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Approach to a Case of Dyspnea

May 05 | 3:30 PM

Dyspnea is one of the most common presenting symptoms encountered by clinicians. The causes of dyspnea can be several and range from cardiac, pulmonary, anemia, obesity, hysterical/psychogenic, physical deconditioning, among others. As these causes are varied, it is essential to differentiate life-threatening causes causes from benign, self-limiting conditions. Let's understand the practical approach to the case of dyspnea with this amazing Medflix select session with Dr. Kamal Sharma.

[Music] good evening doctors thank you so much for joining us on another interesting session on netflix today our topic is approach to case of disney so now we all know that disney is a very common presenting symptom in that all the clinicians face so there could be varied reasons for it and it's very important to differentiate between the minor ones and ones that could be life-threatening today on the topic it is our honor and privilege to have among us our metrics select creator dr tamil sharma it is an honor and privilege to have this opportunity to learn from you doctor dr kamal sharma is a senior interventional cardiologist with past experience of primary angiography stenting valvuloplasty pacemakers and pediatric interventions he has a rare combination of dna degrees in both medicine as well as cardiology apart from md and dm dr sharma has also been awarded 22 gold medals for academic accidents apart from practicing at sal hospital serg has been teaching the subject of cardiology at unwetter institute of cardiology and at beta medical college among the many firms he is first known to have performed the world's first legal nerve stimulation device implant as part of anthem study in refractory heart failure some has also discovered the winking coronary sign of bsr on angiography which is also known as the kamal sharma sign of vsi along with having authored a book titled chemical medicine for the mbbs memory degree courses dr sharma has more than 200 publications to his name and more than 8 000 google citations a fun fact about sir he's the only cardiologist to have cleared the civil services in the first attempt so this is really amazing to have this opportunity to learn from you sir thank you for joining us today hi good evening thank you for having me uh on netflix uh can i have my slides please yes just started yeah so what we are going to do is i'm going to take you uh into as ray's hand if you have any questions shop you can uh share in the chat box and i'll be pleasure to answer them what i'm going to discuss is not i'm going to not teach you how to treat dyspnea neither i'm going to teach you what dyspnea and its question i'm going to take you through a clinical uh appraisal of when a patient of dyspnea comes to you what you do very often uh when you don't know anything a lot of people do is a cocktail of therapy which is actually not the right strategy a lot of times patients who come with dyspnea would begin given injectably uh you know a one trucemide injection one daily filing injection one steroid injection and then hope that it works out that's not the way because you need to know the disney and actually the patient may be nothing but anemic you know hemoglobin is four grams and that's why patient is listening so it's important to approach a case of dyspnea and to arrive at its diagnosis even before the lab reports come that's more important because your your cbcs and your lfts and rfps and bnps will come in a while and you need to diagnose what you're dealing with as soon as the patient is assessed by you clinically so when you need to diagnose that you first need to know what are the possibilities of dyspnea and for that to know you must also understand as they say i see what brain knows if you don't know you will not see it so disney can of course can be cardiac pulmonary metabolic or miscellaneous so we all know that cardiac dysphonia would be like heart failure which can be the obstruction to the mitral valve which can be in form of mitostenosis which is actually the not the lv failure so left heart failure may be either left electrical failure because of obstruction to the inflow which you find in mitral stenosis volvo thrombus and exoma all these conditions lv function is good so what is called as obstruction to the flow to the inflow of the lv and that leads to development of pulmonary edema which is because of the obstruction to the inflow of the mitral valve where lv function is good so anything which will increase the la pressure and in comp as a response to that either obstruction or because of inability of the heart to pump forward is in the case of elbow dysfunction the blood is which is accumulating into the la the la pressure rises and this back pressure is then transmitted to pulmonary veins you know you would sometimes wonder what a fantastic thing it would have been if the pulmonary veins had a valve you know the valves will not stretch backwards and not allow the pressures to rise into the pulmonary circulation but that's not the case pulmonary veins don't have a valve and the la the pressures get transparent to the pulmonary vein and then you get pulmonary venous hypertension and then you get pulmonary alveolar hypertension you get the alveolar edema and then interstitial edema followed by pulmonary alveolar edema and then pulmonary artery hypertension that's the sequence so you have a pulmonary wedge pressure rising and you have left heart failure which is one of the mechanisms that you can have secondly you can have a cardiac disorder which is coming from not the obstruction per se of the lv inflow or the rise or inability of the lv to pump outside but it can happen because of some other structure compressing on to the pulmonary or the cardiovascular or the ra and the rv side and not allowing blood to be pumped adequately to the lungs and the patient may be dyslexic not because there is congestion in the lung but there is not enough blood in the lungs to get oxygenated so which conditions are there where you don't have enough blood reaching to the pulmonary circuit despite good cardiac activity if anybody can comment on the chat box it'll be pleasure to answer listen to your answers uh well the clue is then we all know that the lv pressure is 120 systolic right but the right ventricular pressure is 25 systolic and compare this with say the pressure uh of the ra which is only 5 to 10. so when the ra pressure is low all you need is a pericardial pressure around eight to ten so uh basically what i'm i was talking about that when you need a compression of the chamber to be uh you know susceptible enough to allow congestion to develop in the or the cardiac output to fall the most susceptible chamber would be one one chamber whose pressure is low and the lowest chamber that has got the lowest pressure inside and hence can be compressed easily by outside is right atrium because right atrium has got a pressure of 4 to 8 and for that reason the ra compression uh will cause temporary which compresses first in temporary followed by rv and then later on ph so cardiac tempo not is one etiology where though the lung uh the though the lung is not flooded with the blood but still patient is this thing the dyspnea is because there is good amount of oxygen reaching because of the breathing but not enough blood is reaching to the pulmonary or through the pulmonary arteries to get oxygenated and that because of that reason this inadequate oxygenation it will lead to hypoxia and that's why the patients are this nic so when you're dealing with a cardiac so possibilities when you're looking at you have decompensated heart failure acute pulmonary edema you have in pulmonary embolism again similar etiology and pulmonary cardio or cardiac temporary this can also develop in pulmonary hypertension now uh slides are not changing and because i'm not changing them so once i'll change them beyond cardiac slides the etiology you will see the new slides so i'm still stuck at the five six causes that i mentioned in cardiac etiology so the ideology otherwise is pulmonary hypertension which is so somebody can ask you where the pa pressure rises or shouldn't the blood flow be increasing to the lungs and the patient should actually feel better no it's not the case patients have pulmonary hypertension develop dyspnea because the mechanism of protection of the lung to the flood prevented to be getting flooded because of the rise in the pa pressure is pulmonary arterial vasoconstriction actually the x-ray findings also look at when you look at in the patients who are developing early pulmonary hypertension you will find there is what is called as peripheral pruning pruning means tapering off of the pulmonary artery and they are constricted enough to prevent increased pulmonary blood flow and because of this there is a hypoxia that there is a weak mismatch that develops and thus these are the causes of cardiac uh dyspnea then the respiratory causes we all know there is copd bronchial asthma and ammonia interstitial fibroids pneumothorax hydro pneumothorax plural effusion the list is long and then you have metabolic so you have anemia diabetic acidosis and uranium so these are three which we should commonly remember and nowadays you can also consider hypertransfusion reaction over transfusion uh in a patient who ends up getting a lot of saline being pushed uh as a a patient who actually is already sitting on a brink of lung congestion who's already having mild function uh all these patients can also develop this year so disney when the patient you see the causes you must know are extending from cardiac respiratory to metabolic now i've changed the slide now when you have a patient of disney you need to define whether you're dealing with an acute dyspnea or it's a chronic dyspnea so by definition acute we all know is within days to ma days to hours uh sub acute is up to two weeks and anything which is more than two weeks you call it chronic disease some people say three weeks some people for two weeks so anything which is more than two to three weeks is a chronic dystonia so some people say two weeks some people say two months but anything which is beyond two you are actually dealing with something like sub acute and chronic and then the causes will be different now salil has asked what is angina equivalent fantastic equation i had mentioned in my slide then dyspnea can be angina equivalent not all patients of coronary artery disease will present with classical angina especially elderly women they can present with dyspnea as an angina equivalent which means the patient says when they are walking they don't perceive it because of their differential perception of pain and differential perceptions of lv feeling pressure patient may not feel pain as the symptom but they may feel disney as a symptom when actually it's nothing but the coronary artery disease so this is called as angina equivalent patient actually has coronary artery disease he says exertional dyspnea feels better with nitrate sits down feels better everything else is descriptive and the like the classical angina but basically patient is not mentioning it as a chest heaviness or pain it says gabriel on walking that's what is an angina equivalent so patient may not have heart failure but he has angina which is equivalent and masquerading as this now when you come to an acute dyspnea the acute district patients can have various etiologies triggering it so you can either have a dyspnea triggered by hypoxia which we saw a lot of patients of our covid19 so you have pneumonia pulmonary embolism pleural effusion copd's ild pneumothorax atelectasis mucous plugs and of course pulmonary edema which can be either cardiogenic or non-cardiogenic so cardiogenic pulmonary edem i just discussed it can be lv obstruction lvla in flow obstruction lv inflow obstruction or lv dysfunction or you can have multiple ethologies like pulmonary vein thrombosis etc which are rare etiologies and i'm not going to touch and confuse you further about that but sometimes hypercapnia itself can lead to dyspnea as a perception so what is hypercapnia we all know it's the rise in co2 so if that happens in co2 exacerbation these patients they do lot of effort we all know about pink puffers and blue blotters if you remember blue blotters are chronic bronchitis why are they so because their respiratory perception of hypoxia is not so good they are not concerned and they don't make an effort to improve oxygenation because of their chemoreceptors being desensitized so they are blue because of hypoxia and bloated because of pulmonary hypertension and right heart failure compare this with say emphysema which were classically called as pink coppers will make a lot of effort they will breathe with firstly breathing and hence they will have uh because a lot of effort they have to put to maintain oxygenation they are having a lot of work of breathing and that's why they are lean and thin they lose a lot of calories they spend a lot of energy in keeping themselves pink so they're called pink puffers but because of this they are puffing and they are distinct so hypercapnia is the trigger not only oxygenation but their co2 also when you see they actually try to bring it down in your normal level compare this with say uh chronic bronchitis patients who are blue because of cyanosis and there is a constriction and they are co2 narcosis so they are drowsy they don't breathe it's a vicious cycle and they are hypoxic and they develop pulmonary hypertension and then they develop right heart failure so co2 exacerbation hypercapnia can itself will be a responsible mechanism of acute dyspnea and this is very often the case in acute exacerbation acute neuromuscular disorders like myasthenia atm gbs all the workup is to be focused account around co2 these patients have rising co2 levels uh and they don't have much of o2 initial phase so uh when you're looking at a patient it's not just the o2 saturations that matter you also have to look at co2 that's why a blood gas does much better acidosis is responsible sometimes in patients for breathing a hyperplania iron technique and which can again be perceived as dyspnea now the common causes of acidemia is uh what i call as kusama kusama's breathing so kusama's the causes of kusama's breathing are kusaman what do i mean it's an acronym k for keto acidosis u for urania s for salicylate poisoning s a for aldehyde poisoning m for methyl salicylate or methanol poisoning and l for lactic acid a u s s m a kusaman's breathing as we call it right perfect for keto acidosis u for urania as for salicylate m for methanol a for aldehyde and l for lactic acidosis all on the all of these are the causes of ketoacidosis so uh so that's one keto acidosis acidosis and some other causes of acidosis all will lead to acidemia now poor oxygen delivery so either the oxygen will not be transferred enough or it's be if it's transferred enough it's not being delivered so anemia uh the disorders where the oxygen delivery is poor even the patient is not hypoxic would happen when the hemoglobin is low enough or actually there are disorders where the oxygen cannot be though it is binding well in the lungs cannot be transmitted to the tissues so these will happen in anemia in patients with low output uh heart failure in patients with massive pulmonary embolism cardiac temporary and tension pneumothorax and so as i said in general equivalent and in upper airway obstruction anaphylaxis angioedema these are all miscellaneous causes pain etc so what about chronic disease when you have a dyspnea which is a longer duration you have plural etiology by plural effusion copd asthma chronic pneumonia interstitial lung disease vascular hypertension polymer av malformation cardiovascular point of view it will be constriction heart failure valvular heart disease brady arrhythmia tachyarrhythmia uh angina equivalent again patients with anemia neuromuscular kyphosis renal failure obesity and deconditioning can be miscellaneous causes of chronic disease so once we have known what are the possible causes now we need to know how we will approach these cases now when you approach again you must know there are certain equivalents of this there will be a lot of patients who are you know bedridden they will not come and complain to you that they feel breathless when they exert a lot of classification some and this lecture is not at all about you know your exam preparation this is all about your clinical approach how you're going to approach a case of dyspnea so when you go to see a bed-ridden patient you'll have to ask some other history what's the question that they presume do they have to the relative can say this is a bedridden this elderly daddy is you know bedridden for now quite some time but off late uh she always cuffs at middle of the night and she wake wakes us all up what is that that's pnd paroxysmal children so patients who are actually they go to sleep at night and after two to three hours of sleep they wake up suddenly from middle of the night gasping for the air hunger and after assuming upright posture on 15 to 20 minutes of upright posture they feel a bit better and they can actually have a pink for this put them that's a classical description of paroxysmal that is about nocturnal at night dyspnea now dyspnea is a symptom and decubitus decubituses for the this near this near this is discomfort near means breathing it's a discomforted breathing when a patient has got abnormal perception or discomfort of his own breathing that is called as this near now orthopedia is a posture orthomensity so orthopedia is the posture that patient assumes what post is sitting posture patient assume so when patient is so patient when you don't describe orthonya as dysphea and supine because the position assumed not the position of discomfort position of comfort so patient is breathless and hence he feels slightly comfortable while sitting up okay that's what is orthogonal so patient assumes upright posture and he feels better and that is orthopedia and this you get in heart failure asthma your esophageal reflux at the night also can actually look like it the reflux itself can lead to chronic uh chemical pneumonia in a patient who's got a bad gard and you can have intermittent epi episodes like mi bronchospasm in pe chronic persistent could be copd and interstitial and there are some other trappening platypianis patient feels comfortable in supine and this happens in lm exoma and because see the mixoma when the patient sits up it comes and obstructs the lv inflow into the mitral valve and as the patient lies down it goes away from the step a mitral valve and that's why a lot of patients of lm exoma because it's a pedunculated tumor will feel better when they so lie down rather than they will sit up because as soon as they sit up the tumor plops into the mitral orifice and occludes this is a classical history so when you look at this kind of a history you know that you're dealing with the relay ball wall thrombus or lm zoom etc and it can also happen with fistulas pulmonary hepatopulmonary fissure etc so these kind of histories also should be aware to you that what you're dealing with is uh dyspnea now the pattern is important how what is the prolonged bed rest whether the patient uh but i had prior to the onset of listening it actually indicates for example today only i have discharged a patient this patient the otherwise young healthy you know he was on a road trip six hour single sitting and he was sitting on the back seat and developed swelling in the feet and acute dyspnea so that was a dvt and led to acute pulmonary embolism so prolonged bedrest suppose a patient underwent a hip surgery and was immobilized but there's a very good likelihood that she may develop dvt and this can then embolize and kill permit so you should also look at the history is the patient been adding alone been traveling on the long distances or had past history of recently say covet covert itself is a risk factor of developing dvt and pulmonary embolism does the patient have orthopedia the patient has to sit upright and feel comfortable slightly pnd platipune orthodoxy and trap neurotrapnea means lateral decubitus platypnea orthodoxy means patient is platypic that means he's better when he's in supine posture but deoxy i mean he desaturates when he sits up so very simple look at his saturation when he's supine and check his saturation when he sits up normally when you sit up your saturation improves but if a patient who's feeling breathless and he sits up when the saturation drops by more than five two to five percent actually this is a indication of platypus technique probably so these are simple diagnostic method there is a small asd through which the shunt might be taking place which can also be responsible for or platinum is asking me sir please explain platypnia and hepatopulmonary syndrome good question i thought we had an audience limited to mbbs md level so i would not go much in detail but now that you ask gordolin i'll take care of that uh so in patients with pulmonary av fistula and also in hepatopulmonary syndrome there are basically collaterals that develop into the uh into the lungs from the liver so what is happening is that there is some amount of blood that is cross match that is bypassing the lung fields as well as the liver pathways and is called a causing short circuiting in terms of this is the amount of blood which will not get oxygenated in the lung now when you are sitting upright the gravity is something that these fistulas will have to overcome so amount of shunt through this fistula will be lesser but when you go supine the amount of flow with the with the gravity going away from the fistula will be easier and hence you'll have more desaturation in pulmonary beta pulmonary syndromes or hepatopulmonary fistula same with pulmonary fistulas also what happens is when you're sitting upright it can cause the vq mismatch that you have because of the fistula would be again be much driven by the gravities unlike the supines where the gravity will be nullified and hence patient will be better in clinton orthodoxy with the desaturating when he's sitting up uh pf also mentioned as a cause of platypia because of the direction of the flow uh is there and he's mentioned it very well so what is this is very important in certain job airline fitnesses you know in in divers you have c diver profession in sea diver's profession you are got to make sure that you don't have the diver having a patent for a novel because if he has it he's likely to end up with cases disease what is called as bends the deep sea diverse disease because that's through which the asd would also have the compress the air bubbles or the uh will all of the nitrogen would start escaping into the systemic circulation so there the pfo should not be there and the pfo uh why they desaturate is because of the directional of flow when these patients they sit up versus when they are supine when they are supine the ivc is and the svc is going right in the direction of uh not facilitated by gravity through the ra into rv but when these patients sit up the ivc in the svc the flow is now alleniated towards the septum and because of this the septal flow you will have blood coming in the supine for in the sitting up posture from the ivc svc now going across the international september into the ra and this will lead to desaturation if there is a patent for minor well and that's the other reason why and dr mario this i correctly pointed out that pfo can also lead to political orthodoxy so once you have known these patterns now you need to know how you are going to approach a patient with this firstly uh you will try to treat and manage in dyspnea for sure but you'll also look at his level of consciousness now very often you find that a patient who's uh being on a slightly hypoxic because that's his co2 drive these patients some of these patients you know they remain and maintain their uh so archel in the meanwhile is asking what is trapnia let me address that trapezoid lateral decubitus now lateral decubitus when they assume they feel better in the lateral decubitus that is trapdium and that they feel better because of again the same reason they will lie on the side of the disease uh you feel they make them comfortable again because of the gravity so you have supposed left lung av fistula so patient will feel better uh if he excludes that lung where there is more shunting and you know feel uh comfortable by changing to the posture in the lateral so again hepatopulmonary fistula uh volvo thrombosis all of them can come with so lateral decubitus is called a stepopia one more terminology is because everybody is asking me about terminologies it's called bendopinia now let me finish the all left neos in that matter so bendopnia is this neon bending forward this is actually said to be a sign of early patient ending up with uh interstitial edema pnd or heart failure bendopnia this is relatively a new terminology this is not an old and there was an article i think published in 2019 only this terminology was coined and this actually showed that the patient is likely in the borderline case of heart failure who can actually end up within your class three class four symptoms uh in future so it's a predictor the patients will be listening when they bend forward and this can actually be present in disorders other than that which is like very common in obesity it can also be found in grd it can also be found in patients with sleep apnea or obstructive airway disease so it's not a classical symptom but you should know what is bendopinia also now you also as i was talking about the co2 drive or hypoxic drive a lot of patients uh who actually maintain low o2 levels 3po2 levels like 88 92 saturation and their drive is basically hypoxia they are not responding to co2 as the determinant of their breathing in these patients if you start giving oxygen to maintain 100 oxygen especially in copd what happens is the respiratory drive disappears and these patients can end up with ventilator you know so make sure that your hypoxia is not over treated this is very important if you chase in a patient of copd 100 saturation a previously stable saturation the patient you're seeing is comfortable your saturation is 92 with co2 you've done an abg po2 is 60 and you look at is co2 co2 is almost 40 45 this is good enough you know don't you know try to chase his oxygen to 100 you put his oxygen on his o2 levels go up he is not going to respond to co2 co2 will start rising because he feels that oh co or hypoxic drive is gone and this patient will now not breathe at all so this patients will now that have hypercapnia co2 levels will go to 65 70 this hypercapnia will cause them to now become drowsy the respiratory ends up in a very vicious cycle and will end up in intubation so don't chase 100 saturation in copd that's one of the victims i thought i'll just touch upon that based on the consciousness level again that is the reason why the consciousness i have put ahead of the rest of the things what about degree of central as i said synonym blotters would you expect them to be a bit bloated and blue but in the emphysema patient is actually now becoming cyanotic that's more alarming that's terminal but a patient who's chronic bronchitis and has got mild hypoxia that's acceptable you need to know case to case basis on the other hand you look at a patient of say congenital heart disease who comes with cyanosis and is moving around if you try to chase him 100 you will never achieve it for example a patient of tetralogy you'll never have it without correcting his tetralogy or without doing his vt unless he's into a spell spell the saturations go below 65 where then you treat it and you go up to 85. so 85 is a good enough oxygen and the differentiation for a child who presents with dyspnea whether this cyanosis is respiratory or cardiac the test is called as hyperoxia test which is you give them 100 oxygen for 5 minutes and if their saturation does not come beyond 85 for a minute then you're dealing with a congenital cyanotic heart disease this is called as hyperoxia test this is very commonly used in pediatrics and this helps to differentiate respiratory from cardiac etiology again you must look at angioedema swollen lips very common manifestation swollen eyelids somebody else and these days these chinese masalas in the charts and the poppers and cut trees you think that the food allergy is not common it's very common because of lot of these additives that have come into to you know increase your taste buds what they do basically they release histamine and you know hyper hysteremia is one of the mediation of giving rise to anaphylaxis or even to enjoy edema or for that metabolic area so food allergies are very common patency of the airway is important you might be actually dealing with the patient of upper airway obstruction the child might have swallowed a coin or maybe a marble that's why patient is having this problem so you need to so uh find out what is the status of this ask ram shankar singh is asking scale of dyspnea so yeah there are a lot of that's true you should also be assessing what severity of disney it is but whether it's acute or chronic and whether it is orthopedic class three class four etc and dr ramshankar is saying is saying that the scale of dyspnea also needs to be quantified and we have multiple ways to do that so you don't use nyha classification for respiratory but you can surely use mrc classification and that's not part of the clinical assessment today some other time i'll take into the you know theoretical aspect of that thing the whole purpose of the today's lecture was to assess a patient when you come to this near to you so again you look whether a patient is able to speak in a single sentence or not very simple lot of patients will come and tell you when they feel better so when i came to your last time i was not able to complete my one sentence in the breath now i am able to talk to you uh uninterrupted that's very simple way of assessing how the severity is also you need to look at heart rate blood pressure and what is the cyanosis or peripheral perfusion present or not so uh i've not changed slides i'm i'm going to change slides as i finish all my content i usually keep very few slides so that i can go extend for because my purpose is not to talk to you and go through the slides to be spoken so the important determinant of differentiating cardiovascular from respiratory is very simple if you have a patient who's got a very high sympathetic reflex response you're dealing with heart failure that's very simple so i usually tell a lot of charts a lot of algorithms i usually say by bedside all you need to do is check what is this pulse rate it's very very unlikely that you have heart failure and heart rate is less than 100 unless the patient is complete heart block car patient has been injected with a blocker who has been chronically on even in patients who are 100 mg of metaprolol when they come with acute lvf their heart rate should go above 100 that's the simple way second thing is look at his peripheries is he cold kami is he perspiring that again is a finding of cardiovascular dyspnea patients of respiratory dysmenia don't come with very much of perspiration and they don't have tachycardia disproportionate to this i'm not saying they don't develop tachycardia a bronchial asthma patient can have tachycardia if he comes with you know a cough syrup where he is taken up beta two agonists very often very confident they get these side effects of tachycardia but these two things look at the heart rate or sympathetic tone and the peripheral cold coming of course there are other ways like whether the cuff precedes disney or disney proceeds cuffed this very simple history we have been taught ever since time immortal that in respiratory etiology you will have first the irritant going to the lungs so first you will have cough and then there will be dyspnea while because in the cardiovascular etiology there is first uh pulmonary venous congestion and there is vq mismatch so first patient will just develop dyspnea then he develops prank pulmonary edema which he brings out so cough comes later so dyspnea precedes cough in patients with cardiovascular disorder while cuff precedes dyspnea in a patient with respiratory disorder of course you can go for the history pnd hardest mi traps wrong chi chest is clear not clear heart sounds audible not audible all those things do matter but those sometimes can be very difficult to differentiate simple thing is looking at the heart rate and cold gummy skin those two things that you're dealing with uh heart failure so yes there is work disney or scale there is uh dr ram shankar singh is saying there's the bog disney scale there is a physical activity scale uh there's a visual analog scale uh you can use canadian cardiac society scale you can use nyha for cardiovascular the list is very long but i think the visual analog scale which is presenting most of the nursing chart where you just stick how smiling and not smiling the patient is is much easier so once you've done this and you've looked at the history most of the time that the patient had passed issue valvular heart disease patient had fastest of am i patient is elderly patient doesn't have family history or separation has seasonal variation patient is a history of allergy patient is aspirin sensitive intrinsic versus extrinsic seasonal variability known in therapy etc all these will aid in diagnosis um once you've done that and you know what you're dealing with which of the two you're dealing with you can simply look at of course ecg and echo but then i have tried to summarize all the tests possible in this chart so what are these the labs can include cbc tsh thyroid hypothyroidism can present a lot of times with refractory heart failure recently had a young chap you know he was being seen by a lot of cardiologists but nobody had bothered to look at his tsh his tsh was more than 100 and he he said the moment i started his escalating thyroid replacement therapy he started feeling much better his lve was already 20 20 for almost five six years imagine this guy would have done much better quality of life just this thyroid had been checked so hypothyroidism or even hyperthyroidism can lead to mean lurman scratch where you get but it's not usually elbow dysfunction hypothyroidism leads to elbow dysfunction cbc you look for anemia that's the basic point of pancytopenia where you can have certain cardiovascular disorder you look at chemistry panel which includes sugar you can also look at pulse oximetry and simple and acute setting but very important is your blood gases and biomarkers so very simple test is to do as an nd pro bnp or you can if not available in the pro vp you can do bnp also at your place people do nt pro bnp pro bnp bnp itself a np but there are new markers galactic 3 st 2 and the list is long so i'm not going to touch up on those which are not available we'll just look at b and pure anti-probability remember for that cut off the simple rule is 135 for bmp or 300 for chronic 135 are acute so anything which is up in three digits you should start suspecting for antiprobe entp it's like 1 0 behind your age so if you're thirty three hundred fifty five hundred something like that so uh that up to that level you can actually leave it 450 and above you consider usually heart failure you can look for d dimer for pulmonary embolism you can look at anti-probe and peptides and creatinine also because creatinine influences not only uremia can cause heart failure but creatinine alters the level and implications and clearance of peptides and hence in a patient with crf you may have falsely elevated anti-probe so if the anti-pro bnp air bnp is normal your dyspnea is not cardiac so it's a very very almost 100 percent negative predictive value if your anti-probienpnbnp is normal you are ruling out cardiac this year it is not even so in patients who's got an echo which is showing normal systolic function antiprobe np is elevated that is called as heart failure with preserved ejection fraction or diastolic this function which we previously used to call or fpf so anti-probability is so important you know echo if is normal and anti-probe is elevated falls into half prime part failure with the preserved ejection fraction because dr kaushik is asking about repeat the bnp level so 135 if you're looking at bnp 135 for acute and 300 for chronic and if you're looking at nt pro pnp 450 if you can remember a single figure i usually say anything in three digits be suspicious anything less than three digits forget at any antiprobe npn pnp probe enp whatever test if it is in three digit plus keep working up if it's two digits you're sure that's not heart failure one digit not failure okay so once you've done that you look at the ecg echo chest x-ray and pulmonary function test depending on where you end up with this and then you can go for cardiac ct cardiac mr for the cardiac causes for pulmonary you can go to pulmonary ct bronchoscopy torico vq scan pulmonary function test hrct etc and for other disorders especially like six minute walk test is important to know and prognosticate how the patients are behaving so six minute walkthroughs cardiopulmonary exercises some patients with grd can be required upper gi scopy you can require sinusity for patients with sinusitis and post nasal drip triggering it so those are the methodologies of working up the patients so now this is this was to deal with approach and how to arrive at a diagnosis neither i am teaching here theoretical aspect of categorizing them nor i am going to discuss about treatment strategies you all know that that's a very separate lecture in itself but what i talked about is how you approach so firstly i'll now summarize this was my last slide i'll now summarize firstly you should know what dyspnea can present with in women and sometimes in children it can masquerade as angina it's the angina can masquerade this near both ways it can happen you can have its equivalence like or trepopnea platypnia or topia for the people paroxysmal challenges not all this or not all dyspneas are cardiovascular remember this you can have dyspnea like pnd mimics there are dyspneas which mimic like pnd patient wakes up in middle of the night but he does not have cardiac disease it actually may be obstructive sleep apnea it can be gastroesophageal reflux giving rise to patient to rise up in the middle of the night so what we are dealing with is uh what kind of dyspnea where the patient is and what are its equivalent make sure you're dealing with acute or chronic if the patient has come with acute you should know the acute causes which i've just shared with you look at his sympathetic response look at his heart rate look at his blood pressure look at his perspiration cold calmly skin or whether he's dryness of skin wrong repetitions respiratory versus cardiovascular and then you can differentiate the two of course you can go ahead and do the biochemistry you can do the invasive evaluation of course ecg will show infarction copd am i a imp uh hyperventilation syndrome yes uh dr ashok agarwal is saying patients can masquerade and the best way again would be the approach by looking at the abg these patients will have what would o2 saturation but co2 will be very low co2 will be very low and that's how you know and the way to treat it hyperventilation is rebreathing mask ask the patient to breathe inside itself and of course people give clonazepam which is very common associated with hyperventilation syndrome is associated with mitral valve spectrus excavatum psychological disorders panic episodes uh so you should know the associations of each of them and once you have arrived at a diagnosis and we are sending further one simple test that you can do is a biomarker anti-probe np if you've ruled out anemia thyroid etc uranium as this other disorders apart from abg and once you've done that you can look at ecg echo x-rays spirometry and then you can look at further work up in terms of ct thank you very much thank you for all nice comments shivan etc everybody's even nice comments i'm open to questions thank you yes sir thank you so much that was super informative do we have so many awesome comments pouring in uh doctors in the audience we're giving a moment for you to put in your questions in the comment box also feel free to directly communicate with sir by touching on the raised hand feature you will receive a prompt to turn on your audio video and you could directly direct your question to dr kamal we have a raise hand request from dr mahadev desai yes sir please go ahead yes sir hello yes kamal excellent talk in-depth analysis i must say i'll just add one or two of them that one we have been seeing many times the cyanosis which is not responding to the oxygen and we keep in mind methmoglobinemia because that's what we have seen number of patients right with methamphetamine so that's over and above seopolian causal heart disease that you mentioned that is correct psychogenic you already mentioned otherwise that's one another and many patients who have dyspnea and little dehydrated but no respiratory findings and again just like smalls as you said we have to keep in mind diabetic ketoacidosis and lactic acidosis so in the investigation serum acetone and anion gap is what i would add to what you already said otherwise an excellent talk and very very informative i must say thank you thank you yeah squatting in uh dr madhuri decides point is very valid i did not take cynosis in this but i think in some time maybe in future we'll take cyanosis as a separate lecture so we have you have methamoglobinaemia sulfimoglobinaemia you can have shunts you can have peripheral central versus peripheral differentiating between the two cyanosis which is reversible irreversible sinuses [Music] all four limb cyanosis differential sinuses reverse differential sinuses now we have artificial sinuses which you get in acmo which is called as uh you know north-south syndrome also you've got harlequin syndrome because it looks like an harlequin a joker from the movie so harlequin syndrome that you find in acme therapy patients so cyanosis itself is a big topic but yes then you should keep metamorphoglobulinemia self-image as those two important ideologies that you should know uh uh i think there are a couple of questions that i could see one was how to differentiate hysterical dyspnea and can you show me the previous question what was that yes i accepted a raised hand request dr praveen could you please come on we are using anticoagulant i want to know sir why we are using anticoagulant what will happen in covalent pneumonia good question so anticoagulation is primarily to prevent deep thrombosis because there have been lot of studies which have shown that in patients who have chronic hospitalization or long hospitalization they itself is a risk factor for development of dvt and pulmonary embolism on top of that covet 19 itself is a pro thromboticity of condition so we had our own paper published recently in the american college of cardiology two papers one of them was on a meta-analysis umbrella review which is accepted in reddit jack at the american college of cardiology is published now in journal of american cardiology where we looked at the umbrella review whether the novacs actually prevent rates and we found out that yes they do prevent even traits even in patients actually there was another paper that we did which was on docile is a map that how it prevented atrial fibrillation in patients who were having coveted 19 but did not prevent mortality overall so the the prep the point of anticoagulation was that it should be indicated only in patients who are hospitalized and have severe pneumonia it should not be started for patients whose d dimer is less than 1 000 and is not hospitalized for sure that subgroup is completely out only in pneumonia you can consider that up to 28 days and not be on for sure so there i sometimes see a lot of patients who are online you know been three months and four months they're still on no wax and they're chasing their d dimers can be d timer normally well that's the wrong strategy timers you did not change uh chase and once you've done beyond 28 days of coverage you can surely cut it off yes thank you thank you for your question dr praveen uh so there were a couple of questions yes i missed them sorry yes uh so we have dr nikon asks the difference between nt pro bnp and bnp yes nikon so difference between anti-pro bnp and bnp is that the bnp is influenced very much but it's a short tax thing anti-probiemp is long-acting and the bnp has got false elevations with renal failure it varies according to the body weight gender and age that's why it's not very specific antiprobably is supposed to be more superior and less influenced by renal clearance so preferably you should do anti-probe but it is costlier than bnp so a lot of people sent us they do bnp good thing about both of them is both are normal everything else is i mean hardy this me has ruled out for sure so you can do either of the two but antiprobe np is better uh dr cabela's differentiating hysterical dyspnea yeah so people do lot of funny things actually you should not do them one is pinching the patient's nose or crossing whether she can with older breath or not you know sometimes if the patient is hysterical they will pour a drop of ether on their nose don't do these things these are not required uh simple thing is to hysterical dyspnea is to check most of these patients will develop signs of hyperventilation which is their ph will start co2 will wash out and because of that they don't have a they are not doing it deliberately it's not hyper usually these patients have panic episodes these patients have basic abnormality in their chemo in their respiratory centers and hence these patients they hyperventilate and their co2 levels starts falling and because of that the ph of the patient will start becoming alkalotic and they will find features you will they will complain findings like tingling perestatia perioral numbness uh these kind of features are very common in these patients so best is to look at an abg look at their saturation and they will have associated finding associated triggers stress lean and thin belt uh dietary abnormalities panic episodes uh features and that's how you can differentiate of course you can look and rule out other ideologies before you confirm that the same is there uh dr madhav may mention that if they keep on doing it they can actually develop the telly they can actually end up developing carbohydrate spasm as we call it they can end up with a carbohydrate spasm uh which you can trigger and check their blood pressure and inflate the vp cuff above the systolic the higher hand will go into spasm uh what is called as a coach's hand so which is uh found in patients with hyperventilation but not all patients will develop a cautious hand when you do the carpopular spasm tetany evolution so it may be without it also okay so so we have question from dr kavitha how do we differentiate between a panic attack and an acute disney no acute dyspnea one of the ideologies panic attacks so don't consider that a panic attack is not disney and these patients they don't realize that they are actually coming with this thing because of that so it's it's a diagnosis on differential it's not a different diagnosis these acute panic episode patients can do come with you and of course you require a psychosocial evaluation and of course by confirmation is simply to look at abg when they come with disney because that that time their co2 will be low so simple way is to look at an abg their o2 levels will be very fantastic but their co2 levels and then again the clinical history if you look at there the breath is not deep enough they have technique they are hyperplanic they are the kidneys but they are not hyperthing they are not breathing deep enough if they do they will end up with co2 washout okay so a question from dr ashok d-dimer level and how to interpret them sir yeah d-dimer i think we have to again go by the age i'm hearing my voice echo somebody's probably unmuted i'm not sure so yeah so d diamond levels yeah yeah so d timer level the timer level you have to again go by is usually 500 cutoff is taken as a normal value but again it's something like like bnp i told you you know multiplied by zero so 70 700 60 600 50 years 500 1000 that is two times the upper limit is abnormal so one thousand and above you need to be concerned up to one thousand i don't think in an era of code for anticoagulation you don't have to chase it so don't be much concerned about it but you suspected p diamond to be more than thousand you're probably in acute system setting you're looking at pulmonary embolism but for pulmonary embolism say better is to do an echo which will tell you pa pressure and also look at the proximal thrombus if it is present it's much easier cheaper and more specific rather than you know doing a dimer per se which will add in diagnosis where echo is not available but now with the wide availability of echo and also equally great availability of ct pulmonary angiogram i think that's the diagnostic for these patients okay uh thank you sir we have a question from dr cable in covet patients their own level starts reducing without much disney what oxygen level one must hospitalize the patient their o2 yeah so i think that it varied till it varied from the wave to wave because of the availability of vids so uh in the in the second wave we all know patients were told that you can stay home till 88 in some of the centers and they were patients who were managed like that uh anything below 92 i would definitely suggest hospitalization in the current era you should be very watchful because these patients do get a desaturation very quickly but in first and second wave the cutoffs were like 88 and what is called as happy disney or hypey hypoxia which was very deadly because these patients did have hypoxia for a while and then they started some of them started improving but some of them could deteriorate very rapidly so anything below 88 you should surely be cautious in covid uh 85 and below i believe you must hospitalize but we all have seen and treated patients with saturations of 55 and 65 you will have fantastic waveforms then the saturations would pulse oximeter would just not much you know 55 65 that's how it will move around thank you sarah so we have a question from dr gurleen how anemia can cause heart failure yes so anemia causes heart failure by three mechanisms one is the hypoxia to the myocardium itself so you have less amount of oxygenated blood which is going through the coral reason the heart itself is not getting good amount of oxygen number two hypoxia the anemia itself leads to more work to be done by the heart so it's both demand and supply so there is increased cardiac output and there is more burden on the heart and third is what is called as diastolic heart failure of anemia because the volume the lv end diastolic pressure because heart is contracting with forcefully the heart is not able to relax adequately because of increased tachycardia so when we know that there is increase in the heart rate the what gets shortened is not just it's gas which gets shorter so amount of diastole is short and hence the amount of lv time to fill is less and hence your diastolic pressures will rise your wedge pressures will rise efficiently so patient can have systolic heart failure diastolic heart failure and hypoxia from anemia all three can lead to heart failure in a patient okay so this is coming to the next question what is happy hypoxia the mechanism behind happy hypoxia i think we are ending with covid again so uh high p hypoxia is patient actually so usually what happens in a patient with dyspnea uh usually as soon as the saturation starts dropping below 88 85 patients do feel distinct the problem in kovaid was that the saturations would go down below 85 but the patients would not realize this and this was primarily driven by the tissue perception of oxygen content rather than the central oxygenation what do i mean what i mean is that your carotid bodies are not responding despite your co2 levels going down to say 85 65 normally once it goes below 85 the body will trigger a need for oxygen consumption but because the nervous system the angiotensin receptor mechanisms the lung the peripheral tissues are not able to adequately uh you know sensitize the chemoreceptors to get a distinct sense the tissue is hypoperfused and the tissue saturations are low the peripheral saturations are low because of the constriction also contributing to it what is called as peripheral hypoxia also on top of this impaired central perception in these patients though initial first two years there was a lot of people to talk about what is the mechanism nobody knew everybody was guessing but not to some extent we know that this was through the impairment of the perception of hypoxia that the patient felt happy he was not happy but he felt comfortable despite being hypoxia so this late perception despite low oxygenation both in the lung and the peripheral was responsible for hypoxia it's not actually happy because it does not warn you and it just kills you so it's actually dangerous thank you sir a question from dr chaitanya sir pathognomic signs and symptoms to differentiate between cardiac and respiratory dysmenia i think i covered it but i believe i can revise it no problem so one is you look at so let me go back again from whenever you're asked go back to medical school and start from the name age sex you know those points that you remembered when in history taking so does name help you in this me or no it does age yes how again you go by age young child hypoxia test congenital heart disease not a congenital heart disease gender young female coming with tachypnea is in panic no so it's not cardiovascular elderly male past history of mi yes cardiovascular past is family history family history of anybody having asthma yes bronchitis childhood episodes of similar history in past yes bronchitis seasonal variation does it always happen in winter yes again bronchial asthma doesn't happen in past has it happened now had an angioplasty a few months back cardiovascular dysphonia so you start right from the history then come to your important things which is your examination and which i said again again two important things as i mentioned dyspnea precedes cough and cough procedure usually as i said in cardiovascular because of the mechanisms that i already explained first you will feel dyspnea because of the eq mismatch in the lung and then the spillover into the alveoli of the flooded lungs will give rise to pink frothy sputum and hence the pink rock this time we'll have to the cough later on so fast then caught in cardiovascular in bronchial asthma you have a small infection or an irritant or a gas or a smell or something which gives rise to first the cough and then the bronchospasm leading to this nearby so what proceeds what and then sympathetic tone increased heart rate cold calming spin hypertension or hypotension all will favor cardiovascular etiology apart from and then of course crepes and bronchi s3 if you can hear it thank you sir thank you for beautifully explaining as to us again uh so we have a question from dr thakur uh how effective is hyperbaric oxygen therapy in acute disney and your thoughts on the matter so hyperbaric uh actually if you remember there are two mechanisms of acute oxygen damage to the lung and chronic oxygen damage to the lungs so don't chase hot for lungs for limbs it's good for gangrenes it's good for cases it is good but for acute dyspnea of respiratory or cardiovascular hyperbolic is no no there is something called as acute oxygen injury and there is something called as chronic oxygen injury oxygen can itself damage lung some of times permanently so oxygen is not all all good it has got its own problems hyperbaric oxygen only in selective cases don't change it and if you give hundred percent oxygen for an etiology your first six hours you should try to taper it off as quickly as you can thank you sir so could we take a couple more questions if that's all right yeah sure yes uh so we have dr said says excellent explanation dr ashok is asking the relevance or importance of six minutes walk test especially in ilt or incipient heart failure good question six minute walk test is very often used in pulmonary hypertension in patients with pph even in heart failure for rehabilitation it can be used in interstitial lung disease and in c respiratory etiology to quantify how much improvement the patient is taking place but there are better questionnaires also available if patient cannot walk into a minnesota heart failure yeah there is which is called there is a quality life kccq canon cancer city quality life questionnaire so these are more simple questions if the patient cannot you don't have because six minute walk test has its own rule you need a single straight corridor with at least 30 feet length i don't know how many of you can afford that kind of a clinic where you can have a 30 feet in single corridor where the patient can walk uninterrupted in a dedicated staff looking at the stopwatch and counting what number of steps he takes or what distance he covers so six minute walk is a good test especially in pulmonary hypertension pph patients but otherwise i think you can restrict to quality life question and they're easier to do thanks sir we'll just take one more question so indications for bipap at home for uh hf patient not a good idea if you need a pipe for heart failure it's not a good idea because if your heart failure it can surely be managed with novel therapies it means there is enough or extra fluid in the lung you need bypass for respiratory obstructive etc etc for heart failure if you're requiring cpap means you are under filtrated under diures you are having more amount of fluid and this surely can be managed so bipep at home for heart failure refractory heart failure maybe more of inotropes may be more of iv diuretics but not a bypass but if you do end up that then maybe this patient needs to undergo an evaluation of our transplant because that that will not pull out for much longer because that's not a disorder like lung where you can you know continue a bypass overnight like in osa forever but you need to actually get off by preparing a card patient who is a cardiac failure and requires bypass so that needs evaluation you need to cross check revaluate are you really dealing with heart failure if it's because of heart failure what's the problem with the treatment and if the treatment is adequate until the patient is feeling the same then i think we need to optimize and enroll him for maybe heart study thank you so much sir we have a comment from dr eunice uh who says explain each and every question very nicely so humble and god bless you thank you so much wish you all we thoroughly enjoyed the session looking forward to your next session on heart failure so would you like to see a couple of words in it yeah so yeah i think uh now now that i have touched upon how you arrive at your diagnosis i'm going to teach you in the next class which is two weeks from now you can book yourself away so this i kept at nine because uh she was saying that it's going to take more hits but i believe i've preserved enough seats now for seven thirty five people in the lecture so it should not be a problem so i have i'm going to take you through heart failure we'll discuss the basics management strategies and the future that is there and this would include your new mcqs for your neet preparation also and your exit exam also and your entrance exam also so i'll try to cover that aspect here this lecture i wanted to focus on your clinical assessment how you manage a patient when actually you see a patient no marks for writing a full question yes so that's awesome doctors make sure you rsvp for the coming session uh so it is on heart failure it is a 19th may 7 30 p.m please go to the homepage rsvp for it i am sure you all wouldn't want to miss this as well and i would request them also to subscribe to the club that i own which is two of the clubs where one we used to do debates which i believe will pick up again because of the kovitz and the other clinical actions that we had uh we were doing more of that and but i believe uh on the request of netflix i've gone to this time and but i think we can have the debate things happening in future and maybe we may have some more lectures in the other cardiovascular update club as well sure sir we'll make note of that thank you so much once again for joining us thank you uh doctor yeah thank you for joining us we do have a couple of questions perhaps we could detect them for the heart failure session because it is on that topic yeah will be a pleasure thank you very much thank you bye-bye everyone nice to be connected with all of you looking forward to have you again take care bye-bye good night good night

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dr. Kamal Sharma

Dr. Kamal Sharma

Chief of Interventional Cardiology, SAL Hospital | Author | Researcher | Innovator

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dr. Kamal Sharma

Dr. Kamal Sharma

Chief of Interventional Cardiology, SAL Hospi...

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