Cardiac Tamponade - Causes, Symptoms & Treatment.

right so today we are going to talk about cardiac tamponade already we had a very detailed lecture and on the topic of acute pericarditis right and now we will talk about cardiac tamponade now what is cardiac tamponade let me draw me a diagram first actually cardiac tamponade is the condition in which fluid is accumulated in pericardial sac under pressure under pressure is the real thing what is there fluid is accumulated in the pericardial sac so this is pericardial effusion but pericardial effusion result so much pressure on the cardiac chambers that it obstruct the inflow of blood to the heart right let me make it a very simple diagram let's suppose here lies your heart suppose this is the normal heart with some very simple diagram right heart should be simple anyway clever heart subproblems so it's a simple heart now what really happens that if there is fluid in pericardium and and this fluid in the pericardium develops so much pressure if there is if there is so much pressure that it compresses the heart in such a manner that venous filling is obstructed right for example here the venous feeling is coming right and here there is so much pressure that venous blood cannot be filled in the ventricles properly right or cardiac filling is compromised and of course if there's fluid accumulated and it builds so much pressure I'm not talking about amount of the fluid I'm talking about the pressure of the fluid this is very important if it produces so much pressure that it strangle a it's the heart it strangle a it's the cardio chamber and intra pericardial pressure is more than the filling pressures in heart different Rothery cardial pressure is more than the filling pressures of the heart then cardiac filling will be compromised and you know heart is a pump if you cannot fill in can you get out so what really happens that if venous return to the heart is compromised and heart is not filling then cardiac output will drop if you are not putting the blood in from where you will get the blood out you are getting it so what really happens that cardiac output will drop and we say that patient's hemodynamic stability will be lost and when who the situation develop we say there is cardiac tamponade and I want to make it clear many times patient has pericardial effusion but pericardial effusion does not exert enough pressure to strangulate the heart then it is not tamponade listen carefully if a patient has pericardial effusion let's suppose this is a another this patient also gonna spell card in effusion but a few years is a sort of Lex Lex of Union it is not enough pressure to strangulate the heart then it will be called called pericardial effusion but it should not be called cardiac tamponade so what I am trying to tell first of all what is very hard Ella feel excessive fluid in pericardial sac right normally 30 to 50 ml fluid is there but when there's excessive fluid in pericardial sac with a pericardial effusion is there but every case of pericardial effusion is not cardiac tamponade cardiac tamponade is said to be present only when intra pericardial pressures due to a few Yin become more than the filling pressure the ventricles and ventricular filling is compromised into hemodynamic and stability in the patient am i clear now question is this that this condition cardiac tamponade this is medical emergency because mo dynamic situation is not stable heart is not getting enough blood and it's not maintaining its cardiac output appropriately it's a medical emergency so rapid and correct diagnosis is must it saves life rapid diagnosis and correct diagnosis there's a must right if you miss this temperate case maybe you will be losing the patient you are getting yet this is one cause of shock which is very different cardiac tamponade is one cause of shock which is treatable sometimes only just doing the pericardiocentisis can relieve later on I will tell you there are a few exceptions where you don't do pericardial sentences in cardiac tamponade but mean most of the patient with cardiac tamponade if you draw the fluid out you can do leave the patient at least for a while depending on the underlying causes those are right so it's a medical emergency right it's for one cause of shock which is treatable that is where I'm stressing so much on this disease you can save the life with the rapid correct and prompt you can say right diagnosis now so no question is that that it's diagnosis is clinical right echocardiography is the confirmatory test again I will repeat it you diagnosed this patient on the bedside with signs and symptoms history signs and symptoms a good doctor must be able to make a diagnosis of tamponade is there a right later on if there is not extreme urgency you can do the echocardiography and echocardiography can from your clinical diagnosis or reject but that is later on is that right so let's talk about that first of all how much fluid should be there to produce tamponade how much pericardial fluid should be there to produce tamponade answer is that is really not the amount of fluid actually in to tell it temperate will be there or not in a patient with pericardial effusion it depends on three factors right number one it depends on amount of fluid of course when amount of fluid is more here pressure will go into a very idle mode but more important than amount is the rapidity with which fluid is accumulated repiy detail the rapidity the speed with which fluid is accumulating the fluid is accumulating very gradually the fluid is accumulating very good gradually then pericardium will stretch out what will happen very cardem will stretch out and if pericardium stretches out then intra pericardial pressure does not raise this rapidly the fluid is accumulating slowly then pericardium is trying to stretch out right and if pericardium keep on stretching out and fluid is accumulating slowly then entropy recording pressure will rise very slowly and maybe lot of fluid is accumulated before the empanelled develop before the hemodynamic instability develop sometimes up to two little fluid is accumulated and after that temperature ah but but if fluid is accumulating very rapidly the fluid is accumulating very rapidly then pericardium does not have time to stretch out and if pericardium does not stretch out this is the rapid fluid accumulation even small amount of fluid like 100 to 200 ml fluid is enough to strangulate your heart you get it so what I'm saying this it is not only the amount it is all that also that how fast or slow pericardial effusion is developing and third factor of courses that compliance compliance which is a measure of stretch ability if pericardium is very stiff of course when it little fluid will produce the tamponade but if it is stretchable then what will happen you will larger amount of fluid may not raise the pressure so much so basically primarily there are three things how much fluid is there what is the rate of accumulation of fluid and what is that compliance these three factors interact with each other to produce the tamponade right in the end what matters is not amount what really matters is improv pericardial pressure what is that intra peri Cardinal pressure right if it is more than 15 millimeter of mercury it definitely needs to dampen it why because when pressure here become more than 15 millimeters of mercury it is more than the filling pressures am i right yeah and if pressure here is more than 15 millimeters of mercury tamponade features start developing am i clear right now let's talk about or have pretty simulation of fluid and one of the puzzles and solo accumulation of fluid and what are the causes if there's rapid accumulation then what happens this is sort of a cube situation so cardiac tamponade may be acute or it may be sub acute or chronic sub acute or chronic in the Q cases there is rapid accumulation and sometimes 100 to 200 ml fluid is enough to produce tamponade in the sub acute or chronic cases sometimes up to two liter 2000 ml fluid needs to be cumulated before enough pericardial pressure is there to produce I'm atler now the causes of acute very rapidly developing cardiac tamponade yes who'll tell me the causes of very rapidly developing tamponade due to some reason very very rapidly fluid is accumulating within the pericardial sac first you should not forget free wall rupture of the ventricles right trauma just from I yes very good we can cook like stab wound in the chest right a rupture of the free wall of the heart and blood definitely pours out into pericardial sac so we can say trauma chest from of course right chest trauma leading to the picture of the damage to the coronary artery or damage to the root of a or at all damage to the free wall of that what is this ventricles or atrium and blood accumulates into pericardial sac that will lead to rapid company other call other cause of rapid accumulation of fluid is a section of your eye but before that I would love to mention post and my free wall rupture post myocardial infarction free wall rupture free wall rupture what I really mean that here is your beautiful heart right and unfortunately if someone run up myocardial infarction and here is your pericardium right and if this piece of this area instructed area you know after a few days of infraction it becomes solved right if this area becomes soft and it ruptures the blood may pour into and this bleeding may accumulate rapidly where in the pericardium right and this accumulation can also lead to temper night but remember this is one case of tamponade where you will not Esprit the fluid because if you will not do the pericardial synthesis pericardiocentisis processes you pass a needle to the pericardium and aspirate the fluid out right here if you spread the blood out more blood will come there so this is one contraindication for yes yes very card your sentences because every doctor whenever you think of cardiac tamponade he thinks of you should bring the needle and push it and get everything out that is every doctor good doctor should know that what is the underlying cause maybe myocardial rupture another cause is dissection of Europa actually more specifically dissection in the root of your aortic dissection he or take dissection now what really happens in your attic dissection this is your aorta here is your pericardium as you know that the Ricardian is around all the great great vessels of the heart and this is pericardial sac do the favored tiles in the pericardial sac now let me make this is a your attic valve of course let me make that eurotech wall little thickened right this is the wall of a or da sometimes when there's dissection of a rota right for example if there's a section here then blood this is blood blood which should normally travel in the lumen of your da it punctures the wall of your toy and enter them to wall of Europa and then it tracks within the wall it tracks within the wall of your da if blood enters into wall of the outer on tracking sometimes this ruptures outward and then blood goes into pericardium let me make more clear diagram that here is yota okay and I'm just going to make let's suppose this is blood and blood is going right it's a very simple diagram and here is what pericardial sac I have removed the I'm not showing the right right side of heart now what really happens that if there's a tear here and through this T our blood tracks into wall of your aorta and it may go antic antegrade or it may cut the wall of your toilet ro grade and then if it opens Outworld right blood will come into pericardial sac and very rapidly pericardial sac will be full of blood and of course you do to the rapid accumulation there's not enough time to stretch out the pericardium so intra pericardial pressure will go up and strangulate the heart and cardiac tamponade will develop but again this is another case of cardiac tamponade in which you will not do pericardiocentisis why because again more blood you spread more blood will come here and patient will go to shock you are under straining me right in such cases where this free wall rupture or is a or attic dissection right in such cases if by mistake you put a needle there the blood will come out which is bright red right it is oxygenated blood right secondly it will clot yeah right here also you should not do pericardial sentences here also you should not do pericardiocentisis does that right in this cases the right approach will be while trying to stabilize the patient medically you take it for thoracotomy right and then expert cardiologists or cardiac surgeon or cardiothoracic surgeon should deal with the situation right so these are two cases where you should know the question is that that these are the acute or very rapidly accumulating fluids like trauma post and my free wall rupture or aortic dissection and if you go for chronic accumulation as I told you gradually developing pericardial effusion which leads to infinite when there is lot of fluid accumulated up to one liter or one and a half litter or two later right classical example here will be new play the iron tuberculosis neoplasia and tuberculosis right new plays and tuberculosis then there are other causes of cardiac tamponade there are so many causes I will just mention some other important causes of tamponade one more important cause of cardio tamponade is idiopathic pericarditis idiopathic very hard itis now idiopathic pericarditis is usually not always doodly repeated attacks of viral pericarditis and eventually where we cannot find the cause of pericarditis with routine investigation of course sometimes you bring the CIA to investigate maybe they will find a reason right but what I'm trying to tell you that with routine investigation if you cannot find the cause of pericarditis usually it is viral we think this is idiopathic pericarditis and some people unfortunately when they repeatedly suffer video Pathak pericarditis they eventually may go into cardiac tamponade or they may go first of course they go into situation of pericardial effusion and then eventually they may end up into pericardial tamponade or some of these patient end up with constrictive pericarditis which we will discuss in the next lecture so then there are other causes some other causes of bleeding empirical cardio sac bleeding in pericardial sac already we have said that bleeding may be due to these three causes like trauma post am i free one capture your dick dissection but a very important cause of bleeding in pericardial sac which may lead to tamponade is post cardiac operations or post cardiac interventions especially in modern world it is one of the very important group of patients where you have done some sort of cardiac surgery right and after that right bleeding occurs within the pericardial sac and this is a dangerous bleeding because bleeding is occurring in too limited space and it was blood will accumulate and again strangulate the heart so bleeding may be traumatic may be free wall rupture may be stab injury but more importantly you must remember that post cardiac operations or post cardiac interventions is that right bleeding can occur cardiac operations then sometimes we have done a big mistake patient with acute pericarditis don't give them anticoagulants patient with acute pericarditis acute pericarditis if you give them an to Toa balance they may bleed to death they will bleed into pericardial sac and if not diagnosed in time and managed it was strangled at the heart lead to tamponade cardiogenic shock and death anticoagulants why I'm trying to put into my students mind that in acute pericarditis be careful to give anticoagulants the reason being sometimes as I mentioned in previous lecture yet acute pericarditis present with ischemic leg pain even though classically the pain of a beautifui carditis is central chest pain which is sharp and steppin and localized you are getting it but sometimes acute pericarditis pain will be dull and diffuse and pressure like so dr. may confuse the Spain as an ischemic pain and given to coagulant and that will lead to hemorrhagic bleeding in the pericardial sac and rapidly developing temper Nate why sometimes as I mentioned in the previous lecture why in acute pericarditis sometimes pain is like myocardial pain not pericardial pain because sometimes in Furman acute pericardial information right what really happens that chemical mediators of inflammation present in the pericardial layers and pericardial sac may diffuse into EPI myocardium and lead to inflammation and injury to open myocardium and if EPI myocardium becomes injured as a part of acute pericarditis that will present clinical clinically with the pain which is like my idol in GDP nor dull diffuse and pressure like me you know wait like you know compressing piano squeezing pain you know all those pains of art right okay am i clear then we come to some other causes of pericarditis of course suppurative pericarditis which can lead to superlative pericarditis and if it is not treated and pericardial effusion is not drained right it may lead to tamponade right suppurative pericarditis and then there is something renal failure renal failure renal failure that is uremic pericarditis right Jewry McMurray creditors then that can also end up in - what happen I remember Julie McMurray carditis may be painful maybe PMS right but it can also end up into more often can you tell me another pericarditis which can be painless one is uremic pericarditis tell me just one more cause Nia plays yeah yes - Burke lesson Nia plays yeah very good neoplasia tuberculosis we have written here right so these are some other causes of cardiac tamponade but now I will go to clinical presentation which was the real thing to understand for a good doctor now you I really need all your attention yet clinically how a patient with cardiac tamponade present right when we talk about clinical presentation usually doctors good doctors think about Bextra Jade Beck's prayut doctor back in nineteen nineteen thirties he told that if someone has these three features you need to rule out cardiac tamponade back strangle right now what is Becks triangle let me make it here right a patient who comes with rising jugular venous pressure falling blood pressure and muffled heart sounds muffled heart sounds or soft heart sounds or absent heart song right if a patient come with rising jvp falling systemic arterial blood pressure and the muffled heart sounds you think of what cardiac tamponade remember this classical presentation is more common in patient with acute tamponade because in the toutes pericardial tamponade hemodynamic stability 'he's been lost very rapidly and these chains are showing then system is patients cardiovascular system is not stable this is right now let me explain properly step by step out of these three signs of course this is a sign right leaving jvp changes in geography changes in blood pressure of course I will tell you later okay let me tell you right now I will explain it in detail there is number one jugular venous pressure is very high number two pattern or jugular vein is waveform or pattern in the jugular vein is change as I will explain in few minutes that there is yes there is lost why descent I will explain why right there is lost why descend and there is sharp you can say sharp X descent I will explain what I really mean by this right so actually jeweler venous pressure goes up with lost Y descent and sharp X descent right this is the most sensitive sign of what cardiac tamponade it's the most sensitive sign of cardiac tamponade then there is fallen blood pressure there is fallen systemic arterial blood pressure with paradoxical pulse with para doc sickle pulse or pulsus paradoxus right again I will explain what is pulsus paradoxus alright and when you see there when you hear that they are muffled heart sound usually with soft epic speed there is soft apex beat or absent effects beat right but classical features are three rising you be following blood pressure with muffled heart from the soft heart sounds now let me first explain jugular venous pressure and a patient with cardiac tamponade what happens to jvp stand for jugular venous pressure and gvp also stands for jugular venous pulse so when we are talking about jvp we must talk about the pressure is it normal or not and we should also talk about the pulse pattern that is normal or not right now let me explain first normal doula venous pred a waveform and then what happens in cardiac tamponade right so now be attentive try to understand with both ears and your hemisphere I mean cerebral hemispheres AHA yes let me draw the jewel of Venus this is normal jeweler Venus pressing right actually this is also central venous pressure pressing because jubler venous pressure which is here and pulse form right that reflects that she pressure changes in the right atrium because right atrium spirulina KY and eventually internal jugular vein there are no valves in between so because there are no valves in between right so whatever pressure changes come into right atrium right they are faithfully usually faithfully reflected in internal jugular vein pressure and waveform right let me draw here the right heart that right and here is let's pose is I'm not going to details we have in a caveman eventually you can say here is your what internal jugular vein now individual away and you can say if there's a balloon here and there's a pointer here and there's a pointer here and it is connected with eventually with what is your right heart right now that changes now imagine there is a paper moving under this pointer there's a balloon here so here is your blood okay I will make the balloon color and pointed different just imagine there is a device which measures the pressure here now when pressure changes will occur into right atrium they will be reflected on the back so we can say internal jugular vein is a sort of manometer or hygrometer attached with the right atrium now this ball will move and pointer will move and we can get the tracing even clinically we can see is there right now what really happens imagine start with this atria contract atrial contraction then atrium contract pressure goes up so this will move Lido up and it will little up then pressing will go up and this is called a wave what is this a wave when you trim contracts those are right a wave is formed after that what will happen atrial systole will be terminated and what will happen yes this valve will open or close atrial contraction fluid has come here after that ventricular contraction will start let me tell you at the end of the atrial systole blood has been filled into ventricle then ventricular systole will start right when ventricular systole will start this valve will close tricuspid valve will close so that blood does not go back it moves forward right now when it reacts in pressure went up a wave is formed and when it just started relaxing pressure was going down but suddenly ventricular contraction started when ventricle contraction started this valve closed when this valve closed there's a little jerk here the valve will little bit move when this valve closed right little jerk after that atrium ventricle are not connected with each other because of the closure of the valve now whatever happened to ventricle we are not worried now we have seen what is happen in atrium what is happening now in to atrium it will progressively relaxing when atrium is relaxing you are understanding when atrium is relaxing of course blood will come down and pressure will come down this isn't right this pressure which is coming down due to atrial relaxation this pressure is called what is this X descent what does it called X descent does that right after that what happens when it was relaxed it was progressively relaxing more and more blood was coming and accumulating into that eventually a time will come that valve is still closed and it clears completely full now more venous return is coming now this more venous return which is coming and it has no more relaxing cumulation of blood will slightly take the pressure up this pressure up world is due to venous blood accumulating here we call it V wave what we call it V wave and this jerk which came here due to closure of this value is see wave so here let me repeat it that what really happens it Ria's atrial contraction a wave it just start relaxing but ventricular contraction closes the tricuspid valve and C wave then a tree are keep on relaxing and X descend pressure keep on going down when it becomes full more blood is coming and now it starts flow floating upward venous accumulation V wave eventually this whale will yes will open and when this valve will open the simulated blood will fall eventually when this valve will open then atrial diastole is still going on ventricle has completed its systole and now ventricular diastole or relaxation start and as soon as ventricular relaxation start what will happen this valve will open and as soon as this valve open thus accumulated blood will fall here right because in ventricles laughs intraventricular pressures are very low as soon as intraventricular pressure are lower become becomes lower than de and hydro pressure ventricular filling will occur when the ventricular filling will occur then what will happen that this blood which is accumulated here as this blood will go down this will again go down this ventricular filling or more appropriately atrial emptying atrial emptying immediately after valve opening or when cutolo filling immediately after the valve opening takes the whole Venus column down and this is presented as pressure also going down and this downward going is called wire descent what is it called Y descent right y descent occur during early - play early - lee of ventricle immediately after opening of the tricuspid valve immaculee now we see in these patient what really happen in this patient now again I will just repeat that you can repeat with me again next atrial contraction ventricular contraction valve closure right this is valve closure then the natural relaxation X percent and then Venus accumulation and then ventricular early early diastolic ventricular filling due to opening of tricuspid valve so what is this this is again why descent this is also why descent now after this basic understanding now we come a patient with cardiac tamponade what changes in doodler venous pressure welcome now we'll talk about a patient with cardiac tamponade now imagine that this fluid accumulated here and this is your cardiac situation right stimulated and here was your what was this internal jugular venous system okay now pressure from here what will happen to these situations first of all when it is being strangulated blood will pool behind that will accumulate here and this ball will go a higher level so total Google I'm not talking about waves now talking about the pressure suppose here was the pressure that was three centimeter above the angle of Luis or sternum on Abril joined at 45 angle right as but as temperate start right venous blood which is coming from head and neck it cannot enter here any doctor because it cannot enter here so blood start accumulating so this point will shift upward in the pressure scale right so first thing will happen here that jubler venous prep pattern will go up I'm just trying now the jubler venous pressure has gone up no I'm not going to show other changes just I will show that this whole pattern has gone up this isn't right if simply this pattern go up we say there is raised jugular venous pressure and due to this pressure neck veins will look distended veins will be obvious as distended waves so we will also say that there is jugular venous distention right and play - we call it plateau of this as raised due to pressure now we come to what waveform will be chained we said there will be sharp X descent and there will be loss of Y descent loss of Y descent is more strongly associated with it and I want my students to understand very clearly why why the center is lost because so very very sensitive sign you may not observe very well here but with central venous straight line tracing or right atrial pressure tracing you can see it very clearly that Y of Y descent is blunted or reduced or lost and in constrictive pericarditis when you compare the patient with cardiac tamponade with the patient of constrictive pericarditis one of the classical difference in the Y in case of cardiac tamponade Y descent become blunted I will explain why and in case of constrictive pericarditis why doesn't become very rapid and suddenly abruptly stop that I will explain later now let me explain why there's loss of Y descent right let me explain actually why why the original Y descent was there I told you in the beginning why doesn't occur when which we are open what is this valve opening tricuspid when tricuspid valve open and in early diastole pressure is very low so blood will rapidly enter his blood will enter here and it will come down and by descent will come now you imagine if there is cardiac tamponade is the cardiac tamponade then this will be pressing on the chamber and if it is pressing on the chamber now you imagine if the fluid is pressing here you are understanding do you think when this valve will open it will be very low pressure chamber no again listen if okay just imagine here if they were temperate fluid here and pressing it too much and keeping it compressed when tricuspid valve will open can blood rapidly fall down no you seem intelligent let me repeat it listen carefully normally what happened that when this ventricle chamber open tricuspid valve open right it expanded into in diastole to expand into all directions and when pressure is low this blood will go down that is early diastolic filling early diastolic filling and when this is this blood is going and early diastolic filling is occurring right why doesn't come is it clear to everyone now you imagine here is tamponade here if tamponade is here then this unfortunate right ventricle is pressed it is sort of compression it has some sort of - trolley compression later on I will tell you this - this compression - fully compression also is seen on the echocardiography and help in diagnosis when this is compressing the chamber from the very beginning of - Lee there will be high pressure here from the very beginning of - Lee even in even in early - Lee of the ventricle pressure is high because there is high what enter a pericardial pressure compressing it and pressure to the high can this column fall even if this open so it will not fall so can to find out why descent No so this wild ascent will not be there now in this diagram normal wide ascent is shown here so this y descent will not be seen you will find that after the V wave this will move like that go directly to the it cannot descent down so why doesn't is lost here you understand it this Y descent which was supposed to be there it is not there and we wave directly goes to the a wave because still ventricle will be filled to some extent but under higher pressure so because pressure does not fall Y descent is not they are a my class so again in this case again this is the atrial contraction well Chloe our exit descent a trill relaxation venous accumulation you are getting it and then again well tricuspid valve opening and Y descent but can't this Y doesn't throw at you can blood go no so pressure will remain again like that so this is what is lost am i clear to everyone or only teaching myself enthusiastically so the classical feature is loss of Y descent and patient with cardiac tamponade now good doctor will say oh I know that is you will have energy suspension and there is dual venous pressure raised a very good doctor right who has practiced himself not only to look at the pressure because there are doctors around who cannot find where is the jugular venous where to look the jeweler venous pressure but if you are good you can find the pressure and one day you will become so good you may know how to look at the pulse pattern right and in this case normally you have two pulse pattern a/c is usually not visible here so you find it goes up down up down the second down is lost right so this can be so first mechanism I told you number one Google Irwin jvp what are the changes number one player goes up total pressure goes up number two the loss of white descendants I am a clear there's no question but there is no problem with the EX descent why the exodus enters there let me repeat it reconducted I'm going to normal what are they what is this now it real start relaxing when it really relaxing here the valve closed and now as soon as this valve closed I'm talking about now ex descent how it is produced this valve is closed but because it really relaxed in blood column is still coming down so what is this ex descent is that right now this ex descent now listen carefully this even becomes sharp sharp mean that yes there is ex descent this is right rather than it becoming like this it become more sharp and even deeper there right why because there's a high pressure of blood here which eventually fill it while it is relaxing because pressure the jubler system is gone am i clear but really what you need to understand and remember only two things in googler Venus jvp number one patient with tamponade dougela venous pressure is going up and number two if you're very good you will find why descent is lost am i clear after descent this small thing may be seen in there tracings or central venous pressure but cannot be clinically detected was very difficult I am at left so this was about the jugular venous and jugular venous pressure changes are the most sensitive sign about what cardiac tamponade and now we come to the blood pressure yes okay before that we talk about the muffled heart sound there's not much explanation for that it's very easy to understand that is lot of fluid is there and you are putting this chest wall and then put the stethoscope heart is far away from your that'sa scope they're farmer Bell and you cannot hear that hard sounds very well right and secondly when hard is compressed it's really not beating very ha very hardly and not producing so my sound number one it is less sound II and number two it is away from our hearings mechanism so hard sounds maybe softer muffled or may disappear and of course at that time if you try to find the apex beat because there's a lot of fluid between the apex of the left ventricle and your chest wall right beat may not be transmitted well so there will be loss of FX beat are very weak and FX beat am i clear so this is done with the primer this part of triangle now we have to talk about this part of triangle that there is falling blood pressure and eventually pulsus paradoxus appear rather I will discuss in detail pulsus paradoxus later right now I will tell you why the blood pressure Falls it's very easy to understand that what really happens in this patient patient with cardiac tamponade let me draw a other diagram to explain how the systemic arterial blood pressure drops systemic arterial blood pressure drops it's about the basic hemodynamics let's I will draw only the left heart and their tamponade diagram right okay this is cardiac pericardial fluid now this is pressing here and it is also pressing here and as I told you if pressure here is more than the filling pressures of course here is the systemic venous pressure coming and here is pulmonary venous pressure coming because here the blood which is returning from the lungs those are right now if pressure here are higher of course venous return cannot be maintained very well right well so what really happens there due to higher diastolic pressures because when when to go the left we call it diastolic pressure and actually pressure should be very low so that blood can come and accumulate here and later on it can pop out but what really happens because it is being soaked wheezed from outside or strangulated from outside so pressure inside the ventricle even during what - means higher because pressure is higher so venous return becomes wrong so we can say that sequence of events s number 1s as there is increased intra is Perry cardial pressure when there is increase in properly cardial pressure that will lead to yes decrease ventricular filling and that will lead to decreased end diastolic volume when ventricular filling will become less at the end of the - li total volume here will be less and if end-diastolic volume is less of course and diastolic pressure is also less and secondly when there is under filling of it can it stretch the myocardium if okay leave it and actually qalam is less and when entire Olek volume is less when volume is less change stretch the myocardium valve know now according to Frank Starling law all of you know more you within physiological limit more you stretch the myocardium or it contract less you stretch less contract is very simple it's like elastic you know women know very well right so what happened that's like elastic within physiological limit more stretch more it snaps back so how does something like that right so frank-starling loss when you are under filling it it is under stretching so what will happen and actually volume is less so that will end up and to decrease myocardial stretch when my body stretch become less there is decrease myocardial contractility and when contractility is less then what will happen to stroke volumes stroke volume is less and stroke volume is less than cardiac output is less and that will lead to drop in systolic blood pressure right so as in a patient with cardiac tamponade more and more fluid accumulate and more and more entropy pericardial pressure goes up right that will lead to keep on reducing the ventricular filling and that will keep on reducing and diastolic volume and myocardial stretch and contractility will become less stroke volume will become less and eventually that will translate into dropping blood pressure am i cleared everyone now of course when your blood pressure drop significantly what happens sympathetic overflow occurs compensating mechanism come into action and you develop tachycardia is there too or not so actually there will be tacky cardia even due to anxiety another reason patient will develop tachypnea also and even des Nia so tachypneic and dekap knee I mean increase respiratory rate take opinion tachycardia and sort of anxious look cold clammy hands cold nose or peripheral parts of the body these are features of shock you are getting it tachycardia is very important technique ideas known of course specific for a tamponade tachycardia occurs in so many conditions but there is something very important in write it down if there is no tachycardia there is no tamponade except two or three conditions if there is no tachycardia patient doesn't have tamponade if jvp is not distracted your diagnosis is wrong it is not tamponade am i clear why the reason being when this tamponade hemodynamic disturbances so grave that sympathetic overflow should occur and compensatory mechanisms should come into play and tachycardia must be there so if there is no tiny cardi up there is no temperate except two or three exceptions for example those patient of tamponade who have rural pericardial effusion due to mix edema due to hypothyroidism of course a patient with hypothyroidism as hard rate of 50 he will also get little sympathetic overflow is harder it will become 17 but it will look like normal there is no tachycardia another exception you should remember I'm stressing again if there's no die cardia there's no tamponade right if there's no jugular venous changes there is no tamponade but there are few conditions a very good doctor will be alert there sometimes there may be patient with temper night but no tachycardia classical example is patient talk temperate with mixed edema another classical example is M finaid with uremia you know you really also produce bradycardia and hard blocks good doctor should be knowing it doctor if sahar right so what happens if a patient is transferred from nephrology war is uremic and having a sort of pericardial effusion and even some features of hemodynamic instability are there even clinically or echocardiographic le but tachycardia may not be there is that right third of course any patient due to any other reason who is on beta blockers right and then classical cause patient is unfortunately just about to die in very terminal cases and patient reached to you very late is all unfortunately with very grave tamponade patient may still have unfortunately he isn't bradycardia not technically so told you four condition first the basic rule the synchronous spell is what the sequence follows that if no tachycardia no temperate no tachycardia no tamponade but four conditions a very good doctor will keep in mind is there a patient has temporary due to mix edema tachycardia may not be there or with uremia tachycardia may not be there or due to some other reason if patient is on some beta blocker type drug which tachycardia may not be there and if unfortunately patient is in very terminal state and very terminal stage produces cardio suppressants and tachycardia doesn't occur am i clear what is left here to discuss the paradoxical pulse it is so important it's a very very important clue to the cardiac tamponade I will discuss that into detail but before I leave this part of the lecture I would say the classical Beck Beck's triangle backed by aid this classical back tired of signs and symptoms or you can say this clinical situation classically is seen in acute tamponade in which there is rapid deterioration in hemodynamic parameters but it is chronic tamponade very slowly and gradually developing large effusion and very gradually you can say strangulating the neck with love will happen sometime right if that kind of situations there features of back triangle may not be very pronounced but features like heart failure may be there features like heart failure may be there right for example now again listen here is your heart and it is a very gradually developing sort of very long-term mild tamponade right it may have some features like cardiac failure it is right now these are the pressures and very slow very mild pressures mildly disturbing the compress in the heart in this case of course when there's more pressure on the right side for a long time do Levinas pulse will be chronically elevated even central venous pressure will be elevated and then you know hepatic means can't drain well and that will lead to again what will happen can the blood drain from portal system to this No so because it is being compressed for a long time right so due to chronic elevation of central venous pressures back pressure to the what is the same level may lead to a plateau mughelli may lead to ascites even because of the hydrostatic pressure elevated in all Tripoli's in the body may lead to systemic edema mild with that if left side is unable to receive the blood that pressure to the lungs will lead to yes pulse it will really not lead to frank pulmonary edema will not be there right the but we can say that there will be congestion the vessels in the lungs right and that will eventually translate to some degree of dis Nia remember this knee other very important feature of tamponade so there may be days Nia calf orthopnea or throught Nia's worse Disney or worsening on line just line up or down Lange's point okay that's right thanks fine okay so there may be sort of features of biventricular failure from left-side feature maybe just like how far Desna are orthopnea with forward failure there may be fatigue you know weakness and here there may be a participant in um a gala with societies with little generalized edema but this type of situation is seen in sub acute or chronic tamponade so we can say in a very cute tamponade you will find the classical backs triangle but in sub acute or chronic tamponade there may be some mild features of X triangle right with that there will be some features like heart failure a mcclure now in these patients who come with the tamponade what other clinical features can be appreciated what other clinical features may be there as I have discussed up to now only I talked about those clinical features which developed due to chemo dynamic instability but of course there may be clinical features due to underlying cause for example if someone develop tamponade due to tuberculosis he may have clinical features of tuberculosis also weight loss or night sweats or night sweats remind me something yes night sweats low-grade fever anorexia you are getting it or if he developed let's pose tamponade due to uremia he may have some features of course other features related with renal failure so what I'm saying or he developed just you to a acute pericarditis due to what is this SLE so the features of SLE will be there systemic lupus so what I'm trying to say if a patient come with tamponade first of all to be sure the patient really has temperate or not you have to demonstrate clinically that hemodynamics system is undergoing destabilization with rising JQ following blood pressure and and muffled heart sound and if it is chronic then features like heart failure should be there but with that whatever is the real underlying cause of pericardial effusion features of that may be there right and then many of these patient have developed tamponade due to acute pericarditis due to so features of acute pericarditis may also be there so we can say that total features which should be probably may be present in these patient number one category is features due to hemodynamic instability which include the Becks triangle and in chronic cases failure features like failure secondly signs and symptoms of underlying cause of pericarditis underlying cause of pericarditis because first there have to be a disease produce pericarditis like first diseases for example tuberculosis which lead to pericarditis in some patient and in some more patient with tuberculous pericarditis tuberculosis even to a lab and in some more patient of young goes into tamponade so disease may be like this that primary cause primary cause then it may lead to parry card itis that may lead to pleural pericardial effusion and some of these patient develops tamponade so features of tamponade of course which is related to the plural of Ian may also be there right and it's not pericardial effusion please correct me if I'm wrong and then feature of acute pericarditis may be there and feature love underlying cause now features of acute pericarditis I told you in more dynamic instability features then clinical features related with the underlying cause and of key underlying cause should be a signs and symptoms of underlying cause etiology of acute pericarditis and features of acute pericarditis may be present in some of these patients right what will be the features of our underlying cause I told you as it depends on really underlying cause right if it is renal failure of course those features will be there if it is tuberculosis those features will be there if there is mix edema then hypothyroidism feature will be the earth then come features of acute pericarditis like chest pain right features of chest pain may be there I have discussed features over to Erica in previous lectures into detail right that the movie just mean but you should not forget that tuberculous neoplastic or genomic acute pericarditis maybe painless then pericardial rub can be there some most of the time as pericardial effusion enlarges pericardial rub disappear but in some patients it may be still there right then there may be ECG changes of acute pericarditis which I will discuss later that in the cute fairy cardiac test there is ST segment elevation and PR segment depression right which we have already discussed in previous lecture and then final feature of acute pericarditis with effusion with the fusion there is a feature called a wart sign that also we discussed in the previous lecture that in the left lung right sometimes pericardial effusion compresses is so much that lower part of the lung left lung become consolidated collapse right and then then this sound which is coming bronchial sound right it does it cannot divide into smaller pockets and become vesicular so it remain bronchial you are under straining again in some cases with the pericardial effusion right it may compress the left side of the middle part of the lung and this part of the lungs when it become consolidated right then bronchial sounds which are coming through bronchial tree cannot divide into this small area and convert into vehicular nature so bronchial song can be heard here we of course back of the chest at the angle of the scapula and there can be dullness to percussion this is right this is called a ward sign so what did I say that when we are talking about clinical presentation to talk about clinical features related with hemodynamic instability clinical features may be pointing towards the cute pericarditis and there may be clinical feature pointing towards the cause of acute pericarditis is that right a very good doctor has a responsibility to find all those things right then we'll go into detail of pulsus paradoxus as I told you with fallen blood pressure pulsus paradoxus is a very important clue to this condition right now what is pulsus paradoxus before any I go to the pulsus paradoxus I want to explain a very important physiological concept related with the respiratory cycle and arterial blood pressure and then I will tell what is pulsus paradoxus right now let me tell you that I'll draw it here blood pressure you know blood pressure if if you put a manometer in my brachial artery I hope this is a brachial or femoral brachial okay so brachial artery sometimes I forget anatomy right so a brachial artery if you put a manometer when heart contract pressure goes up that is systolic and then heart the relaxing went left tentacle is relaxing pressure when goes down it is called diastolic blood pressure so let's suppose my blood pressure is ideal even though I don't have many things the ideal but I'm happy with my life is true so what is there that system your blood pressure measurement the systemic arterial blood pressure it fluctuates like this it goes from 80 to 120 down now what is this this is systolic blood pressure then come - trolley then systolic then diastolic then systolic then - slowly right you understand it very clearly everyone understand now actually during the respiratory cycle this fluctuation in systolic blood pressure you must be knowing systolic blood pressure mainly depend on cardiac output if left ventricle is producing more cardiac output if left ventricle is producing more cardiac output systolic blood pressure will go up for example if my left heart more strongly contract right systolic blood pressure may go up right or if my left heart contact very weak then systolic blood pressure may be less than normal so what I'm saying the systolic blood pressure depends on the performance of the left ventricle systolic arterial blood pressure this is your left ventricle right this is the well now let me tell you what really happens during the respiratory cycle if there are changes basic concept if there changes in left ventricular output there will be changes in which pressure systolic blood pressure is that clear if there changes in cardiac output or left French because there will be changes in systolic blood pressure now we see during the respiratory cycle what really happens this is your chest right there from here lies your right heart and let's toes here is your left heart right okay let me make the septum were clearly this is left heart okay this is your right heart right now listen actually normally pericardium which is around it is there it is not it is filled with 30 to 50 ml fluid and not interfering with dynamics of the heart right and when the inspiration occur what happened first I will talk about when inspiration occur what happens when inspiration occur you know lungs are challenging or expanding now let's suppose this patient undergoing inspiratory process so naturally chest wall is expanding diaphragm is going down and in to excessive pressure is becoming more negative intrathoracic pressures become in more negative so that the air can be sucked in the purpose of when they affirm goes down and chest wall expand enter posteriorly and side-to-side laterally would happen intrathoracic pressure becomes negative when there is intraspecific pressure become more negative it sucks the air in it sucks the air and that is what we call inspiration that is what we call inspiration this is it right but with that it also sucked the systemic venous blood chest cavity the venous return from here and venous return coming from other speed of energy one few of energy white also become faster again listen during inspiration right chest is expanding thoracic cavity is expanding pressure intrathoracic pressure become negative as air is pulled in enlarging cavity and increased more negative intrathoracic pressure also pull the venous blood from spider vena cava and also venous blood from inferior vena cava so venous return to the right heart during inspiration is less or more more is that clear to everyone so venous return to the right heart during inspiration becomes more so when there is more blood coming here so - what largeman top right ventricle it is slightly over failed when right when tickle is slightly overfilled it will expand in all dimensions right ventricle will expand in all direction during inspiration it will expand in these directions free wall will expand as well as higher amount of blood will not only push these walls it will also push the septum also push the septum so during the spiration not only this extra amount of fluid which is accumulating here not only free wall move outward this free wall this will move outward this septum intrumental or septum is pushed versa left but this pushes very slight suppose this is the septum during inspiration it becomes slightly not very severely slightly deflected to the left so during inspiration due to the right / right side you - overfilling there's slight deflection to the left side so filling - left side will become slightly less this is one reason why during inspiration left-sided heart is slightly under fault there is another reason why left side is under failed during inspiration during the special lungs are expended during inspiration and spiritual lung they are spending and longer expanding the pulmonary circulation is compliant stretchable so when lungs are expanding not only air pockets expand but also vasculature of pulmonary vasculature also explained so capacity of pulmonary vasculature during inspiration become more or less more sweet become more capacity so it try to hold the blood during inspiration so blood from the lungs going to the left side of heart will be less or more less your understanding so during inspiration two things happen one thing is there is a negative intrathoracic pressure pull more blood to the right side of the heart and menticles overfilling slightly pushed the septum to the left and that make the left slightly under failed second reason is that in left side of the heart is receiving the blood coming from pulmonary circulation and as the lungs are expanding pulmonary circulation is compliant for every circulation expand and venous return to the left heart become less of course when venous return to left heart is less and also septum is slightly deflected there so this will be overfilled left side or under health yes so during inspiration right overfill and left under cells but still this can expand there is very slight movement of septum because expansion can occur in this direction and also in this direction now but in normal person right now when you go inspiration left side is under fill' of course end diastolic volume is less what will happen and actually pressure is less myocardial stretch from the left ventricle is less contractility is less stroke volume is less cardiac output is less and systolic blood pressure slightly draw this is physiological draw this is the logical drop in normal person with normal respiratory right healthy person during every inspiration left ventricle become slightly under filled and due to that reason cardiac output becomes slightly less and systolic blood pressure becomes slightly down during yes during inspiration and reverse will occur during exploration so we can say let's suppose this is inspiration right okay let's start the cycle with inspiration and let's start with exploration because it will become easier to explain in exploration opposite occur what will happen during exploration chest cavity is becoming smaller and trucks massive pressure is less negative right what will happen there Kable blood will be pulled less efficiently so venous return during expiration with Nas returned to the right side is less and because longer being aqueous during exploration venous return to left side is more and cardiac output during expiration becomes more and systolic blood pressure goes up now if you very carefully check the blood pressure during let's both this is 80 and this is 120 systolic blood pressure during exploration in spas if it is 80 120 during inspiration it will fall right during inspiration it will fall and in exploration again it will go up and then again inspiration it will fall and then exploration it will go ah and then in inspiration it will fall now this fall this inspiratory fall this inspiratory fall during inspiration this inspiration fall of systolic blood pressure do write and spirit Ori fall of systolic blood pressure if it is this fall is less than 10 millimeter of mercury it is a norm for example blood pressure during expiration is 120 by 80 and blood pressure during inspiration is suppose 114 by 80 how much is the defense six so this is normal so normal inspiratory drop and systolic blood pressure should not be more than ten millimeter of mercury is that right pardon can you say more loudly I will not talk about that later but if you really want to know what is the difference in diastolic the reason being during inspiration sympathetic slightly overflow occur a little technicality as there and arterioles constrict so - leak may go slightly change but right now in the explaining of pulsus paradoxus I will focus on systolic blood pressure so what we have learned up to now during expiration systolic blood pressure goes up and during aspiration systolic blood pressure come down in normal person and this difference should be less than 10 millimeter of mercury right then it is normal now what is pulsus paradoxus actually listen what is pulsus paradoxus pulsus paradoxus is our condition in which inspiratory drop and systolic blood pressure is more than 10 millimeter or monthly again repeat i will repeat what is pulsus paradoxus or paradoxical pulse paradoxical pulse is a situation in which in during inspiration systolic blood pressure drop or decrease more than 10 millimeter of mercury then we say there is pulsus paradoxus even though or another way to mention it is that pulsus paradoxus is a condition in which normal physiological drop and systolic blood pressure is the exaggerated normal physiological drop in systolic blood pressure is exaggerated beyond the normal image emmaclaire now so example classical example of this can be let's suppose this is another person in which systolic blood pressure is going like this normal tracing is going like this but here it becomes like this here it was 120 by 80 during expression and if there is pulsus paradoxus I will explain why poses paradox is developed just in two minutes for first lesson what is pulsus paradoxus pulsus paradoxus condition there during inspiration the drop which is supposed to be less than 10 millimeter it is too much a drop rather than here was normal person I am just giving an example it was 120 and it was 114 or 110 then it is horrible but if this is 120 and this is let's suppose it is 100 systolic blood pressure right in this case we will say the systolic blood pressure total blood pressure during the what is this expiration it is 120 by 80 and maybe during inspiration it has become 100 by 80 pulse volume has become less sometimes it become so less that pulse is very weak very few pulses become very weak or rarely they may be absent your understanding during inspiration and what pulse should appear during expiration if it is epsilon all the time with some of the hoodie all right a mic left so now what we have learned up to now only we have learned one thing what is pulsus paradoxus pulsus paradoxus the condition it in which normal physiological its parietal drop in systolic blood pressure is exaggerated it is more than 10 millimeter of mercury am i clear now pulsus paradoxus is one of the important clue towards the what cardiac tamponade even when some patient comes with the cute pericarditis an effusion even if cardiac tamponade is not there you repeatedly check the patient's pulses check the blood pressure and jvp and heart sounds and if jvp start rising and pulsus paradoxus appear with the hypotension you have to think of cardiac tamponade boy am i clear now why the pulsus paradoxus appear in this funny situation we are discussing what is that yes my friends card yet come on man yes I was thinking you are having silencer in your mouth okay now we need to explain why process paradoxes is rather than tamponade let's see what is the server said her heart okay this is our very sad heart it is a very simple diagram now this is of course what is this this is cardiac tamponade pericardial effusion under high pressure right it's more than the filling pressure so it is compressing the ventricles here you need to remember low pressure chambers are compressed more easily for example atria are compressed easily right ventricle is compressed easily left ventricle is difficult to compress pakodas I will take wall you understand so you any compression or collapse during the day asleep this collapse of the free wall or compression is seen in the right atrium and right ventricle now listen carefully what really happens during inspiration during inspiration in a patient with cardiac what what is this cardiac tamponade in cardiac tamponade because it's pressure first of all when blood will when blood will be filling into ventricles can ventricles significant significantly expanded this no because in cardiac tamponade crowded chambers are encased or entrapped in a fixed area where fluid filled cavity is not expandable you are understanding if it was stretchable there will be no impaired actually so temperate only to Allah when this is surrounded by such a fluid filled cavity which has enough pressure does not allow it to expand now the real computation will develop because the little space in which right ventricle has to feel as well as left ventricle so both ventricle will try to fill in the same little space during inspiration what happens during inspiration I told you during inspiration there is increase venous return to right side and less venous return to the left side but usually in a normal person not patient with cardiac tamponade normal person during inspiration when there's a overfilling of the right side right chamber will expand in all directions will expand in all direction but patient with cardiac tamponade when there is increase venous return to the right heart can this free wall expand here so there will be too much pressure on what is this wall septum so there will be too much deflection of interventricular septum towards left side you understand there is exaggerated motion of interventricular septum towards the left side during inspiration I told you in normal for some also very little deflection of septum occurred to the left but why in normal person this little deflection because heart is Right chamber is expanding in all dimensions but in case of cardiac tamponade cardiac chambers are encased in a small in fixed space surrounded by a fluid-filled cavity which is not expandable and both chambers have to compete for the ventricular filling and during inspiration our physiology is favoring the right side because during inspiration and specially inspiration become more deep due to respiratory distress and intrathoracic pressure become more negative so there will be more traction on the systemic blood during for filling during inspiration so what happened in patient with cardiac tamponade during inspiration when there is right side going to be overfilled it cannot expand into all dimension so there's exaggerated push off what interventive is septum towards the left side so left side with during inspiration normally under fill' now it become extremely under front if it is pushed towards that side can it fill well no so normally left ventricular filling during inspiration becomes slightly less and now in tamponade due to strong abnormal leftward deflection of what septum and left ventricle become moderately or extremely under felled and when it is under failed the meaning story you know and diastolic volume less stretch last contraction last stroke volume drop significantly and if stroke volume dropped too much cardiac output during inspiration dropped too much and systolic blood pressure drop too much and that is what produces pulses there are doctors so what am i clear now so let's see again this is suppose expiration right inspiration normal person expiration inspiration you are understanding now if template start developing expiration through the middle hypotension is their exploration with given inspiration exploration during inspiration now you see this drop here drop was less than ten and here drop has become more than there Desi's pulsus paradoxus now how do you clinically assess in the patient because the no-fun learning this theory if you cannot pick up into the patient am I right doctor of Thoth you need to pick it up so how do you pick it up it's very simple as you know I will not go into detail of fine detail of how to do the blood pressure measurement I understand you know that very well I will just tell you how to pick the pulsus paradoxus what you really do that you port properly what is this handcuff okay so figma manometer cough okay says with Momina metric cuff you put it here and inflate it more than what significantly more than the systolic blood pressure now you start dropping de for example you have inflated up to 140 you start dropping it slowly okay you start dropping the blood pressure okay I want to show this is first is paradoxical now how you will catch it you store the sperm animated pressured slowly during exploration right if you reach up to 120 and systolic blood pressure is about 120 and the pressure of 120 vessel will allow some blood to move blood will move through this vessel as soon as cuff pressure becomes slightly less than the systolic you are getting it now this will first crack off sound will appear this sound will appear during what time exploration let's suppose this is 120 we for our understanding we call it the sound is appearing at 120 we call this sound k1 chronic of one start appearing at pressure of 120 after that you start bringing the blood pressure down very very slowly sorry not blood pressure cuff pressure when you're bringing it deflating it very slowly right during exploration during x-ray inspiration sorry during inspiration systolic pressure valve let's pose imagine it 100 and you bring the pressure of 110 during exploration when pressure has brought from here here the k1 came this k1 appear only during exploration when it will become here at this point will the blood pass through the artery no will you hear and sound no so during the through what yes inspiration through the inspiration you will not hear the product of sound but as soon as you go to exploration again sounds will appear you are understanding so what happened that we come here that first found was this was the exploration this was inspiration what was this expiration this is inspiration same here exploration inspiration exploration aspiration exploration inspiration now let me help you to understand cuff pressure was here when you brought it here these sounds will start appearing is the right when cuff pressure and strongly pressure are almost equal crota cough sound appear but when you are when inspiration come because inspiratory drop is there if you are maintaining almost above it cuff pressure sounds will disappear now you keep on bringing the sound sorry you keep on bringing the cuff pressure very gradually down again when exploration come again Cradock of songs will start appearing again when inspiration come what will happen they will disappear then again in next exploration you have to root very with patience during next exploration it will appear but now gradually you have come significantly down let's suppose you have come 200 when your pressure is equal to lower end what will happen that during expedition song girls appearing but as soon as your cuff pressure is somewhere here somewhere here suppose it is 100 then sounds will appear not only during exploration particular start appearing during inspiration also so this is when souls are heard through the respiratory cycle during expression as well as during inspiration we can call it k2 this pressure is k2 it is not k2 okay so k1 was let's suppose 120 and k to us let's suppose and we are just posing k1 was 120 and k2 was what 1 112 is there pulsus paradoxus know very good right now it is 120 and this is 112 the difference is a as you need to take classes in mathematics right so then what happens that we say there's no process paradoxes but let's suppose that patient sound product of sound which appear only during expiration came on which only appear during exploration is at 1:20 but sounds appear in exploration and inspiration both right add the pressure of let's pose 100 then that systolic drop during this fresh inspiration is more than 10 millimeter of mercury this should be called so this is how you mayor da pulsus paradoxus then of course you will keep on taking the blood pressure down eventually all sounds disappear and you say this gas holy blood pressure is that right so this is how you measure God what pulsus paradoxus remember one thing when you are mining the pulsus paradoxus don't ask the patient to take a very deep breathing because that will produce false positive results you want a normal person like you if you take very very deep and hard breathing right you can produce some degree of verses paradoxes so some doctors becomes super intelligent they ask the patient I'm checking for pulsus paradoxus you take a deep breath even if it is not there it will appear you are under straining so don't ask the patient to to do inspiration deep specifically deep inspiration and hold that got that may produce false positive result now actually pulsus paradoxus is not specific for cardiac tamponade it can be positive in some other conditions anthem for example pulsus paradoxus may be present in chronic obstructive airway diseases like asthma if you have asthma and you are breathing very strong here you can say that when chronic obstructive airway disease or even sometimes a cute obstructive airway disease is there and to take the air in you have to generate very negative pressure in the chest you take very strong and hard breathing with difficulty then what happens you pull the air with lot of power in you also pulls ah what is this venous blood very rapidly and there is exaggerated motion of the ventricular septum producing pulsus paradoxus so pulsus paradoxus may also be present in herve diseases then pulsus paradoxus may be present in constrictive pericarditis but less often here I would love to mention that pulsus paradoxus is more common in cardiac tamponade and less common in constrictive pericarditis about 30 percent patient with constrictive pericarditis may have pulsus paradoxus and co small sign co small sign is that during inspiration not normally normally during inspiration jugular venous pressure goes down but if during inspiration jubler venous pressure failed to go down or even goes up this is called Co small sign whose small sign is present less often in cardiac tamponade and cou small sign is present more often in constrictive pericarditis that I will explain in the lecture with constrictive pericarditis then some other conditions in which pulsus paradoxus is positive one I told you of course cardiac tamponade then there is obstructive airway diseases where there's too much negative intrathoracic pressure then pulsus paradoxus may be also present in pulmonary embolism because if there's pulmonary embolism right heart cannot pump into lungs so right heart will become too much overloaded and pulmonary embolism and left heart is not receiving the blood very less is just massive pulmonary embolism and pulmonary artery is significantly blocked right out become overloaded and left heart become under loaded so naturally inspiratory blood pressure will significantly drop systolic blood pressure so pulmonary embolism also can produce pulsus paradoxus and sphere hypovolemic shock also can produce persist paradoxes now let's have a break and then we'll talk about the management of this condition okay plastisol okay now we will talk about the diagnostic studies in patient with cardiac tamponade stick studies and these traditional confirm or point towards is their tamponade or not and then we'll later on talk about the lab work which we have to look for the underlying cause right now in diagnostic studies here the gold standard is echocardiography that is echocardiography as I told you in the beginning that true diagnosis of cardiac tamponade is clinical but you can confirm or reject the clinical diagnosis by the echocardiography now echocardiography there can be basically two types you know they are transfer a thoracic echocardiography and there can be trance esophageal echocardiography and when we do our doing transfer seek echocardiography again there can be two types of echocardiography that there can be yes two dimensional 2d findings and Doppler I don't know what are the real spellings of Doppler this is double P oh my god people are happy with 1p D or double P and ER Doppler echocardiography or Doppler ultrasound okay so now really it's very easy to talk about this because we have talked about basically problems or changes hemodynamics changes and abnormal movement of different components of the heart right those will be discovered of this right let me tell you as we talked about previously that what happens to the heart during this situation cardiac tamponade right so we can talk about like this suppose this is your heart and here is your cable system right now what findings you can find on two-dimensional echocardiography very simple as I told you there is fluid around it and the pericardial sac and there's pressure in the fluid and I told you tamponade developed when pressure in the pericardial fluid become more than the filling pressure in the ventricles or the cardiac chambers then of course what really happens that temperat develop now we should really look at the interaction of pericardial fluid pressure and the cardiac chamber pressure during diastole during - Lee when left ventricle is right ventricle and it yeah they are relaxed now what really happens that this fluid which is all around here now this fluid this is compressing of course it is compressing the right ventricle and also compressing the you can say right atrium and also compressing right atrium right ventricle left ventricle in left atrium but as you know right-sided chambers are low pressure chambers and left-sided chambers are higher pressure chamber so which chambers can be collapsed easily by external pressure right there's no need to remember what is the infinite fluid accumulation pericardial sac with the high pressure and this pressure should be enough to compress the ventricular impede the or obstruct the ventricular filling right so right-sided chambers will be compressed more easily by this pressure so what you would you really see is right atrial collapse and right went it'll collapse especially during yes during what during diastole right during gastly right this is a collapse and here is the collapse so first feature we can say like that one by one we talked about that first then we start from here this is the first finding what is this right atrial diastole collapse collapse during their sleep and pressure glow is here pericardial pressure will push it in or diastolic compression number two this is the feature what is this right ventricular diastolic collapse or compression is it difficult to understand number three when it is too much compressed right and during - Lee it cannot move outward what will happen to the septum right so third finding will be exaggerated what is this or abnormal portion of interventricular septum so I have a normal motion of interventricular septum does it right do you think you need to remember it's easy to understand so easy to understand as you know if someone kick your head it will be compressed if it's enough in the same way there is a pressure here pressure here and eventually pressure there there's no need to remember it and then do you think because these areas are compressed inferior vena cava can push the blood here no so what will happen to inferior way acaba it will be the standard and stool so Bolin with the blood so there will be inferior vena cava plethora plethora mean too much abundant blood or excessive blood or we can say dilated inferior vena cava am i right what is this finding dilated inferior vena cava you may be thinking why not speedo vena cava gravity assist the speed of well I'll give up our gravity is opposing the inferior vena cava such more this language than the spear of an Akiva right so this is the stranded hammock left with that a very classical feature here is normally during inspiration I told you that blood very rapidly empties into normal right heart in normal person during inspiration table blood rapidly I chosen to the right side so during inspiration normal person in fear vena cava collapses or its eyes become slightly less but in these cases where there is tamponade right during inspiration even though the filling to the ventricle right side is more than exploration but still it's not enough to truly collapse it or significantly reduce the diameter so we can say that during inspiration there is no collapse of inferior vena cava on 2d echocardiography but again no need to memorize it it's very simple right that there's fluid on the heart which is compressing it right into chambers the low pressure chambers so do you - Lee they are compressed more so atrial compression is diastolic compression going to load that right ventricular diastolic impression with the septal abnormal motion and inferior vena cava dilation and which failed to collapse during collapse significantly during inspiration then if fluid is really too much not in case of a cute but in chronic cases when the fluid is really too much a heart will be dangling and - or swinging into this cavity you will need dangling entró posteriorly right I'm not doing any I'm just trying to tell about the heart that this heart is not properly fixated anatomically at its own place because it is surrounded by a fluid filled cavity so it's it starts freely floating into that fluid the word which is used it's a swinging heart I'm not talking about swinger of the heart that's a different thing this is swinging heart and this is only seen when there's significant effusion so actually this swinging heart and troposphere Li can also be noted in what two-dimensional echocardiography right swinging heart so these are - these findings now we come to the Doppler finding you know Doppler actually tell about the blood flow right Doppler will tell you about the blood flow or different how the blood is moving through different chambers especially across the valves right so let me make another diagram then what you will see Doppler echocardiography these findings are 2d echocardiography findings now what are the Doppler if you choreograph e now it's let me draw the diagrams this isn't the right side and here it is of course the blood here is coming from where from pulmonary veins now it's very easy to understand first go to the normal and then we go to the abnormal there as I told you normal person even during inspiration right heart overfill and left heart under this is normal but this normal phenomenon in pericardial tamponade is exaggerated as I told you in pericardial tamponade this normal phenomenon is exaggerated and right heart / overfilled and left heart under under fills this is it right now listen carefully in the right heart blood has to pass through which areas what is this well bicuspid valve and then what is this well foramen ovale left heart blood has to pass through which what is this valve mitral valve and then a or attic valve so these are right-sided blood flows and those are left-sided blood flows yes all right no if I say as we discussed in previous part of the lecture that during the inspiration the right-sided flow become exaggerated there's over filling and left is under filling it's very natural to understand if more blood is passing through during inspiration if more blood is passing through tricuspid and pulmonary well trance well Bloods lusty will become slower fast so easy that if you have bringing more even you put a water here you put in more water flow will be fast here you're putting less water flow will be less even primary class primary class child can understand that so in the same way you are thank God you are very very educated me first you cannot intellectual people don't need to remember what are the Doppler changes you understand very well yourself what will happen in Doppler changes during inspiration right flows are increased left flora degrees so we will say that trance valvular city in pulmonary valve and sorry tricuspid valve and pulmonary valve will increase right so velocities on the right side will increase and velocities pulmonary venous return mitral valve flow and aortic valve flow will decrease and these are the top of - that's it 2d findings again 2d finding atrial - holy collapse ventricular diastolic collapse abnormal scepter movement yes dilated and Funaki Basel is swinging hard the oppler finding look at the velocities typically there is in spirit right inspiratory dominance that right-sided flow the faster and left-sided flow are slow so we say in these patients as compared to exploration during inspiration tricuspid flow 40% increase on left side during inspiration as compared expression during inspiration mitral flow 25% decreases so there's no need to remember this right so any question up to this now we come to trance esophageal eco-car echocardiography this is very sensitive test right but this is done especially when we are suspecting that either there is a rhotic dissection because if you can diagnose the aortic dissection also all free world of chair or more importantly original section and when there is tamponade after cardiac surgery why because after cardiac surgery template something local ated localized loculated tamponade develop due to local a trait accumulation of fluid especially behind the left atrium there's the most common site after the cardiac surgery cumulation of the blood and transfer acid echocardiography virtually misses it it cannot really judge very well the fluid accumulated behind the left atrium and post cardiac surgery if tamponade start developing and sometimes it is look related fluid accumulated which is compressing the cardiac chambers right then it's preferable to do trance esophageal echocardiography is there right so especially this is good in hemorrhagic appeals now we'll come to some other investigations but classical investigation is echocardiography it is very good for empanelled you know why number one echocardiography is very sensitive for tamponade secondly it is very specific right it gives specific changes remember echocardiography I didn't mention it also shows the echo flow free zone around the heart echo free zone troves operate it can also in 2d it can also show the echo free zone around the heart but just finding echo free zone around the heart tells that there is plural pericardial effusion it does not tell this tamponade or not I told you every case of pericardial effusion is not tamponade for tamponade you have to see these stem this is showing that there is significant in more dynamic strangulate you know problem going on it the significant strangulation there is that right now some other tests but echocardiography is a very good test because it is a sensitive test for tamponade it is specific tests which have specific findings it can be done on the bedside and of course it is non-invasive test and it can be done rapidly isn't it now we come to some other tests for example what you may find on ECG on a CD number one feature graph of cute pericarditis may be there which we discussed in detail in previous lecture that features related with acute pericarditis that is ST segment right concavity upward right remember as I mentioned previously with this history segment elevation with what is this am i right this is a sad face it's a bad face right st-segment is elevated with concavity downward myocardial infarction transmural of course but if segment is elevated in very crowded rows you can ST segment is smiling that is not as dangerous diagnosis as myocardial infarction just a segment elevation with PR segment depression right I will not go into detail of these we have discussed already in the pericarditis lecture what really I want to mention that voltages will be low in ECG there will be low number one is ST segment elevation PR segment depression then voltages on why the voltages are low it's very simple because the fluid is not conducting very well and now I am now I come to the real and real an important electrocardiographic finding right which is important that is the electrical alternans electrical alternans I will tell you what it is actually what really happens that this is the fluid filled cavity and heart is dangling into it and moving right now heart is moving like this actually it's so cardiac major ventricle cardiac vectors normally major ventricular depolarization vector is directed downward leftward and backward to the right now this cardiac vector if hard keep on moving this vector also keep on changing the direction right so naturally let's suppose if we put the label eight number two minuses here and positive in here you know I'm positive negative here and positive there so what really happens if heart heart is like this right and it's axes are directed towards this then fluctuations will be amplified but when it's dangled other direction or it swings away then vector has gone another direction only a component of vector is along with it so amplitude will become less then hard swing back and it is directed towards electrode so amplitude will be high and then again it swings back and amplitude will be low so what really happens because heart is swinging in this fluid filled cavity so when for any positive electrode when it is vectors directed towards that right amplitude of QRS become high when it directs slightly away amplitude drop so when you took look at the ECG changes you will find that let's suppose this is an ECG pattern you are as complex now maybe next beat it become low amplitude then again it may become high amplitude so then again it will become low amplitude this is a write it just like that I'm facing to your eyes you can see the full face and now you see a part of it then full face part of it in the same way hardest turning its faces you are getting it so vector is of course the face here is electrical vectors right sometimes of going directly to the electrode and sometimes of way due to this reason beat to beat V to beat QRS morphology or even its what is this amplitude it varies right this phenomenon can be seen not only in QRS but it can also be seen in P wave or T wave but it is meant better highlighted in amplitude of QRS wave those are right this is called electrical alternans right this is a very important feature which tells that there is large amount of effusion and heart is swinging into that so these are the ECG changes then we come to the chest x-ray what is investigations we have done up to now echocardiography we did the electrocardiography now we are talking about chest x-ray what we can find in chest x-ray echo we have done then we did that yes you see G and now we are talking about chest x-rays chest x-ray but you will find the cardiac shadow will be lied if pericardial effusion is more than 250 ml because and very acute now this is important why it very acute kind of cardiac tamponade fluid will be just hundred ml or up to 200 ml and this may be enough very rapidly developing tamponade effusion the 100 to 200 ml fluid is enough to strangulate the heart but that may not show a large cardiac shadow or large cardiac silhouette right so what really happens that in these patient depending upon suppose this is normal cardiac shadow right so this card is shadow will become enlarged and heart will become sort of I don't know what kind of bottle flask shape or globular heart this is the logo yeah it can become hardest really not globular cardiac shadow is global her heart inside is unfortunately compressed you are getting it so we say then enlarge cardiac silhouette is the right or shadow but remember this will happen only when there is fluid is more than 250 ml right but one more thing it large cardiac shadow you always think of cardiomegaly and you should think of pulmonary edema and pulmonary edema lung fields are not clear but in cardiac tamponade specially lung fields are clear and lung fields are usually in cardiac tamponade within large-hearted shadow lungs fill the fields are clear right they are not showing all those features of pulmonary edema then you can do CT scan yes if you want to CT scan and MRI advantages of these two tests are the they are good for anatomical detail that you can see there what is this of course exact amount of a fusion you can see but a fusion can be seen and echo although very well it can show you look related effusions and these can also show you some malignancies or some mass liam's adjacent to the very card IAM and in the end yes but it is less commonly done julie diagnosis is made before that but if you do cardiac catheterization cardiac catheterization the most important thing in cardiac catheterization is that all the chambers are surrounded by pericardial yes fluid and pressure is the right so during the - lee all chamber than the same pressure almost same pressure you could could you get it because it is just like that you have four chambers and compress all of them with the same force right so all of them will have C pressure so we can say that - colic pressure this is important because during systole pressure very too much chamber the chamber but during - laye right we say there is near near equalizations of pressures in all chambers of the heart right and this is what will be really pressure that is determined by what is the pressure and very card iam any question of the sirs now we come to the other investigations other investigations are to look look for underlying cause right is there tuberculosis or is there SLE as mr. demora renal failure right these tests we have already discussed in detail when we were talking about yes previous lecture in acute pericarditis so all those investigations will be applied you have to apply diligently depending upon history and what you suspect according to that you will do the investigations right that and of course you will if when you will do pericardial sentences you should not forget to send the fluid for analysis does that right so those investigate will not discuss into detail again right now we move how would you manage this case patient with cardiac tamponade how you are going to manage right I would say that let's suppose you have a patient with acute pericarditis with a few Yin remphan it has not yet developed in your ward you have a patient who is already diagnosed with acute pericarditis and patient is developing a few Yin right actually you should diagnose that tamponade as soon as it drops this is the right so what you will do you will ask of course will keep the patient hospitalized or even in outpatient the patient come with the cute pericarditis and some of Union right you have done your tests you will immediately hospitalized the patient so you hospitalized hospitalized the patient and then monitor the patient first step is in case of acute pericarditis with pericardial effusion step number one is hospitalization and with that you monitor the patient now you will monitor for what of course you have worried that patient should remain hemodynamically stable and you keep on looking for the signs of hemodynamic deterioration as I told you that your monitor the pulse course patient should be on cardiac monitor on ECG right there's no need to tell that and look for the back triangle that you will repeatedly look for jugular venous pressures you will look for what blood pressure right repeatedly and you will also heart sounds so you keep on looking that jubler venous pressure is not rising and blood pressure is not falling of course you will also look for pulsus paradoxus and heart songs are not becoming distant or muffled or marital sounds may be already destroyed and buffering when there is pericardial effusion but you have to look for these two things specifically there should not be rising jvp with loss of Y descent and there should not be falling blood pressure with pulsus paradoxus if these things start appearing to temper natives there am i clear and of course again don't forget the pulse or the that he cardia told you without any cardia Julie tamponade is not there almost all tamponade of tachycardia except temperate with max edema uremia fish on what drugs a bit of blockers drugs and and very terminal stage unfortunately right so it will monitor the patient and of course you will do serial echocardiography right you will keep on doing serial echocardiography then we come to pericardial synthesis if it really develops then we'll go for pericardiocentisis while before you put your needle in you must know the temporary it is not due to aortic dissection and you should know it is not due to rupture what post am i free wall rupture this is that right after that these two things you are sure or not they are then you plan for pericardiocentesis but before really I I talk about pericardiocentisis I want to tell you something very interesting that even a very small amount of fluid is when it is released patient feels dramatically improved hemodynamically and even echocardiographic le the question is that if someone has let's suppose 500 ml fluid and you just remove 100 ml and patient dramatically become better on hemodynamic parameter and echocardiography why is such a small amount of aspiration of fluid can make better it is actually volume pressure relationship I'm going to explain now volume pressure relationship of pericardial effusion suppose this is pericardial effusion and if we are measuring what is the relationship between volume and pressure let me make up here it is volume progressively increasing volume and here is the pressure in a cube case of course pressure will go rapidly up because it cannot stretch up this is not linear ship is not that you people the volume and the same rate will pressure will with the same proportion and three is no actually it is curvilinear you know what does it curvy linear or it's up sloping very steep initially even pressure is increasing sorry initially even prior ideal a few and volume is increasing the little increase in pressure but once it reach to maximum stretch ability and further it cannot stretch a little increase in volume will take the pressure very high this type of graph is called curvy linear of course this is in a cute case let's suppose if I say here is the pressure is here the volume is suppose 200ml and here volume is 100ml then it is acute case but in chronic cases it because fluid is accumulating gradually it keep on stretching so lot of volume is accumulated accumulated and then suddenly when it cannot further what is this stretch it will become like that right now the art of under straining is this that let's suppose here pressure is where your patient is at the situation that volume is 200 ml and pressure is let's suppose 20 right but if you bring it you move the volume you have spread the fluid and volume moved from 200 200 pressure will not become 20 to 10 it become maybe 4 it became drastically down right so sometimes we or even you just remove 50 ml here I'm just giving an example it is 150 so pressure from 20 become less than 10 you are under strain in the same when Corona cases when you remove a small amount of fluid right volume has gone little from here to here this much volume is reduced repression significantly reduce so that is why you will really see clinically and echocardiography that when you start aspiration even though it is a device you should aspirate as completely as possible but usually you rated slightly or small amount patient him blood pressures start going up this is paradoxes start disappearing jelly please start going down that's right emmaclaire in the same way if you are doing a co cartography while you know you should do echocardiography before and if you are being echocardiography guided needle pericardiocentisis you will really see that while you are doing aspirate in the fluid the future of echocardiography normalize that you will see that right atrial : - truly collapse disappear right ventricular diastolic collapse disappear motion of interventricular septum become relatively normal and even fewer vena cava plethora or enlargement disappear emmaclaire so now what is pericardiocentisis that is very simple that this is actually with the needle which usually 18 to 22 gauge needle we aspirate the fluid what we do remember before espera espera in the fluid you must put the patient on IV line preferably on say a line or dextran or depending upon is olymic situation right because we should give the saline why we are trying to prevent the diastolic collapses right so anyway so the folding pericardiocentisis get IV line access puts the say line arrange some blood cross match if this enough time and usually there's not enough time if patient is really very advanced then you can choose the approach you can go subsea fight or epical or parasternal depending upon your experience depending upon the localization of fluid you will keep the patient on 45 angle and I'm not going to into detail of procedure right so this basic process that you will take 18 to 22 gauge needle push if suppose if you choose for subsea 5 which is most commonly shows your direct direct it at about 45 angle with the sky and needle should point towards the left shoulder right and then you start as soon as you reach to pericardial cavity you start aspirate in the fluid but important point is that you keep an eye other both eyes on this fact that you may not be injuring the myocardium this is a right of course patient is on the cardiac monitor and on ECG myocardial injury changes if they appear it means you are messing messing up with the myocardium right so usually these the needles when you pass they should be guided echocardiographic Allah of fluoroscopic Aries so you really know where you are putting your what is that needle right so you will expect the fluid as much you can and after that some it's always wise to leave a multi hold catheter pigtail catheter or multi old catheter so that fluid keep on braining right for a few days and when further draining become of course with their time if patient is getting better and you are treating the underlying cause also then further drainage will become less and when less of fluid is coming oh very less fluid come you can pull out the drain also right so this is what is the basic things you do in pericardial synthesis but remember one thing if there is hemorrhagic fluid it should be dark colored and it should not clot please refer to the right colored and it clots you are doing something very wrong because usually if it is have magic fluid then it should be should be dark colored which means it is deoxygenated blood there and it should not be clotting it shouldn't have clotting factors like a fresh blood but if you are bringing a fresh blood out and this is bright red then well oxygenated looking and with that there is you can say it clots also believe me there's something drastically going wrong right after that then in those cases where there is recurrent tamponade that you drain and again it come so those cases where there is a recurrent tamponade you cannot keep on a spreading because sometimes you are not there to aspirate and temporary develop and kill the person then you have to be taken some more serious approach if their different template or they look elated through it or if you fall diagnostic purpose you have to take that tissue sample then it's better to do surgical drainage surgical drainage is done by subxiphoid limited subs if I'd thought of thoracotomy right just subsea fire you put a small in CN and you drain it well and also you take a tissue sample is that right and you drain it as completely as possible then sometimes in very case those cases we are repeatedly you can say fusion keep on coming like cases of neoplasia right and you know that again and again effusion will develop then you develop pericardial window what is pericardial window that you open this area and remove a piece of pericardium and open a window between the pericardium and pleural space so we also called it creation of pericardial pleural fistula very cardio pleural fist relies the right so in this case pericardial fluid is being formed but it is being drained it is continuously draining into pleural space and mediation lymphatics and to lymphatics all of those areas very large area keep on absorbing their tough union so risk of tamponade is not there am i clear so what was the first thing pericardial sentences that is needle aspiration with leaving a catheter for drainage or if there is going to be a recurrent and you have to take a tissue sample of the local at it you go for surgical drainage so right and if there is very recurrent and long-term fusion coming and coming then you go for pericardial Laurel fistula that is pericardial window then some cases specially in malignant cases we do pericardial pieces I will write it down pericardiocentisis Perry cardio sentences that with drain then what was the second yes surgical drainage surgical drainage that is sub defied limited thoracotomy right these cases are done when recurrent or do you want to remove as complete as possible or this loculated or you also want a tissue sample like diagnosis of tuberculosis then pericardial window pericardial window you will need to open the left pleural cavity right then you can also do your dishes thorough this is flora diseases in pericardial space you inject you introduce tetracycline or bleomycin actually right bleomycin or tetracycline or the agent when you push into this these article or raising agent they irritate the pericardial lining and activate the fibrotic reaction and severe fibrosis occur and that fibrosis made the pericardial layer adherent with each other and pericardial cavity disappeared for example this layer and this layer they become fibrotic and they become sticky where the fluid will accumulate right so such cases specially in malignant cases to prevent repeated pericardial effusion and tamponade risk of tamponade we can also do pericardial this's pericardial disease is a process in which we are putting a the closing agent in pericardial sac like bleomycin or tetracycline or any other signaling agent so that sclerosis of cavity occur and there's no more cavity then yes very good question it can eventually do can do a lot not always but it can duel of constrictive pericarditis but my friend I told you we are doing this case and terminal cases of cancer so as usually they unfortunately most of the patient died before the dual of the concept of pericarditis right it is a sort of pin the ativ mahir in those patients which have very advanced degree of malignancy right those cases would do it but you are right that if you do oversee chlorosis or oversee chlorosis occur then you will get rid of tamponade risk but you may end up with some sort of constrictive pericarditis you are right in that the patient survive long enough here we can use steroids you can use steroids to prevent what fibrosis and that will discuss in lecture of constrictive pericarditis right okay then we come to the last resort surgically remove the pericardium and throw it somewhere else out of the patient body what is that called Perry called yet to me Perry of course you take care of the phrenic nerves right there are phrenic nerves on the sides I don't remove them along with the pericardium right so Perry cardiac tomy right this is the last resort when you cannot do anything you just remove the pericardium so that no pericardial sac no risk of fluid accumulation and no risk of temperature and strangulation of the heart right recently they have also introduced another method we just called balloon Perry called the or to me okay that is balloon then known Perry called D or Thome in this case actually they introduced to the small and seen here they introduced a sub C felt to introduce a small deflated balloon into pericardial sac and then they inflate the balloon and then pull it out while it is coming out it produces a larger window in the pericardium right so that fluid does not accumulate there and keep on draining into mediastinal structures and floral area so that risk of temporary is reduced am i clear any question no question yes okay he is saying that it's an emergency situation in a remote village where there are no medical facilities available and someone some family call our doctor and tell that this is our man and he is having some destiny and tachycardia and he looked net winds are distended right and hard homes are no more there so he strongly suspect there is cardiac tamponade and it's a very advanced stage and there's not enough time to come to the city and bring all these things and what you should do I'll say at least still if you can't do pericardial sentences you do it of course you will not do in a proper manner but at least your finds in your doctor should carry a box and that box there should be at least four needle directly you push that needle in and stir even with 5 ml 10 ml syringe and emergency Trude you try to bring the fluid out right so that I this is what I was trying to push in your mind even a small amount of fluid brought out will relieve significant relief in the patient until you can take the patient to better medical facility where we can take better care of the patient right class dismiss

Channel: Dr. Najeeb Lectures

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Keywords: cardiology, cardiac tamponade, medical lectures, medical videos, usmle, usmle step 1, armando hasudungan, lecturio, medicine, usmle step 2, medical education, medical videos channel, medical school lecture, pathology, Cardiac Tamponade (Disease Or Medical Condition), USMLE, FMGE, AIPGMEE, cardiac, tamponade, Health (Industry), Medicine (Field of Study), Disease (Cause of Death), Osmosis, Pathology (Medical Specialty), what is, nursing (field of study), dr najeeb

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Length: 142min 4sec (8524 seconds)

Published: Wed Mar 06 2019