Approach to a case of RHD

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Approach to a case of RHD

27 Oct, 1 PM

welcome about our guests our speaker for tonight is Dr Kamal Sharma he is the chief uh Interventional cardiologist at Sal hospitals with over 25 years of experience he has an expertise in the field of currently angioplasty stenting valvoplasty pacemakers and pediatric interventions like PDA ASV closures Etc he also has numerous Publications to his name like clinical Cardiology ECG simplified and clinical medicine which are textbooks for fellows in training for Cardiology and MD Mbps students also has done the world's first uh wiggle now stimulation device implant and has also discovered the Winking coronary sign of VSR on angiography which is also commonly known as the Kamal Sharma sign of BSR uh really honored to have you sir once again with us on Netflix um so getting started uh on today's lecture um so this is the presentation and the flows all yours thank you good evening so today we are going to discuss how do you approach a case who's got a multivalic disease of course now you can do an echocardiogram and you know you can do evaluation in terms of a cardiologist reference and things can become pretty easy but then clinical examination not echocardiography firstly may not be available easily quickly at the right moment at the moment that you want to diagnosis and secondly it may also not be a very cost effective tool in lot of rural territories or where the cost of echocardiography is exorbitant and it's not covered so what we all need to know is go back to our basics of History examination and clinical findings to come to the diagnosis as which is the dominant lesion what is bothering the patient is the aortic viral disease or a mitral valve disease whether it's a stenotic lesion or a regurgitant lesion and based on that you can actually think of the therapies I think therapies I will leave open to question answer session because what our idea for today was to how do you approach clinically and try to diagnose and reach to a diagnosis of rheumatic heart disease or a multivalial disease and which of them is a dominant lesion now we know that a lot of common symptoms that Cardiology patients do come across and come present with so common cause of chest pain when you're looking at of course you must always think of the other causes like ischemic heart disease or mitral valve prolapse or even some severe cases it may be dissection but remember all not not all chest pains are cardiac pains they're pains because of respiratory etiology like pneumonia call them the embolism pneumothotics or local causes like rib fracture teeth syndrome or even peptic ulcer pancreatitis cholecystitis all can radiate and mimic a chest pain of cardiac geology dyspnea though it's often a presenting specific finding of cardio respiratory etiology you have non-cardic non-respiratory causes of dyspnea as well for example a patient diabetic ketoacidosis or a needle failure or a patient with respiratory paralysis can all present with the same in cardiac disorders however ischemic heart disease and LV dysfunction or even valular heart disease like Nitro stenosis or mitral prolapse can be the presenting cause same way with hemoptysis a patient may not always come with hemoptysis in pulmonary tuberculosis it may be a mital stenosis or it can be a pulmonary congestion in pink frothy's putum from LB dysfunction or pulmonary apoplexy as they call from pulmonary hypertension and since the you should be aware that these symptoms can mimic and present with cardio maybe a manifestation of their cardiovascular disorder a lot of times you may come across a patient who's come with breathlessness and you may be confused whether you're dealing with a case of respiratory disease or a cardiovascular disease and very simple in symptomatology Wise to ask is what was the relationship between the cough and the breathlessness if breathlessness has preceded cough it's very likely that it's cardiac because the first thing that will happen will be the VQ mismatch because of pulmonary interstitial edema and this edema will impair the development of adequate oxygenation of the tissues and hence patient will be posed breathless this later on will be preceded and for followed by cough because of the then later on ulab alveolar edema while a irritant cough in bronchial spasm would later on trigger a bronchospasm and ends usually in bronchial asthma or respiratory etiology it's the cough that precedes the breathlessness the quality of scrutinum presents of classical peroxis neurological distance palpitation would also help you in distinguishing the same game past history is a very important feature that's why you need to ask but the patient has got ischemic heart disease or valvular heart disease or hypertension diabetes or migratory polyarthritis as a residual etiology in the past which may be responsible for the symptoms and manifestation that the patient may be having when a patient who's known case of previously stable disease like valvular heart disease if he comes with a sudden deterioration the possibility allergies need to also we looked at very often in a patient or mitral stenosis who was previously stable a worsening or certain development of failure may be triggered by a development of new episode of atrial fibrillation also any infection or rheumatic fever or infective endocarditis may be responsible for worsening of the lesion and this can lead to worsening of the symptoms as well very often in mitral stenosis pregnancy itself can worsen the symptomatology because of the additional volume of the fetal circulation now coming on to the cardiac cardio in the cardiac output and the narrowed fixed orifice is now not ready to compensate or is not adequate enough for allowing the blood from the fetal as well as maternal to pass through that narrowed orifice which was barely able to compensate in the maintain stability in a non-pregnant women now will become stable unstable and the same is case with anemia when there is a hyper volume state hyperdynamic state more amount of blood is passing through and oxygenation is also impaired because of the low oxygen delivery by hemoglobin reduction can also lead to a sudden worsening of symptoms before you understand what we are dealing with in a patient who is presenting with a while will a heart disease you should know what are the normal hemodynamic parameters in various uh cardiac Chambers so normally the right atrial pressures are not exceeding the range of 5 they're usually in the range of one to one to five millimeters of mercury RV pressures are below 25 the mean pressure more than 20 is now called as pulmonary hypertension and wedge pressure is always less than 12 millimeters of mercury also in terms of wood units if you were to think remember one good unit can be converted into glass uh in the nine seconds per centimeter to the power minus 5 by multiplying with a factor of eighty eight zero pulmonary vascular resistance is less than one and systemic vascular resistance is never more than 20. so 10 to 20 wood units or 700 to 116 1600 nine second per centimeter to the power five is the classical normal value of these parameters now what happens in mitral stenosis there is narrowing of the mitral valve so blood is now accumulated behind the mitral valve into the LA so the pressure that rises is the LA pressure and the pulmonary back transmission through the pulmonary veins which don't have a valvular uh valves to prevent the backflow to coming from the language into the pulmonary veins from the LA would give rise to rise in the LA pressure as well as pulmonary capillary wedge pressure while the because the flow is reduced to the LV the end diastolic LV pressures are low this can trigger basically reactivity in the pulmonary vascular bed and Rise the pulmonary arterial hypertension this also will then be reflected into the right ventricle and endoscolic pressure and rise in the array pressure in the long run while in chronic Mr because of there is extra blood so blood is contracted partially into the systemic circulation and partially because of the leakage into the LA this additional blood will now have from the next cycle coming from the both the next cycle that comes in and also the regurgitated blood and hence there is more amount of volume of blood that's coming back to the mitral valve into the LV in the next cycle so the LV and diastolic pressure can either be raised in the later stage when the heart starts failing and the in the chronic state the LA will remain dilated try to accommodate as much of blood that it can take from the regurgitation and hence the wedge pressure would rise much later but it is often reflected as a rise in B wave as compared to a wave which corresponds to the ventricular cystole so when there are two waves in the Atria a wave and the V wave the V is more than a because of the regurgitation pulmonary hypertension is very late in mitral regurgitation which is chronic because of the compliant delay in aortic stenosis the price is in the pressures of the LV the failing ventricle only will have arising in the volumes of the chamber so the peer pressure the same way as you go away from the pulmonary arteries are structures which is you're going now from mitral mitral to aortic the pulmonary hypertension will be very less likely to develop it is classically characterized because of the obstruction a narrow pulse pressure and a raised LV systolic pressure The Chronic regurgitation however will give rise to rise in the LV and diastolic pressure because blood is coming back because of the leakage and also from the subsequent cycle again pulmonary hypertension is rare and what is characterized is a wide pulse pressure now how do you determine what valuular disease you are dealing with so there are simple nine rules or nine methods of evaluation to tell you which is the dominant lesion because a lot of patients can have more than one disease now what is giving them trouble is what you need to identify and to identify this you assess a patient for you need to assess right from the history as I said but these nine features will tell you what you're dealing with apart from chest x-ray ECG or Echo these are all clinical findings that I'm talking about not even talking about investigations because the list of Investigations go can go right up to cardiac MRI and CT and nuclear majoring and uh cardiac path you can go on and on but clinically you need to look first whether it's a which is the dominant symptom remember in aortic valve disease the symptom Triad is angina dyspnea and syncope while mitral valve because of these stenosis will come with dyspnea or a left pulmonary congestion so most of these patients will have either palpitation if they have atrial fibrillation or between them again between stenosis and regurgitation because of stenosis if it's mitral they come with dyspnea and congestion in the back pressure so dyspnea pnd palpitation Etc while regurgitate and lesion whether aortic or mitral will present with low cardiac output because some lot of blood is actually going back to the LV or to the LA and fatigue and tiredness is very often and also pre-cordial activity which means patient will complain of palpitation because the blood that is coming now to The ventricle is twofolds one that is from the next cycle and second what it had regurgitated from the previous cycle so aortic regurgitation blood or mital regulation blood will also join in the next subsequent cycle blood flow and more amount of volume is now kicking in into the left ventricle which because of the Frank Sterling law will now get stretched further and will kick more forcefully and hence these patients will complain of increased forceful precordial activity sometimes people can confuse it with palpitation where actually it is often reported as one is the rate other is force of course the duration of illness would also tell you how often these patients are presenting because natural survival in a patient who's symptomatic of certain disorder may be lesser as compared to the other so if the patient has been symptomatic say for a decade you know that certain disorders are ruled out pulse characteristic narrow pulse white balls water hammer Etc what is the blood pressure how is the jvp what is pulmonary artery hypertension how is the Apex speed What is the characteristic of first heart sound and what is the characteristic of murmur would also help you to determine the dominant lesion so coming to each of them one by one mitral stenosis the symptoms are dyspnea of palpitation and palpitation is either because of atrial fibrillation or sinus tachycardia sometimes as the pulmonary hypertension develops they will present you with right heart failure which is edema Rays jvp ascitis pedial edema Etc mitral regurgitation as I said will present with fatigue because of some amount of blood going to the LA ins in the cardiac cycle and not all blood going to the systemic circulation and hence the muscles are deprived because whatever amount of blood is now going into the circulation will be first given to the vital organs so brain takes it kidneys take it other important structures take it so the structures that are deprived of the reduced output that is happening but after subtracting the rigidity and blood will be the muscles and the intestine so muscles because they get less amount of blood will be perceived as fatigue aortic stenosis as I said this is Brunswick's Triad as they called angina syncope and failure while aortic regurgitation there is never syncope the symptoms remain in China and failure or they also can present in a regurgitant lesion with palpitation so with these symptoms we know that how often these are likely to live in a mitral stenosis 10-year mortality for a functional class 4 is 100 but a lot of patients who are class one or two means mild or low asymptomatic patient will love up to 10 years in majority of the cases and hence a patient of valuable heart disease if he has survived 10 years it's very likely with symptoms that he's suffering from mitral stenosis while this has been analyzed in other series also or less in series or Rapaport series again 10-year survival is around 60 to 70 percent while mitral regurgitation a if it's mild it's very good prognosis but a severe symptomatic Mr if the patient has symptoms like in a flail mitral leaflet 10 year survival is 50 57 but if the patient is having valvular heart disease of rheumatic etiology and he's having dyspnea five-year survival is less than 30 means a patient of Mr with dyspnea is very unlikely to live beyond five years same has been analyzed in aortic stenosis and aortic regurgitation Eva patient comes with angina and he's having aortic stenosis median survival is five years syncope it is three years and failure is two years while aortic regurgitation enjoyed as four years in Failure is two years so which means practically a valvular heart disease surviving Beyond five seven or ten years is very very likely to be suffering from mitral stenosis and not any other lesion so aortic stenosis in Brunswick series as I said the median survival was five three and two though lot of it depends on the what amount of gradient is there for practical purposes for you all guys remember this as a simple basic differentiating rule in chronic AR again lot of patients will become symptomatic every year a lot of them will proceed to Velvet dysfunction and average mortality is 0.9 so with mortality rates in patients who are asymptomatic is low but if a patient who comes and sees you is very likely he's symptomatic so for a patient who's symptomatic annual mortality in ARA is almost more than 10 percent every year again uh there is something called as paradoxical dyspnea relief so if a patient says this is very classical of aortic regurgitation these patients will feel better because when they exert their heart rate picks up because the heart rate picks up the diastole shortens and the diastole shortens so the amount of time for the blood to leak is gone down in aortic regurgitation because the leaking neurotic regurgitation is happening in diastole so if there is tachycardia the last three shortens dicely shortens a duration of the severity of air decreases and hence these patients will feel better on exertion so this is known as paradoxical dyspnea so patient comes and I feel better on exertion and ease of valuable or heart disease you are probably dealing with the aortic regurgitation so a lot of times actually you can see what symptoms they have and based on that what you can predict on chest x-ray a patient who's symptomatic on routine activity likely which pressure is 12 to 8 and the first finding on x-ray would be upper lobe redistribution which is also called as antler sign a patient who's class 3 which is exertion symptoms on less than routine activity these patients would come with interstitial edema this is also true for patients who present with a paroxysmological dyspnea and class 4 patients actually would be bad swinging appearance so a lot of times you need to know based on these whether the patient is having rheumatic heart disease so there is some rhd criteria so definite rhd criteria and are have been defined and these are that if the patient has got Mr on Echo with two morphologic mitral valve features of rhd or if there is a gradient more than four on an echo or any individual less than 20 with borderline disease of both aortic and mitral while disease or less than 35 who's got AR and at least two features of rhd of my aortic valve in these patients you should suspect it to be of rheumatic etiology now remember in India these patients are much younger usually rheumatic heart in India has got more than well well there'll be multiple episodes of rheumatic fever so there is a rapid progression with a lot of complications like atrial fibrillation embolism heart failure Etc and there are a lot of problems with profile access you need to give them penicillin every uh 21 days a lot of patients may not take it a lot of centers may not be able to give it there might be a fear of an injection Etc so these are the problems in India and in India we have known that the isolated mitral oil involvement is also possible in 70 to 75 percent while both the valves are involved in 20-25 percent as a disease so in an acute phase you may have both valves involved but one of the valve may not have any residual disease left behind and ultimately only mitral valve will be diseased so isolated aortic valve however is less occurring only in five to eight percent now once you've known this history now you will go ahead and check the pills of the patient in atrial fibrillation if it is present very likely it's a mitral valve disease because aortic pressures are not getting transmitted to LA and mitral stenosis or regurgitation will cause la dilatation which will be responsible for atrial fibrillation mitral regurgitation because of high amount of blood actually being kicked out rapidly in a lot of blood actually dissipating into the LA lot of initial force will have a rapid fall and that is called as collapsing pulse aortic stenosis the pulse that is described is inacrotic or pulses parvatic Tardis low Rising late picking pulse while aortic regurgitation it is a water hammer pulse rapidly collapsing pulse so in aortic stenosis usually if you can get a normal looking pulse think of some other Associated disorders like Associated aortic regurgitation or some anemia-like disorder or hypertension Etc we all know there are a lot of signs these are 30 signs that will be named after the rapid uh distal runoff in aortic regurgitation from landolphia Men's Backus bosolos minervies mullers corrigans looks locomotor corrigans palm trees uh pennies Queen Keys Hills that we classically read in our mbbs so there are a lot of signs basically all of them uh the names may not be so important in clinical practice what matters is that the blood flow is having high amount of output and because of peripheral vasodilatation the blood is dissipating very rapidly into the peripheries so all these signs tell you a high output state with low systemic vascular resistance basically there is say blood flow coming into the capillaries into the peripheral vessels high amount of flow passing through a vessel and dissipating very rapidly into the peripheries all these signs are basically manifestation of that so you hear a duruzia's murmur you hear a murmur over the femoral artery when you compress because the flow is so high in the artery though it's of a normal caliper a lot of blood is passing through a normal caliber giving rise to a turbulence and that's why you hear a murmur same way he'll sign upper limit lower limb blood pressure difference again there is hydrostatic column giving rise to a difference but the high output is giving rise to a higher pressure and then it's dissipating to the periphery so those signs do tell us that what you're dealing with is a high output high volume state and these signs help you to distinguish aortic regurgitation another simple thing is measuring blood pressure in mitral stenosis the systolic pressure may be slightly blunted because of atrial kick is not so contributing because of the narrow mitral valve so blood that is coming through the normal cycle is able to go but systolic important of the Atria is not contributing much and hence the systolic pressure is going to be slightly low diastolic remains normal so pulse pressure becomes slightly narrow while mitral regurgitation systolic may be normal or raised but because of collapsing nature the blood going back into the La by the LV contraction the diastolic pressure will be low in aortic stenosis pulse pressure will be narrow more severe to the stenosis more narrow is the pressure and in aortic regurgitation we know that systolic is very high diastolic is very low so the pulse pressure is very high when the right heart is involved which means pulmonary hypertension doubles which is more likely in patient of mitral stenosis you will have jvp elevated remember in 30 percent of Indians even tricuspid valve can be diseased and that's why you can get a giant v wave the RV Contracting into the array with the tricuspid regurgitation that pulse waves are transmitted to the jvp and this is a positive giant v wave seen in the neck when it is called with obliteration of the excess this is called line CC sign and so you get obliteration of existence and prominent y with the fusion and that's called as Len CC sign this is how you look at the jvp you lean across the patient flash your light tangential to the skin and see the neck movements of the next skin of the neck where the jvp is actually collapsing that's where you while X and Y descent and pulling when there is a forceful contraction so this is how the jvp is looked at and this wood you would find early pulmonary hypertension would as I said because the chambers that is most likely to be Associated or closer to the pulmonary circulation is going to be mitral valve which is in stenosis while terminal pulmonary hypertension can later on develop when the LA is not able to take any more blood from the regurgitation that the pressure will transmit into the pulmonary vasculature will happen in chronic Mr so pulmonary arterial hypertension if it is bound it practically in an isolated aortic valve is rules out mitral valve disease pulmonary hypertension in aortic stenosis means there is some hidden or some amount of mitral stenosis always present other way around if you have pulmonary hypertension you have mitral stenosis also and what are the findings of pulmonary hypertension you will get rust away with parasternal heat loud P2 and TR marmar PR murmur of grams tail but the etiology on looking at the second art sound can also help you in differentiating what kind of Mr you are dealing with so you may have Rheumatic Mr where the a2p2 will be widespread a narrow splitting in MVP and reverse split in lb dysfunction this is how you demonstrate parasternal if when you put your hand on the patient's chest the hand will be lifted up because of the RV contraction the force being so high and this is a sign of pulmonary hypertension you can look at palpate the dance click shock which is the palpable second heart sound again it's a feature of pulmonary hypertension also first heart sound when you can hear loud it's mitral stenosis except in calcified valve Etc while in mitral regurgitation it will be soft because there is nothing like mitral valve to close if the valve is damaged it will be leakage and this will give rise to soft S1 aortic stenosis can it is usually normal because it's the mitral valve with give rise to S1 not the uh aortic valve and AR however because of lot of blood coming back will allow the mitral valve to grow slowly and it can become soft however if you get loudest one in mitral link and so it's the other way around also if you hear loudest one in MVP it means either you have Associated mitral stenosis or you have tachycardia or you have MVP or you have acute romantic fever or it's a thin chest wall so this is how you should actually palpate epic speed we all learned from the front but this is one more technique of palpiting from the back because this can localize it properly and can tell you where the apex beat is and you can appreciate what characteristic it is so in mitral stenosis FX would be tapping in characteristics it just touches and goes from the skin because the LV comp La component into the LV is lost so now LV is touching and just going away because of slightly reduced output while large amount of blood coming to the LV both in AR as well as Mr will have the force of the LV better perceived but because it's just the volume not the pressure it will be forceful but it will go away immediately so forceful but not sustained which is called as hyperdynamic while in aortic stenosis there is force but also high pressure that's why it is forceful and sustained for long duration the beat is perceived so once this is understood we know what valve we are dealing with the murmurs are of course characteristic mitral stenosis you get opening snap and diastolic Midas right Mark aortic mitral regurgitation you'll get uh uh pan systolic murder on top of that if it's severe you will also get mid diastolic number aortic stenosis is a long peaking so systolic murmur an aortic regurgitation is also a longer murmur means severe Mito stenosis so mitral stenosis versus mitral regurgitation you can differentiate by presence of third heart sound murmur ending before S1 resistolic accentuation thrill and Associated Mr in patients with MDM or vital regurgitation while mitral stenosis will have opening snap you can get loud S1 and pre-systolic accentuation usually present with Associated thrill uh now coming how to identify which is severe and which is not severe or which is the how severe is each of the valvular heart disease now mitral stenosis is said to be severe if you have class three or four symptoms also presence of pnd hemoptysis atrial fibrillation would suggest at least moderate to severe vital stenosis and so also right heart failure like fetal edema you may have hypotension low blood pressure low cardiac output prominent jvp short A2 OS interval long murmur presence of loud P2 presence of peristal heave also gram cell or PR murmur all are features of severe mitral stenosis while a severe Mr would lead to a wide a2p2 split because what is happening is lot of blood is going into the LA because of regurgitation so less blood goes to aorta and hence aorta will well close earlier so A2 comes early and that is why you have a to p2s widening out further so why day two p2s played pulmonary hypertension developed so you have loud P2 pal paper S3 because it represents the flow across because of the more blood coming from the regurgitant cycle and the next cycle presence of mid diastolic Pro murmur this also flow of the previous regurgitant cycle will now enter through a leaking valve and this can give rise to mitral uh stenosis so there is a presence of brisk Carotid pulse presence of thrill atrial fibrillation displace the pecs and Loud intensity murmur earlier late pre-systolic impulses severe aortic stenosis is picked up by paradoxical splitting because of narrow valve now A2 will be late there is S4 parvastatus late peaking of marble long duration of murmur it is said that a very no pulse pressure of 30 and a blood pressure systolic more than 200 rules out because there is so much of obstruction that you cannot have a blood pressure of 200 and you can have aortic stenosis so blood pressure of 200 you rule out aortic stenosis it you can also look at AR by wide pulse pressure if its hill sign is more than 60 long diastolic murmur this variance pulse soft S1 Austin Flint murmur if you have diastolic pressure less than 50 in presence of elevated blood pressure systolic again it's a severe AR if you have forceful sustained FX lvs3 all our features of severe aortic regurgitation severe TR can give rise to head bobbing even proptosis eyeball sessions or systole earlobe pulsation or liver pulsation or ascitis or neck veins all our feature of severe TR so when you need to identify the severity of lesion look at the evidence of rheumatic activity look at the ECG axis look at the X-ray look at the Echo and if required you can do a cat all these findings clinically can tell you which is the case of rheumatic heart disease so you can do ASO ESR CRP to look out whether the ongoing activity of rheumatic fever is there use Jones criteria for diagnosis of a presence of acute rheumatic fever look at excess if the patient is having pulmonary hypertension rewrite axis on ECG chest x-ray look at the pulmonary venous hypertension or arterial hypertension look whether LV is enlarged lanyards which chamber is enlarged and that's how you can also find out which valve is getting involved and of course Eco will always get you how do you treat them so once you have diagnosed that the patient is having acute rheumatic fever or carditis in that case if there is no carditis just give aspirin if there is carditis which means on Echo you find new lesions like severe Mr Etc developing of acute card ideas you'll have to give steroids so aspirin is given remember the dose is 100 milligram per kg per day for two to three weeks and four to five divided doses while for acicarditis it will be uh prednisolone 2 mg per kg for two weeks followed by tapering till the ESR becomes normal another important question once you find a patient of rheumatic heart disease how long to give this therapy so for the profile axis in a rheumatic fever with carditis and residual heart disease which means rheumatic heart disease so you had a Rheumatic so three things can happen when you have rheumatic fever you get a rheumatic fever heart is not involved patient goes home and is fine so there is no residual disease he had a rheumatic fever in such patients you need to give for five years or until 21 years of age for patients who had some involvement of heart in the acute phase but there is no residual disease so pain patient had acute romantic fever heart got involved rheumatic fever disappeared now heart is okay these patients you give it to 10 years or till 21 years whichever is later but if you have a residual heart disease which means if you have rheumatic heart disease patient has got some valvular problem in such patients you'll have to give it for 10 years or until 40 years of age whichever is longer and probably you might have to give lifelong profile access in some some patients who in high incidence countries like ours where the penicillin profile access is to be given lifelong so that brings me into the my presentation and I would be happy to take questions uh over to Univision thank you sir for that wonderful uh presentation we'll start getting in questions in the comment section and uh or you can also use the raise hand feature to come up on stage and have a conversation with sir foreign approach as in we what we're looking at is for day-to-day practice because not everybody is an echocardiographer not everybody is an Interventional cardiologist and you cannot always be looking at the only Eco report so the whole purpose was to identify how would you clinically suspect a patient to be having a valuable heart disease and which of the two or the three or five L's are involved So based on that uh these findings you can always think of course you can send for an Echo and things will become much easier for you to send across which patients to look for what you should suspect because the point is that a patient of mitral stenosis can have a longer survival for example a patient is having say uh some 30 year female needs uh is planning to conceive or has say become pregnant now these patients will tolerate regurgit and lesions much better she'll feel I'm doing much better you know as compared to when I was not pregnant that's how what the patients will feel like so that's important for you to diagnose from day to day practice as to which patients would end up with a good prognosis for the current situation and who need to be sent across for surgery now remember the simple rule for sending somebody to surgery is you don't operate asymptomatics unless it's severe or with a complication this is a general dictum across medicine not just Cardiology you don't treat anything let's let it be covered you don't admit all kovitz do we no mild disease no asymptomatics no this is a general dictum in medicine you treat aggressively or operate or intervene seriously ventilate intubate operates replace remove all these things are done one if it is symptomatic has to be symptomatic patient need to have complaint you don't treat reports you treat patient and number two patient is not having problems asymptomatic but it's a severe disease but it's a severe disease so that is what you need to identify based on your evaluation so patient who comes to you is very likely that he's coming with some campaigns and symptoms so he's symptomatic so once he's symptomatic you need to intervene if one it is severe or two has got a complication so what are the complications the mitral stenosis it may be say he's got pulmonary hypertension or somebody's got no atrial fibrillation has got to end stroke iotic valve who's got syncope who's fallen down who's got an angina he's having failure on echocardiography is showing dilatation of The Chambers lb dysfunction has come in is Chambers are getting dilated he's getting lb dysfunction he's developing pulmonary hypertension so that I could have shared the ACC kapura algorithm of all the four and it made it more complicated for you that's not the point the point is to make simple lessons how do you pick up in your day-to-day practice and they'll remember simple dictum and simple rule in cardiology this is not a Cardiology lecture uh this is a lecture for everybody and for that purpose the whole idea is you pick up a disease who's symptomatic think what is this uh which valve is predominantly involved get them investigated if it's symptomatic read or intervene if it's severe or with complication if asymptomatic mild without complication not severe you can manage it conservatively Dr s was asked is there any role of Azithromycin in prophylaxis so it's a good question so how do you give profile access I deliberately skipped that slide here primarily because uh I wanted this to be discussed in question so one is that when you give propylaxis you usually get this this is also rheumatic fever is caused by gaps group a beta hemolytic streptococcus which are very sensitive to penicillin so you give penicillin most of the times it works every 21 day you have to give anybody who's less than 27 kg you gave 12 lakh units every 21 day deep intramuscular with a negative as those and remember it is to be given with negative test those every time it's not normal so now I need not give every injection do a test those because it's anaphylactic reaction which can happen even if you have been taking it for 20 years every single test now penicillin if the patient is sensitive or cannot take the other option is to give oral if the patient is not having oral penicillin or good point that was raised is Azithromycin or erythromycin erythromycin 250 milligrams BD daily to be continued is an alternative that can be chosen in these patients yes thank you sir and I think we have one more question by Dr Arnav Chaudhary who's asked the role of noacf in valvular uh atrial fibrillation it's a good question you don't give no Acts in patient who's got one bulb replaced and two stenotic lesions but yes smiled disease mild regurgitations mild stenosis you can give this you can give nox but the indication is atrial fibrillation not prevention of embolism because of the mitral stenosis in early calculate development so low acts are otherwise indicated in non-valvular atrial fibrillation remember that no XR the treatment of afib prevention in non-valveal in valvular never give imposed replacement never there is actually a bad outcome but in patients who are native disease natural world disease but mild disease because mild is unlikely to cause Afib so still be a non-valveera oh valvular is a coincidental finding that is where you can give otherwise no X are not given only buffer or vitamin K enterprised thank you sir and we have Dr Ashok Agarwal who's asked so he has a patient 40 year old female rhd dominant Ms with MBR uh with a mechanical valve that was done 10 years ago now uh she has Global hyperkinesis with LV dysfunction with her lvef is around 35 percent what is the cause and how to manage this good question fantastic well a lot of times you get this one you need to know whether this LV became down immediately after surgery so what happens lot of times when they operate they are not able to do a complete caudal preservation so when you chop off the diseased mitral valve you take out their posterior papillary or anterior papillary because it's like that when you take out the calcified valve you'd end up taking some amount of papillary muscles or the Cordy along with it which leads to loss of some amount of contractile reserve of the muscle and that's why if the lb dysfunction had developed immediately post surgery it means it was resultant as a post surgical case where the disease the etiology is a bit different but more like that this patient if it was operated long long back and has now come with April LV dysfunction it can be one because of metabolic etiologies like hypothyroid anemia etc etc to Associated or new development of coriatry disease you must rule out three this this age is unlikely at 40 to be having CAD it's more likely that the patient has gotten rheumatic fever chronic ongoing rheumatic fever and she was not on Rheumatic profile access lot of these patients uh once they end up with surgery profile remember rheumatic fever the talk was not today romantic River was approach to valvolar disease maybe sometime other day we will take about acute traumatic fever also but remember rheumatic fever is not involvement only of the valve it is also involvement of The myocardium and also to some extent pericardium so it's a it's it's a pan carditis as they say put a heart involved with that so though valve has been changed your new infection will come and now will destroy the muscle to make it weak so if the patient was or not Rheumatic profile axis maybe that's the cause on one more possibility is tachycardiomyopathy if the patient is in atrial fibrillation for long duration and the rate is not controlled the heart will get tired Contracting too rapidly too fast too often and then it will get into dysfunction so you need to control the rate so find out whether it's the rate related lack of profile access related immediate for surgical metabolic or it's a new coronal artery disease you need to treat this because mitral stenosis with element dysfunction in the long run is not a good outcome and it can actually end up with while thrombosis also in future or maybe development of new alveolar disease you have a pair of algor leak you have development of aortic regurgitation now you have got pulmonary hypertension now impairing your LV function so you need a good Echo and a good evaluation and treat you it's very important because you cannot treat lb dysfunction just like lb dysfunction you need to find out what is causing that lb dysfunction reads the cause and there will be dysfunctionally thank you so I think there's one last question by Dr Hari uh he's asked AF with rhd uh developed ischemic stroke can be thrombolised good question you should thrombolize every stroke a lot of times there have been cases that the patient has been anticoagulated you may have to reverse the anticoagulation and thrombolis a lot of people do that uh there have been cases like patients have been on low acts and they've been treated with antagonists of Novak like you have debitron and it's antagonist which is available in Susie map reverse it in a patient who's on say vitamin K antagonist you look at the INR give it them in K give ffp and thrombolize and there are patients so it all depends on thrombolysis will depend of course whether there is a need of it you may have a minor stroke if your score is low you may not do it but in a major stroke you'll have to thrombolize because you'll then that case probably give ffp vitamin K reverse their bleeding Tendencies with their parameters and go ahead and lies that the patients having acute stroke but now with development of Interventional neurology lot of centers if you have availability instead of lies in these patients they are taken into the cath lab they have done thrombectomy and you can open open up their cerebral and the vasculature structures and open up the circulation rather than end up with thrombolysis so that's the other option but in a devastating stroke just because you have a valve and use anticoagulated don't think that is a contraindication of you know saving the brain it's not that the heart is at the cost of brain or brain is at the cost of heart both are vital for a human health your life uh so we have a couple of more questions come in I know it's post 7 30 could we just take them sure okay so again there's another question by Dr Hari he said rht is usually multi-valular so what's the role of beta blockers what are the indications and contraindications yes good question again mitral stenosis and elbow dysfunction are two indications where beta blockers would be good beta blockers will reduce the rate and because of reducing the rate which will prolong the diastole so when the diastole prolongs you get more time for the mitral valve to remain open so that more amount of blood will pass through the LA to LV and hence the congestion in the lung will be less because of the more amount of blood emptying from the stenos mitral valve across the mitral wire from the so it's for symptom relief and also chronotropic competence that's why beta blockers are good in patients who develop lb dysfunction also we know that the beta blockers are one line of the therapy but you don't give beta blockers to aortic stenosis because these patients when you give beta blocker their LV contractile Force goes down and because of that the flow that is barely managed by this LV which is Contracting forcefully across a narrow wall can actually decompensate and present with syncope or failure so aortic stenosis be cautious aortic regurgitation vital regurgitation free goes slow with the treatment regime of heart failure mitral stenosis no problem go at the way you do because your resting heart rate should be 60 exertional heart rate should be 80 you have good amount of dastly for blood to empty beta blockers are a good line I prefer to use the heart failure to approved beta blockers but then people have used in mitral stenosis anything all across the beta blockers can be used symptomatic uh river oxiban is a Novak as I said you don't usually prefer in a valvular heart disease your question about River oxyb and per se is not related to the current topic but because you've asked I will answer all questions that come across anything in cardiology or medicine that I can take so River oxiban there are four dosages this is one Novak that you should know is I can we can have a noac as a separate topic someday but river oxiban is the only Novak which has got four dosages one dose is 2.5 milligram BD where do you use it you use it in a coronary artery high risk patient whom you want to prevent long-term cbot outcomes which means you don't want stroke you don't want mortality you don't want death but not atrial fibrillation so that's called a compass trial data which uses chronic coronary syndrome there is a new terminology like now CCS chronic coronary syndrome like you had acute coronary symptoms any acute coronary beyond the ear is now called chronic and to prevent new occurrence of event in these chronic you the dose uses two point by BD which you can start after one year of acute episode that is one dose again in that dose is also used in peripheral vascular disease not in DVT you have a atherosclerotic PVD star 2.5 BD you prevent limb amputation limb ganglion second dose is 10 milligrams that is given as a profile axis in patients undergoing knee replacement hip replacement people also use that dose in covet third dose is 15 milligrams daily so 2.5 milligram is twice there 10 15 and 20 is once a day 10 milligram is used for DVT profile axis 15 and 20 are used in prevention of stroke in non-valular atrial fibrillation 15 is dough used in high bleeding risk patient which is elderly patients lean and thin patients low egfr patients those patients you give 15 milligrams and otherwise the dose recommended is 20 milligrams or DVD for patients with atrial fibrillation prevention so where do you give these indications you give early if these implications do give early I've already told CCS dose is after one year but I would not prefer to use vivaroxaban in rheumatic heart disease as I said referred dose is uh that is VK which is buffering like drugs thank you sir and I think one last question easiest way to differentiate systolic and diastolic uh murmur yes so if you are not a cardiologist this remains a question that we started off right from first mbbs and it persists throughout your life so best time when you heard murmurs if you're not in cardiology is your mbbs day after that probably if you're not in medicine or in cardiology a lot of times you would not actually be a much Keen or be able to differentiate so how do you different very simple trick I teach my students put your stethoscope put the Bell or the diaphragm instead on the chest and your other hand uh thumb on the patient's character so this is how you palpate you put your stethos patient's chest and your thumb on the patient's carotid so if you hear the murmur with the Carotid that you palpate it's a systolic murder if you hear a murmur that is not going with the Carotid pulse it's a diastolic number very simple so systolic will go with Carotid pulse this diastolic will not go with Carotid pulse so if the murmur and the Carotid calls are together are not together there is a delay between the hearing of the murmur and carotid pulpation then you are dealing with a diastolic easiest way simplest way because history is carroted lastly is when you're not getting um thank you so I think we've answered all the questions so thank you so much even though we've gone beyond the time and we will look forward to the next session always thank you and I look forward to being on the next session yeah thank you so much and thank you everyone for joining in we look forward uh to seeing you in the other sessions that we have lined up thank you so much and we'll see you again thank you sir goodbye thank you good night everyone have a good weekend bye


In May 2018, the 71st World Health Assembly (WHA) adopted a resolution on rheumatic fever (RF) and rheumatic heart disease (RHD), emphasising the need to treat RHD as a health priority and to establish specific actions to address the needs of people with RHD. Rheumatic heart disease (RHD) refers to the long-term cardiac damage caused by either a single severe episode or multiple recurrent episodes of ARF. While the carditis associated with ARF is a pancarditis, valvular pathology almost exclusively dominates chronic RHD. Mitral valve involvement is seen almost 100% of the time. Tune in LIVE on Medflix with our master mentor Dr. Kamal Sharma to learn in depth about its pathophysiology and management.


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