You have got the LA pressure tracing, not LA-LV, before doing the BMV, from the hemodynamic monitor. Okay, we'll come to that later.

00:43:07Candidate12-lead ECG with half standardisation, 25 by 5...

00:43:07FacultyVery good, half standardisation.

00:43:15CandidateRegular rhythm, heart rate of around 80 beats per minute. P wave...

00:43:23FacultyThis is standard, no? This is normal standard.

00:43:26Unclear25 by 5 is written below.

00:43:31FacultyNo, this is half standard. Okay, go ahead.

00:43:35CandidateRegular sinus rhythm. P wave: there is left atrial enlargement, according to the Morris index. Then the QRS axis is...

00:43:59FacultyMacruz index and Morris index you should know. Yes, okay, go ahead.

00:44:03UnclearThe P wave will be double this; that is half standardisation.

00:44:07FacultyBut is it really half standard? The standardisation box is there on the left, it's half standard, and at the bottom also it is written 5 mm per millivolt. Oh, 5 mm is written. Okay. It is written; that's right.

00:44:42Yes, okay. There is obvious left atrial enlargement, and the right atrium also is enlarged; biatrial enlargement is there. The axis is...

00:44:55CandidatePlus 40 degrees.

00:44:55UnclearThen 40, yes. aVL is [unclear]... 15 to 30... [unclear] 55, but towards the positive side, around 15.

00:45:22CandidateThen there is LVH also, sir. Comparing V2 and V6, according to the Sokolow-Lyon index, LVH is there.

00:45:29FacultyAnd you want to consider the severity of the aortic valve disease?

00:45:37CandidateYes.

00:45:41FacultyBut the BP, the pulse, everything is against it. So by ECG, LVH is there. Okay. But is it a pressure overload or a volume overload?

00:45:54CandidateThere's no Q wave; this is pressure overload.

00:45:57FacultyBut the T is not inverted.

00:45:57CandidateT is not inverted. There is no strain.

00:46:13FacultyOkay, I don't think we can get anything more. It is sinus rhythm with no [unclear], no right axis deviation, no RVH; so it is sinus rhythm with only some signs of LA enlargement. Okay, next: X-ray.

00:46:31When was this taken? Describe this X-ray.

00:46:35CandidateChest X-ray, PA view, overexposed, with rotation to the right side.

00:46:40FacultyAP view, taken when she was in failure in hospital. First describe the lung fields.

00:46:44CandidateIn the lung fields there is a bat-wing appearance: grade 3 pulmonary venous hypertension, pulmonary edema. The CT ratio, although it is an AP film, is around 0.65.

00:47:10The right atrial border extends only two intercostal spaces; there is no obvious right atrial enlargement... It's two and a half intercostal spaces, so right atrial enlargement is there. Left atrial appendage: LA enlargement is there. Splaying of the carina is not seen; the bronchus is not clearly visible. There is no double density. Both RA and LA enlargement are there, and cardiomegaly of LV type is there, with pulmonary edema, grade 3 PVH.

00:47:51FacultyAny other X-rays from when the patient was not that sick?

00:48:13Okay, yes, this is much better. This is much better. This is PA view; this is also overexposed. What are the situations in which this patient can present with the previous X-ray picture?

00:48:25CandidateAF, severe anemia; AF is the most common condition.

00:48:32FacultyOkay.

00:48:36CandidateIn this patient, what is the date of the X-ray?

00:48:42FacultyThe 14th; recent only.

00:48:42CandidateOkay. The cardiothoracic ratio is 0.65. There is cardiomegaly of LV type, right atrial...

00:48:53FacultyNo, I don't think it is 0.6. LV type... Stop going down to the [unclear].

00:49:04CandidateRight atrial enlargement is there, and straightening of the left heart border. Coming to the lung fields, grade 1 cephalisation is there: grade 1 pulmonary venous hypertension.

00:49:15FacultyIs there LAE or not? Is there LAE?

00:49:22CandidateThere is straightening of the left heart border, but the carina... and the double density is not clearly seen.

00:49:26FacultyDouble density is not very clear.

00:49:37Please explain: so the aorta is dilated?

00:49:42CandidateThe descending aorta.

00:49:47FacultyWhy are you seeing the descending aorta there? Okay, fine.

00:49:59Okay, any calcification you will look for in this patient, with a very long-standing history of mitral stenosis?

00:50:07CandidateCalcification in the mitral area; the left atrial wall also can be calcified in very old patients with long-standing mitral stenosis.

00:50:17FacultyCan some calcification occur in the lung fields in very chronic mitral stenosis, with chronic pulmonary venous hypertension? What will happen? What is that called? It is rare only, very rare.

00:50:36CandidatePulmonary hemosiderosis can occur.

00:50:36FacultyOkay.

00:50:45Okay, from the ECG, what is your [unclear]?

00:50:49CandidateYes, I would like to evaluate the AS. Maybe the severe MS was masking the AS severity in my case, but the apex was still not heaving type.

00:50:57FacultyOkay. The position of the apical impulse and its character is the most important determinant.

00:51:01CandidateYes. In both AS and MS it would have been the same position. But the thrill was there in the right second intercostal space; that's why I kept AR, AS and MS.

00:51:16FacultyOkay, go to the echo.

00:51:20CandidateTransthoracic echo, parasternal long-axis view. There is concentric LVH; the AML is...

00:51:27FacultyHow will you know whether your BMV is going to be successful or not from this view?

00:51:34CandidateThe pliability: the doming and pliability of the valve can be assessed in this view.

00:51:46FacultySo first of all, in diastole, the separation between the two tips of the anterior and posterior leaflets [unclear]. What is the normal, or the value below which it is considered severe mitral stenosis?

00:52:01Candidate5 mm [unclear].

00:52:07Unclear[unclear figures: '0.5, 0.7, 0.8'].

00:52:07FacultyYes, okay. Read this echo.

00:52:16What's this first one? No, okay, read this echo. Which chambers are enlarged?

00:52:25He went to concentric LVH; that was the first thing he was telling. The most important thing here is the dilated LA, and the aortic valve is affected.

00:52:33CandidateYes. There is doming of the AML and restricted movement of the PML. Small, spotty calcification at the tip of the PML.

00:52:50FacultyWhile you are trying to explain, don't go to the concentric LVH here. The main pathology has to be explained first, rather than going to concentric LVH. What about the RV? Is it dilated? Because you are considering TR.

00:53:04CandidateYes, sir. I would have to measure it, but it looks dilated.

00:53:09FacultyThe RV is not that dilated. But RV function definitely is normal; it looks normal only. Okay, go to the next one.

00:53:20CandidateColour Doppler across the mitral and aortic valves. There is mild subvalvular disease, mild to moderate...

00:53:33FacultySevere subvalvular disease? No. One more important thing: you are planning to do some intervention. Are you happy seeing this view? By the way, I will not comment on the subvalvular apparatus in this view; I am hardly seeing it. You have to see the leaflet, from the tip of the leaflet to the tip of the papillary muscles, the papillary muscles and the ventricle; then I will comment on the subvalvular apparatus. You need the information on all this before you can comment. Do not comment on it here.

00:54:09The most important thing here is the long jet of AR, crossing the tip of the AML and going right up into the ventricle. You have to open it up; then you have to see the LVOT properly and take the width. And there is no mitral regurgitation; that is the one that matters when you are planning BMV. The valve is not that calcific, the AML is still doming, there is reduced leaflet separation, and MR is not there, in this view at least. Okay.

00:54:46For the AR jet, is the width important, or is the length more important?

00:54:52CandidateThe width: the width-to-LVOT ratio is more important.

00:54:52FacultyHow much ratio?

00:54:52Candidate65%. More than 65% is severe AR.

00:55:00And there is concentric LVH. Parasternal short-axis view: concentric LVH; there is commissural fusion, bicommissural fusion, with thickening of the mitral leaflets and calcification. There is no dense calcification of the mitral valve; some specks of calcification are there in the AML. The commissures are free of calcification, and both commissures are fused. This looks suitable for BMV.

00:55:30FacultySuitable for BMV.

00:55:30CandidateI would like to confirm that there is no MR [unclear] and no clot in the other images.

00:55:40FacultyOkay, forward. Which is more reliable for the mitral valve: Doppler, or planimetry?

00:55:45CandidatePlanimetry. Short axis at the papillary muscles: LV function is normal.

00:56:01FacultyOkay, forward.

00:56:16Yes, what are you seeing?

00:56:16CandidateThis is the short-axis view at the aortic valve. The leaflets appear slightly thickened.

00:56:26FacultyIs it restricted? You said aortic stenosis. You should see the opening, not the closure.

00:56:35CandidateThe aortic valve area is decreased. There is no calcification of the aortic valve [unclear].

00:56:40FacultyWhat other important structure are you seeing? You are planning a procedure, and that will help.

00:56:48CandidateThe left atrium and appendage are seen; there is no clot.

00:56:52FacultyYes, the appendage is very clearly seen; it is free of any clot. Okay. The aortic valve is not grossly thickened, but it is thickened, with restricted opening. Okay, what is that structure? The other white structure you are seeing?

00:57:08UnclearSmall... okay.

00:57:13FacultyYou are planning balloon mitral valvotomy again. Would you like to do a transesophageal echo or not, as she is in sinus rhythm, in this case?

00:57:23CandidateTEE, to rule out clot.

00:57:26Faculty[unclear] is not able to see the image properly. It is mandatory to do a TEE before, except probably in pregnant patients undergoing BMV in sinus rhythm, where you can probably avoid it. Otherwise it is mandatory to do a transesophageal echo to rule out clot. And we are doing it now for the second or third time.

00:57:46CandidateYes, and she had a history of palpitations, and we don't know whether she had paroxysmal AF, especially with this [unclear].

00:57:56FacultyThe small structure, the small white structure... Left, [unclear]. Yes, go ahead. Okay.

00:58:13Apical four-chamber. Yes, go ahead.

00:58:20CandidateApical four-chamber view: LA enlargement and concentric LVH. Mitral valve: there is thickening of the anterior leaflet and restricted posterior leaflet motion. Subvalvular disease is moderate: moderate subvalvular thickening. I would have to see the colour Doppler.

00:58:43FacultyThe LVH is not very gross. Borderline. Yes, okay, go ahead.

00:58:52CandidateSevere... There is increased turbulence in systole in the subvalvular area, and the AR also [unclear]; this is not focused completely.

00:59:05FacultyOkay. Show the Doppler, the mitral Doppler.

00:59:18CandidateContinuous-wave Doppler across the mitral valve: mean gradient of around [unclear].

00:59:23FacultyYou have reported the mitral valve gradient. What important thing is missing? It could be calculated, but it has not been. What is it? V max, V mean, everything is written, but one thing is not written.

00:59:38CandidatePressure half-time.

00:59:42FacultyNo. See, the mitral valve gradient always depends upon the heart rate. You have to mention the heart rate. Okay. Something is written. Okay, 69. Okay, here it is.

01:00:09CandidateSir, the mitral valve gradient is not that high.

01:00:09FacultyYes. What is the orifice area?

01:00:19CandidateThe 2D valve area was not done.

01:00:19FacultyNo, it must have been done.

01:00:23UnclearThe measured view was not that one.

01:00:28FacultyWhat does it say? 0.7. Okay.

01:00:36What is low-flow, low-gradient mitral stenosis?

01:00:39CandidateIn cases like this patient, with a low heart rate, the stenosis is severe, but because of decreased flow the gradient is low, only 7 in this condition. On exercise we can again assess for symptoms, murmur and gradient.

01:00:55FacultyAgreed. There is an entity called low-gradient MS; there are a lot of series on that. Nowadays, when we do BMV in our hospital, the patients are all above 60. The young patients with very pliable valves, that era is over. Now they all have low gradients with a severely reduced 2D valve area.

01:01:22What is the severity of AR?

01:01:22CandidateAR is moderate in this: the jet is occupying less than 50% of the LVOT. To quantify it, I would like to see the pressure half-time and flow reversal.

01:01:41FacultyOkay, they have given you the pressure half-time.

01:01:47Candidate430. It is moderate only; less than 200 is severe.

01:01:51FacultyAround that it is mild only; mild to moderate.

01:01:58Okay, so what is this?

01:02:02CandidateThis is the AS Doppler: around 32. Since it is low flow and the cardiac output is low... 4 metres [unclear].

01:02:08FacultyHow can it be that, sir? How do you know from this tracing that it is not flow-related but organic aortic stenosis?

01:02:17CandidateIt could be due to the AR flow. The shape of the envelope...

01:02:22FacultySo, if it is [unclear]-shaped and peaking in the early part of systole, it is probably not that severe; but if it peaks late [unclear]... Clinically also you will get a slow-rising, late-peaking murmur. So it is like an open envelope and a closed envelope, as we call it.

01:02:55Do you think the AS is severe or not severe in this case?

01:02:59CandidateNot severe. The murmur is grade 4/6, but it is early peaking, so flow could also be contributing, and the mean gradient is only 32 [unclear: '30, 32']. The AR can increase the flow. So it comes under moderate only: less than 40.

01:03:14FacultyOkay, so what is your final diagnosis after all this?

01:03:24There's a question on the group: can he use the pressure half-time for AR when MS is there? Somebody asked on the group: is it valid?

01:03:31UnclearNo, it cannot be used [unclear].

01:03:35FacultyI think it cannot be relied on. Can pressure half-time be relied on for AR severity when MS is there? No, it is difficult. MS is there, so we can't use it; you couldn't rely on that. Also, you can't depend on one parameter. You should not decide on a single parameter.

01:03:55Okay, so what is the final diagnosis? I think our time is going.

01:03:55CandidateSevere MS, moderate AS, moderate AR, normal LV function, in sinus rhythm, with moderate pulmonary venous hypertension.

01:04:10FacultyOkay, what will you do for this patient?

01:04:10CandidateI would consider BMV for her symptoms, but there is a risk that the [unclear] can become significant after BMV. We should reassess the patient.

01:04:26FacultyOtherwise what will you do? If you are not considering BMV, what is the other option?

01:04:34CandidateDVR, sir.

01:04:34FacultyWhat is the mortality of DVR?

01:04:39CandidateAround 9 to 10%.

01:04:39FacultyOkay. What is the longevity of a patient who is coming for DVR? I don't know: 50 years, this socio-economic background, 10 years, 20 years? More than 60% mortality after DVR; high mortality on follow-up.

01:05:02On the LA pressure tracing, when you see it before BMV: if you see a prominent c wave, just as you see on the right side, it means your balloon [unclear]. The presence of the c wave tells you that the descent of the base of the mitral valve is quite good; hence it will open well. That's what you feel. There are other parameters also: DE amplitude more than 18 by M-mode, and many other parameters.

01:05:31Okay, this patient is going home after a BMV; you have done a successful BMV. What is a successful BMV?

01:05:36CandidateAfter BMV the valve area should increase by 50%. Valve area 0.7 and a gradient of [unclear]... An area increase of 50%, or more than 1.5 cm², without any increase in mitral regurgitation of more than 2 grades.

01:05:53FacultyOkay, and this patient is going home after BMV. What is your prescription?

01:06:00CandidateFor heart rate, a beta-blocker after BMV.

01:06:00FacultyBeta-blocker [unclear]. Second option: there are other drugs given for rate control in mitral stenosis other than beta-blockers.

01:06:08CandidateCalcium channel blocker.

01:06:11FacultyCalcium channel blocker. Any other drug tried in India? There are so many Indian studies.

01:06:15CandidateIvabradine.

01:06:18FacultyIvabradine. There are two or three Indian series; all of you should know them.

01:06:23Okay, beta-blocker. Then, not for this case, but I will just ask you for aortic stenosis: what is the value of the dimensionless index in the assessment of severity?

01:06:31Candidate0.25. If it is less than 0.25, it is severe AS.

01:06:35FacultyOf course, it will not be that here.

01:06:40Okay, what are the drugs, you said?

01:06:40CandidateBeta-blocker; then, since she has pulmonary venous hypertension, I would prefer diuretics also; then, if sinus rhythm... if AF, then [unclear].

01:06:51FacultyNo, these two... We don't give prophylaxis?

01:06:55CandidateProphylaxis, considered lifelong.

01:06:59FacultyWhich is the best prophylaxis: intramuscular, or is oral better? What is the event rate? How much will you give?

01:07:08CandidateLess than 27 kg...

01:07:08FacultyNo, she is an adult. You said BMI 24.

01:07:12Candidate1.2 million units every third week, sir; every 21 days.

01:07:16FacultyOkay. Suppose it is not available; then the next best? It is not available, and in Kerala nobody is giving that. Then oral penicillin. What are the two preparations available, and which is better?

01:07:34CandidatePenicillin V and penicillin G. Penicillin V is preferred: 250 mg BD [unclear: '500 mg BD'].

01:07:40Unclear[unclear] for chronic prophylaxis.

01:07:45Candidate400 mg BD, sir.

01:07:45Faculty400 mg BD is penicillin [unclear]... TID? No, that is why it is called BD. Then why are you giving it BD? The name itself is printed [unclear]. Then why are you giving it BD?

01:08:01CandidateSir, you said you give 400 mg BD for prophylaxis; the other is for treatment.

01:08:04FacultyTreatment, okay. If that is not available, then?

01:08:09CandidateAzithromycin, erythromycin.

01:08:09FacultyNo, penicillin: there are two preparations. Penicillin G can be given. What is the dose? Which is available?

01:08:18Unclear[unclear brand name] is the one which is available. Now it is called Pen[unclear], 250 BD.

01:08:24FacultyPenicillin is not available, or she is allergic to penicillin. What else?

01:08:31CandidateNext, azithromycin is not [unclear]. Sulfadiazine is recommended, [unclear: possibly 'one gram'].

01:08:42FacultyOkay, I will... thank you.

01:08:45But what are the two or three recent trials in RF secondary prophylaxis that you named?

01:08:50CandidateRecently, in 2022, the GOAL trial compared prophylaxis in subclinical carditis. The recurrence rate of rheumatic fever was 8% in those who did not receive any prophylaxis and 0.8% in those who received it. In both arms the regression was the same; it didn't change. The regression was the same, but the recurrence was 8% versus 0.8%. The [unclear] trial compared IM with oral, sir; that study has yet to be published.

01:09:22FacultyPublished. And what's the alternative hypothesis of rheumatic fever? Have you read that?

01:09:30CandidateThe alternative hypothesis: besides molecular mimicry, the older alternative hypothesis is that it is inflammatory, not just an autoimmune reaction. There is an article which [unclear].

01:09:43FacultyWhat is the newer advance in chronic prophylaxis?

01:09:47CandidateVaccines...

01:09:47FacultyVaccines are being developed, but not that: penicillin prophylaxis. What is depot penicillin?

01:09:52CandidateThere are some penicillin preparations being tried, once in 3 months; you can give one for up to 6 months. It is given as a depot injection.

01:10:02FacultyWhat is the role of colchicine?

01:10:09CandidateIf rheumatic pericardial involvement is there, then you can...

01:10:09FacultyNo, in rheumatic heart disease. Any study done from any centre? An Indian centre?

01:10:21CandidateA trial from GB Pant [unclear]; it came in JACC last year, in all RHD.

01:10:28FacultyYou said azithromycin. Any RCTs done on azithromycin in rheumatic fever?

01:10:36CandidateNot that I know.

01:10:36FacultyWe have done an RCT on azithromycin once weekly, but it was a failure. It was a negative trial; we have published it in the Indian Heart Journal. [unclear] two patients out of [unclear] had recurrence of throat infection, not rheumatic fever. That was a failure, right?

01:10:54Okay, but your assessment: I think he has said it very well. It is a simple case, no doubt, but in a simple case people always falter, and it is a little difficult in the exam. But you have answered very well. Very good. Your [unclear] also is very good; very good and confident. I think this is the way you should present. Good presentation. Come on, give him a big hand.

01:11:21CandidateThank you, sir.

01:11:21FacultyThanks.

01:11:21CandidateThank you, sir. I thank all the teachers for this.

01:11:26FacultyI am really sorry, sir, we are going to make you talk again. Can you just continue the OSCE? Sorry for this. And all of you will have to answer now, so that he talks less. We will fix the laptop. The next presenter will be presenting after the tea break; he is here. The presenter of the last case is also around. She is here, right? She is there.

01:12:21They will not get a break, sir, but they'll talk more this time. I'm really sorry for this.

00:00:03FacultyBack. That's possible; there could have been a migration. We'll start from the middle; that's safer.

00:01:32Is the chest X-ray showing? Okay. That mic has a light, so I can see in the dark also.

00:01:49CandidateNon-homogeneous opacities in the right upper zone, the right lower zone and the left mid zone. There is straightening of the left heart border.

00:02:16FacultySo obviously there are significant shadows on the right side, not on the left side.

00:02:20CandidateYes, sir.

00:02:20FacultyOkay, so what is it? It is a rare thing, but it can happen. You have just seen one X-ray with bilateral shadows, the patient we just discussed. This patient has right more than left; it is a unilateral pulmonary oedema. So what is the commonest condition?

00:02:57CandidatePulmonary vein stenosis.

00:02:57FacultyOkay. But the most common condition is acute severe MR with an eccentric jet which goes to the pulmonary veins of one side, producing pulmonary oedema mostly on the right side. That is the most common condition. There are other conditions you can read about, where the oedema is in one abnormal lung or where one lung is spared. So if there is right-sided oedema, think of acute MR. That is the one we have to think of.

00:03:35These two are from the same patient, taken within a few seconds of each other. Go on describing.

00:03:44CandidateAngiogram showing a proximal RCA occlusion.

00:03:44FacultyVery good. Are you seeing something here? And what do you see in here?

00:04:02CandidateThere is staining in the second angiogram.

00:04:02FacultyOkay, so what does it indicate? Do you see any particular appearance here?

00:04:18CandidateChronic. CTO.

00:04:21FacultyCTO? Why should it stain? Staining indicates what? Staining indicates a recent thrombus, where the contrast gets in and stains it. So what is this appearance called, where the contrast goes to both sides of the thrombus? What is that sign called?

00:04:50The faculty are answering, but this is called the meniscus sign. Okay, meniscus sign. Can you see it if you look closely? There is a thrombus, and on both sides of the thrombus there is contrast. So this is indicative of an acute occlusion of a coronary artery. You can see that the stain is there at the point where the meniscus is. So this is the meniscus; you must have learned in physics what a meniscus is. This is different from a chronic occlusion, where mostly it will be a tapering type of stenosis.

00:05:29Can the next person read this? The OCT.

00:05:37CandidateCalcification.

00:05:45FacultySame patient. This is the same patient's OCT. At this point, you see what is there inside? This is the same patient after the angioplasty, one of our patients done recently. See that; what is that? Is it a red thrombus or a white thrombus? Which one produces a shadow? Okay. Next.

00:06:17Who is having the mic? Sorry, somehow it is not playing continuously.

00:06:33CandidateSir, parasternal long-axis view showing a hypermobile structure in the atrium, going into the inlet and coming back, going into the LV and then back.

00:06:58FacultyIt is not going into the LV, no? Repeat. Where is it getting obstructed?

00:07:13CandidateIt is obstructing the mitral valve.

00:07:17FacultySo what is that called?

00:07:22CandidateBall-valve thrombus.

00:07:22FacultyBall-valve thrombus, okay. So what is the most common condition? But what about the mitral valve here; what is the aetiology?

00:07:39CandidateRheumatic, sir.

00:07:39FacultyRheumatic? You have seen rheumatic valves; is it like this? There is no rheumatic involvement here. The mitral valve looks okay; it is opening well. The mitral leaflet separation is around 20 millimetres, and the atrium is dilated. Most likely it is atrial fibrillation. So this is a ball-valve thrombus which is producing obstruction. What will be the symptom in this patient?

00:08:04CandidatePostural variation of dyspnoea, due to obstruction of the mitral valve.

00:08:04FacultyOkay. Usually the most common association of a ball-valve thrombus is severe mitral stenosis with thrombus formation. But here the mitral valve opens well, and most likely it is atrial fibrillation. I don't know exactly what it is, but it is a ball-valve thrombus. All these slides were made with AI [unclear].

00:08:41Next. Can the next person have the mic? Chest X-ray PA view. Where is the person? Okay.

00:09:02No, start by speaking about the bones, the cardiac size, the situs. If you see all those things, you can go on describing. If there is silence, that will prompt the examiner to ask more questions. You go on describing the normal things so that he stays engaged.

00:09:26CandidateDilated RPA, sir.

00:09:29FacultyOkay. Any prosthetic material you are seeing there?

00:09:32CandidateYes, sir. Sternal sutures are there.

00:09:38FacultySternal sutures are there; okay, great. It is a postoperative patient. What else are you seeing here?

00:09:49CandidateThis is probably in the pulmonary position.

00:09:52FacultyPulmonary position; what is there? What all things can be there? It is a pulmonary valve; the valve had some problem. What type of valve is it? Is it a prosthetic, a bioprosthetic?

00:10:22CandidateBioprosthetic.

00:10:22FacultyVery good. So it is a pulmonary valve replacement with a bioprosthetic valve. The reasons are different. So how will you identify that this is the pulmonary position? In the previous case we discussed the line; that time when I drew the line, it was not coming accurately, but you can see that this is the line, in the AP view and the lateral view. In the AP view, draw a line from the cardiophrenic angle to just below the pulmonary bay. You can see the [unclear] valves will be above that, and the atrioventricular valves will be below that. In the lateral view, you draw the line from the anterior-most point [unclear] to the carina. Then you will get the same representation. These were created using AI.

00:11:38Who is having the mic? Go ahead.

00:11:38CandidateChest X-ray PA view showing an ICD with—

00:11:51FacultyWhy do you say ICD? How will you differentiate between an ICD lead and a pacing lead, the coils? Anybody else? We saw an ICD lead in the morning, no? Okay, this is a pacemaker lead. Where is it pacing? Many of you have done or assisted pacemaker implants, no? Is it in a normal position or is it abnormal?

00:12:38CandidateNormal position.

00:12:38FacultyWhat else are you seeing? There are two dots seen here, and something coming below and going like this. What is that? That is an epicardial pacemaker which was put earlier; the patient might have had a congenital heart disease, and at that time an epicardial pacemaker was put, and now the patient has grown up. An epicardial pacemaker is done when the child is very small, when you cannot put a transvenous lead for many reasons. So this must be an epicardial lead placed over the RV.

00:13:17Okay, so are the thresholds the same, endocardial versus epicardial? There are some mild differences. For an endocardial lead, an acceptable implant threshold is less than 1.5 volts; for epicardial we usually accept slightly higher, 1.5 to 2. The impedance is almost the same. The battery drain is more with epicardial leads, because we need a higher output. All those points you should know. Okay, next one.

00:13:51Who is having the mic? Go on. If somebody knows it, don't give the clue.

00:14:14CandidateCoarctation of the aorta.

00:14:14FacultyVery good. But you should not go and tell the diagnosis straight away, because you may be wrong. So how will you describe this X-ray? When you see a normal-looking X-ray without much of a problem, always think of coarctation. Okay, so what are the signs you see here?

00:14:35CandidateFigure-of-3 sign and rib notching.

00:14:35FacultyYes, where will you see it? I discussed this in the morning case, no? You should know why you see it in ribs 3 to 8, what the situations are where you get unilateral rib notching, and why it is seen in the upper ribs. I think that candidate was discussing all those things correctly. So these are the figure-of-3 sign and the E sign. The E sign is seen on the barium swallow, and the figure-of-3 sign is what you have seen here: the two bulges of the pre-stenotic dilatation and the post-stenotic dilatation, with the coarctation segment between. Rib notching of ribs 3 to 8 and all we have already discussed.

00:15:25Who is having the mic? Go on describing.

00:15:30CandidateThis is an angiogram with a pigtail in the left ventricle.

00:15:30FacultyOkay, which view is it?

00:15:36CandidateStandard RAO view. Contrast is injected and the LV is filled, and it is ejected into the aorta.

00:15:51FacultyAgreed. But you have to mention the pathology also, in between. Don't distract the examiner with so many normal findings; in between, you have to say the pathology.

00:16:12CandidateThere is a prosthetic ring.

00:16:12FacultyVery good. In which position?

00:16:19CandidateMitral position.

00:16:19FacultyOkay, agreed. What was it done for? There is a clue in the angiogram itself. If you know where I am coming from, you will give the answer.

00:16:42AudienceChitra valve?

00:16:46FacultyNo, not a Chitra valve. It is not a Chitra valve; it is a mechanical valve. No, it is not a ring. We are coming out with a ring, but that will take one more year.

00:17:03What is happening to the LV? Is it a normal LV or something abnormal? What is happening to the LV apex? The LV apex is obliterated, no? It is like a clenched-fist appearance. So it is EMF.

00:17:21But what is the ring for, then? It is a recurrence of EMF. Initially a repair was done: an LV endocardiectomy was done and a mitral ring was put. Subsequently the patient again developed symptoms and had a recurrence of EMF, which is rare, but it has happened. And what is the other catheter? There is another catheter there, no? And EMF is common in Kerala.

00:17:53There is one more finding; if you state that finding, you will get an extra mark. If you just say MR is there, you will not get any mark, probably a negative one. But what type of MR is it? MR usually happens in systole, but here it is diastolic. Diastolic MR happens when the LV end-diastolic pressure is high, but probably it can also happen due to the ectopics. So it is diastolic MR, and the other catheter is in the PA; from the RV it has gone to the PA. So it is endomyocardial fibrosis, which you can identify by the obliterated LV apex and the post-repair situation.

00:18:47AudienceTapioca.

00:18:50FacultyTapioca; we don't eat tapioca now. See, I will tell you the reason, to wake you up. Lord Parashurama went to Kerala, threw his axe into the sea, the sea receded and Kerala was born; God's own country, it is called. The beaches of Kerala have thorium and cerium, and this gets deposited in the heart. This was found at the Sri Chitra Institute, and they didn't realise it until the Germans started taking the sand from the Kerala beaches. I think Cochin now has a BARC centre, the Bhabha Atomic Research Centre; that sand is full of radioactive material. Am I correct? Thorium is actually the future of India. A lot of thorium is there; we don't have uranium resources, so we are developing thorium-based atomic energy, and I think our future will be on thorium, which is very much abundant in the Kerala sand.

00:19:52That is one of the propositions for the development of endomyocardial fibrosis in the particular area where the thorium sand is, the Chavara area, etcetera. And there are other theories also: the tapioca theory; cassava and banana consumption was proposed; protein allergy and malnutrition were proposed. And there is a belt in the tropical region. In Mozambique it is very common: when they screened the population, they could identify EMF in around 20% of the population. That is one of the largest series of EMF seen. But there is a change in the pattern of EMF. There are a lot of studies on EMF, probably from our institution; go through them. Another place where EMF is found is a place in Jammu and Kashmir [unclear]; it is a pocket. That is also because of thorium, and because of the wars, you know, all the radioactive material. Even in the Mahabharata, I think, they used radioactive material. That's okay.

00:20:54This is one investigation done, and based on that, some therapeutic intervention is done. What is that? One test is done, a haemodynamic evaluation is being done on this screen, and subsequently a procedure is done. What is being done in both? Who is having the mic? It is simple only. First identify this. What is this?

00:21:34CandidateDevice closure.

00:21:34FacultyDevice closure of what? It is a PDA device closure. You can see this is done across the tracheal shadow; this is an ADO I device. And what is being done before that?

00:21:54CandidateBalloon sizing.

00:21:54FacultyNot balloon sizing. Balloon sizing we don't do now; balloon sizing is not done even for PFOs or ASDs anymore. This is done because the patient had PH: we occluded the PDA and saw how much drop in the pulmonary artery pressure there is. This is a balloon occlusion test for assessing the reversibility of pulmonary hypertension, how much of it is contributed by the shunt. So this is a balloon occlusion test for assessing the operability of a PDA.

00:22:34We will give a little time for this one. Who is having the mic?

00:22:34CandidateYes, sir.

00:22:40FacultyGo on assessing the saturations and the pressures. Don't give clues; you can have your own assessment. And if somebody is willing to answer, I will give the mic to him. How will you go about it, given these saturations? Is the SVC saturation normal? What are the normal venous saturations? Very simple: 65 to 75 is the normal venous saturation, and 95 to 100 is the left-sided saturation. These should be very simple things: 65 to 75, and 95 to 100. So this is between 65 and 75; 72 in the SVC, and the SVC and RA are normal. Okay, then what is happening in the RV?

00:23:31CandidateRV step-up. There is an RV step-up, 98.

00:23:36FacultyThen what is happening in the PA?

00:23:48CandidateStep-down.

00:23:51FacultyOkay. Is the PA corresponding to the SVC and RA? Okay, come back to the LA saturation.

00:24:10CandidateThe LA saturation is normal.

00:24:14LA, RV, aorta... CTGA.

00:24:23FacultyThe LA is connected to what? The LV saturation is normal, the LA saturation is normal, and the SVC, IVC and RA saturations are normal. So then what has happened?

00:24:31CandidateCTGA, sir.

00:24:31FacultyNo, you describe what has happened. The LA is connected to what?

00:24:36CandidateThe LA is connected to the RV, and the aorta is connected to the RV, and the LV is connected to the PA.

00:24:53FacultyAnd what about the pressures?

00:24:58CandidateRV and aortic pressures are the same, with the diastolic step-up [unclear] in the PA.

00:25:13FacultySo is it a TGA?

00:25:19CandidateCorrected TGA, sir.

00:25:19FacultyYes, corrected TGA. Correct. Okay, then I will go to the next one.

00:25:33I think some of you must have assisted in this procedure, since it is still done in some hospitals; this device is available. What intervention is being done? Where is the position of the valve, which we just discussed in the last case? What is this balloon called? It was developed by an Indian; we are all proud of it.

00:26:05This is the JOMIVA balloon, the Joseph mitral valvotomy balloon, developed by Dr. George Joseph from CMC Vellore. This is an over-the-wire balloon. You can see a sheath here; the sheath comes up to probably the IVC-RA junction, and the balloon is tracked over the wire. You can see the wire, and this is the balloon, which is dilated. So this is called the JOMIVA balloon, an over-the-wire balloon.