Pericardial Diseases | Clinical Medicine

foreign engineers in this video today we're going to be talking about pericardial diseases again this is going to be a part of our clinical medicine section if you guys like this video you benefit from it it helps you please support us and you can do that by hitting that like button commenting down the comment section and please subscribe also if you guys really do want to benefit more I really suggest you guys check out the link in the description box below it takes you to our website we have notes illustrations we're developing courses for those

taking the step one step two the pants Etc check that out also we had a lot of merchandise that you guys can check on get some swagoo going on let's start talking a little bit about pericardial diseases though so pericardial diseases there's a couple of them right the biggest ones are going to be acute pericarditis constrictive pericarditis there's also going to be this intermediate that we'll discuss a little bit about called the pericardial effusion and then the mac daddy the one that scares you and makes you pee at your butthole cardiac tamponade this is the

fearful one so what happens in these process what's the pathophysiological process what's the causes how do we differentiate them so here we have a heart right and we have this normal pericardium which is in pink this is usually a double layer if we go back to our anatomy right you have the visceral layer and then you have the parietal layer and then you have the pericardial cavity which is filled with serious fluid in between when a patient develops acute pericarditis they develop inflammation of their pericardium that's the underlying process right so there's some type of

inflammation that is actually occurring here that's causing the pericardium to become angry and we'll talk about what those causes are in just a second but there's definitely inflammation which is going to be stimulating or triggering the formation of acute pericarditis now let's just say here that I got an angry pericardium right so this pericardium is super super angry you want to think now what will cause this guy to become super angry and oftentimes generally it's idiopathic and what that means is we don't really know why it occurs but the ones that we kind of generally

assume is that it's oftentimes what's triggering this is usually infectious and what do I mean by that so infectious there is two different types of infections that I want you guys to think about one is viral and oftentimes this is Coxsackie B virus all right so that's one and then sometimes in certain patients who are immunocompromised or there where it's very high populations or endemic populations tuberculosis can be another infection that can really plague the pericardium the other one is post Mi if you guys remember if a patient has an N stami or a stemi

we said that that can create a local inflammation and agency of the pericardium and if it's like one to three days it's called fibrinous pericarditis and if it's 14 days or more after they had an MI that's Dressler syndrome another one really really big one is uremia so uremia is a really really big one this is when a patient has usually some type of underlying chronic kidney disease or a terrible Aki so look for this in a patient who has like CKD or an acute kidney injury and what happens is they're bun and they're creating

a really really high and that can cause uremic pericarditis one of the complications all right so look for a patient who's had any features of infections like a low-grade fever look for a patient who's had just had an MI and look for any underlying kidney disease the other one that I want you guys to think about is usually radiation therapy so if they have cancer and they've had some type of radiation therapy to the chest that's another particular trigger because that's going to injure the pericardium the last one is usually someone who's had cardiac surgery

so a post-operative pericarditis this is pretty common especially if someone's having a cabbage they're having open heart surgery for any reason we also call this called post pericardiotomy syndrome so these are big things that will cause inflammation all of these things right here my friends will lead to inflammation and that'll cause this pericardium to become inflamed and angry now whenever the pericardium becomes inflamed generally it'll precipitate a chest pain and I'd say that this is by far for acute pericarditis the Hallmark feature when this becomes super inflamed it produces what's called a pleuritic chest pain

so it produces what's called a pleuritic chest pain what does that mean all right imagine you take a breath in when you take a breath in your lungs expand and press on what's next to the lungs the heart what surrounds the heart the pericardium so when you take a breath in and they expand they push on the pericardium and it precipitates pain the other thing is that this pleuritic chest pain is positional so I want you to think about this it's a pleuritic chest pain that is positional what does this mean all right what this

means is when you have a patient lay flat what happens is their diaphragm pokes upwards into their actual thoracic cavity and what's right there just above the diaphragm the heart and what surrounds the heart the pericardium so when patients are laying supine it's worse and when patients are actually leaning forward what happens is it brings the diaphragm down and that puts less pressure and offloads the pericardium so what I want you to understand with positional is it's worse supine and better leaning forward this is pretty high yield and and high yield and very very common

on patients who have pericarditis all right so that's high yield stuff there now we know these are the triggers for patient developing acute pericarditis you know what else is a very interesting thing when the pericardium becomes inflamed sometimes what it'll do is it'll cause these like these cells the viscerum parietal epithelial cells to start secreting some fluid and it can start secreting fluid and fluid and can accumulate in this pericardial cavity and get a little bit bigger normally we have a little bit but if you start accumulating a lot look what can start happening now

fluid is really really accumulating inside of this pericardial cavity this is now whenever it gets more than the upper limit of normal it's called a pericardial effusion so whenever there is a increase in Cirrus fluid production usually precipitated by what inflammation of the pericardium this will stimulate a pericardial effusion so acute pericarditis can lead to a pericardial effusion because you inflame the pericardium causing it to make more serious fluid what else can they acute pericarditis do it can potentially progress and let's say that you have a patient who has repeated repeated inflammation so I'm talking

repeated bouts of inflammation so I'll put repeated inflammation what's out of the ones up there in the top for causes what are those particular causes which if consistently keeps happening can cause constrictive percolysis think about it would it be infectious it could be if they have TB TB is a definite one because it's a chronic disease what about post am I no what about uremia not really what about radiation therapy 100 tuberculosis and radiation therapy happen to be the most common causes of repeated inflammation which can then cause this angry pericardium to become fibrotic so

now it's going to be replaced with all this fibrous tissue look at this I'm going to put all this here in Black this is all going to be fibrous tissue and now imagine having this big rock hard fibrous tissue covering the heart now this dang heart can't expand now what happens is normally the pericardium should let the heart kind of stretch a little bit but whenever the pericardium is very very fibrotic so you're gonna have a fibrotic pericardium the problem with this is that this actually is going to be making it hard for the ventricles

to fill and what that does is that actually will lead to a reduction in ventricular filling and that is one of the big pathophysiological processes that occur in constrictive paragonies you get a fibrotic pericardium and this will then inhibit the ventricular filling process because look it's making it hard this this heart has to stretch but it can't because this pericardium is super hard and fibrotic and not allowing it to stretch so this process right here my friends is going to be inhibited you can't allow that to occur and that's the big concept that I want

you to understand here that's for constricted pericarditis okay so so far we have a pericardium that's become inflamed if it becomes inflamed it can cause this classic chest pain it also can cause serious fluid to accumulate which can become a pericardial effusion and if you repeatedly inflame the pericardium becomes fibrotic and reduces ventricular filling constricted Perkins we now know the differences between each one of these but all of these are caused by the same thing we come to another scenario let's say a patient has pericarditis they develop a pericardial effusion in the pericardial effusion continues

to grow so you develop a growing effusion so this thing continues to grow nice and slow and as this starts to happen and you grow this effusion what happens is normally your pericardium gets time to stretch and so if it's a very slow growing effusion it has time to stretch and accommodate that but whenever it grows enough that it gets to the point where the pericardial stretch limit has been reached then what it does is it starts to squeeze on the heart and squeeze the heart and prevent it from being able to fill now look

it's squeezing it like constricted pericarditis is and so now this filling process which is supposed to occur here is being impaired that's being inhibited that's one very important concept so whenever you have a pericardial effusion that's becoming tamponade here's what I want you to remember let's see here we have this graph here we're going to say this is the stretch limit whenever you reach this point and you go above it the pressure inside of the pericardium is high you squeeze the heart we're going to use this blue arrow here where this person is accumulating volume

slowly slowly slowly slowly slowly they finally hit the stretch limit and boom they pass the stretch limit and now the pressure in the pericardium is high enough but it's causes cardiac tamponade so this is when you have a slow effusion let's take the worst case scenario the one that makes your your stank hole pucker a little bit we take a patient and we decide that we're going to push tons of blood into their pericardium what's that called that's called a hemopericardium these are rapidly accumulating the big one most patients probably just die when they have

this one is you get what's called a free wall rupture you guys likely remember this from the coronary artery disease lecture right whenever a patient develops a very large LED occlusion they infarct this entire wall it then ruptures blood spills from the left ventricle right into the pericardium that's terrifying another one is a proximal aortic dissection so this is that Stanford a right so that proximal aortic dissection if you have the root of the aorta and it just dissects right into that and boom right into the pericardium that can also be a big one and

then the classic one's trauma right or surgery so you really want to think about this in two particular scenarios did the patient just have an MI do they have any features of ripping tearing chest pain that's classic of aortic dissection or did they have any trauma and surgical procedures usually these are the super super obvious ones what they do is is they precipitate a hemopericardium to form hemo pericardium the scary thing about these as I told you before is that when this happens they cause blood to form super quickly into the pericardial cavity so now

let's fill this pericardium with tons of blood and usually in these particular scenarios if this doesn't occur slowly this occurs extremely fast so now when it occurs very very fast what look look at this example here right here's volume it may only take 200 CC's as compared to like 500 cc's it may only take a Teensy bit but it's going to occur so quickly that it reaches the stretch limit so quickly that the pericardium doesn't have time to compensate and stretch so boom guess what it does Shoop goes right into this high pressure area pericardial

pressure Rises what does it then do squeezes on the heart and reduces it from being able to fill this is an example of a rapid effusion in this case this is usually something like a hemopericardium is the most common cause but in both of these scenarios what are you noticing that the pericardial pressure is going to be high once you've reached that stretch limit and both of these the pericardial pressure is going to be high and what is that going to do to the actual ventricular filling process it's going to compress the heart when it

compresses the heart so you're going to have right ventricle is the first one to be compressed as well as the right atrium the last one is usually the left atrium these all get compressed and whenever you compress them are you going to be able to fill them properly no and so this reduces the ventricular filling process massively so in both of these scenarios we'll just use this one as an example there's an increase in the pericardial pressure due to hemopericardium or a serous fluid from a pericardial Fusion this then stimulates the compression of the right

atrium right ventricle and massively decreases the ventricular filling process like significantly and this is what you see in cardiac tamponade all right now my friends at this point we have talked about pericardial diseases we should have an understanding of it now let's talk about the complications the scary things that you can potentially see with these pericardial diseases when you have a patient who has a pericardial disease you want to figure out what's going on with these patients so why are they complicated what are some issues what are some of the things that can arise first

thing acute pericarditis this one doesn't have any scary complications be thankful for that right it can potentially progress and we'll talk about that but oftentimes the most particular classic findings that are usually seen in patients with acute pericarditis is pain so whenever this pericardium becomes inflamed usually what happens is these patients develop what's called a pleuritic chest pain this is usually the most classic finding now we'll represent CP as chest pain the big thing about the pleuritic chest pain is that it's positional so what do I mean if a patient decides to lay supine so

whenever they're laying supine what happens is is it causes the diaphragm to kind of push up and if the diaphragm pushes up it pushes on the pericardium and when it pushes on the pericardium it precipitates pain so supine will actually worse worsen the chest pain all right that's one thing whenever they're sitting or they're leaning forward particularly what it does it brings the diaphragm down offloads the pressure on the pericardium so usually sitting or leaning forward will actually improve the chest pain or decrease the chest pain these are usually some very specific signs that I

want you guys to remember the other thing that can happen here and this is also very important is that not only when this pericardium becomes inflamed it becomes angry and causes pain but also when patients are getting auscultated what happens is the layers rub up against one another during the actual cardiac cycle and this produces this classic thing called a friction rub so if a patient comes in and here's what I want you guys to understand because acute pericarditis is a clinical diagnosis if a patient comes in with chest pain that occurs during breathing it's

positional and they have an Associated friction rub it's almost completely diagnostic of pericarditis another thing that I want you guys to remember for pericarditis is the potential complications so it does have the potentiality to progress so let's say here you have an angry pericardium what did I tell you could happen it could start secreting some of that serous fluid and the serous fluid could potentially accumulate accumulate accumulate in the actual pericardium and if it does what is this called an effusion so one of the other potential findings that you can see here is these patients

can get pericardial effusions that's another classic finding that you would see in a patient who has pericarditis they get a pooretic chest pain a friction rub and an effusion on echocardiogram yes this effusion could potentially progress if it keeps getting bigger and bigger and bigger it can become tamponade which we will talk about we talked about a little bit prior the other thing that we said is with repeated bouts of inflammation what can happen this tissue can become super fibrotic and when it becomes super fibrotic it actually reduces ventricular filling and this can lead to

constrictive pericarditis so the big things that I want you to remember from acute periditis is the classic findings and the potential to progress to an effusion sometimes to cardiac tamponade and also with repeatabouts of inflammation can progress to constrictive pericarditis all right let's talk about the next thing constricted pericarditis we know that this can be a formed by a patient having acute pericarditis that has repeated bouts of inflammation you guys remember the triggers radiation therapy TB those are usually the biggest things sometimes malignancy as well but we won't go too far in that the classic

finding is that this pericardium is so rigid it's so fibrotic that what it does is it compresses the weaker ventricle which one would you say is a little bit weaker not as much of a thicker muscle layer the right ventricle and so what it does is it compresses or it releases reduces The Filling of the right heart now if you compress this imagine blood trying to come in from the right atrium into the right ventricle it's going to be inhibited and if this is inhibited what's it going to do it's going to start backing up

into the Super vena cava into the actual jugular veins or backs up into the inferior vena cava and down to some of the actual structures there in the abdomen or in the lower extremities and what happens here is this is usually we use a particular terminology called central venous pressure this is usually elevated and because it's elevated what it does is if it's in a superavena cave it extends all the way up to the jugular veins and plums those poppies up and at least is something called jvd Super Classic sign here another thing that I

really want you guys to remember though as patients that have constrictive pericarditis sometimes this jvd is super intense and you can even see potentially a variant of it and what we call this is we call this a cool small sign so it's basically like jvd but it's in a weird particular scenario and let me explain what I mean here so this jvd can potentially also present as kusumal sign so this right heart is being compressed it's having a hard time feeling when you take a deep breath in normally your intrathoracic pressure drops and you suck

blood into the right heart but if you're being if you're compressing that right heart it's not going to fill so during inspiration their jvd stays distended and that's paradoxical so they can have a paradoxical distension of their jugular vein during inspiration classic cool small sign what else do you see that in do you guys remember restrictive cardiomyopathy can also have this the other thing here is this central venous pressure can also extend to the liver and cause hepatomegaly right so it can cause hepatic congestion and if you cause hepatic congestion we said that this makes

it harder for blood to be able to get out of the liver right this will cause injury here and this can progress to potentially liver failure like cirrhosis all right the other concept here is that it can even extend to the lower extremity veins when it extends to the lower extremity veins this can even cause edema so sometimes these patients can experience what's called pitting edema so you push on their lower extremity leave like a big old indent in it super classic here as well the last thing is it can also increase your portal pressures

so it can cause patients to develop portal hypertension and this portal hypertension can cause fluid to accumulate within the abdomen because the pressures of the peritoneal capillaries become increased and they develop something called ascites so these are all and at this point you guys should understand and it'll become so like second nature at this point the features of left heart failure and right heart failure this is classic features of right heart failure so the question then arises how do I know if this is different than between other types of causes of right heart failure or

difference between restrictive cardiomyopathy because that's how they love to try to trick you on the exam they both have cousine they both have right heart failure you know what else constricted pericarditis is interesting this pericardium is so rock solid that whenever the ventricles try to actually distend it bumps up against That Rock Solid pericardium it makes like a knocking sound and this is classic it's called a pericardial knock and that's one way that you can try to differentiate these based on the clinical findings here that are suggestive of constricted pericarditis other words you'd have to

go down the routes of echocardiogram to really determine that difference or other modalities which we'll talk about all right this is constrictive pericarditis we come to the Mack Daddy of them all this is cardiac tamponade so cardiac tamponade is the scary one we said that this can be formed because of the hemopericardium so a proximal aortic dissection will be a one left ventricular wall rupture where it just explodes trauma cardiac surgery something to that effect or a progressively enlarging pericardial effusion due to pericarditis viral infections post Mi uremia things to that effect when these patients

develop these accumulations we're just going to say here in this particular scenario This Could Be Blood this could be fluid it doesn't really matter in this example all we know is that the pericardium has this collection and remember I told you this is kind of the confounding factor and it brings about cognitive dissonance we think that the amount of fluid in the pericardium is the problem that's not the case you can have a little bit of fluid in the pericardium but it accumulated rapidly and compressed the Heart during diastole or you could have a ton

of fluid that has accumulated over time it's reached the stretch limit of the pericardium and compresses the right heart it doesn't matter about the volume it matters about if it's able to compress the actual right heart so in this scenario what do we see we see right heart compression particularly it compresses the right atrium and then it compresses the right ventricle and then if it gets really really high it can compress the left atrium as well but the whole concept here is that it makes it impossible for blood to come down here into the right

ventricle right so what you're going to do is is this is actually going to cause a reduction in right ventricular filling all right then if you reduce the right ventricular filling another thing that also happens here is that your right ventricular pressure is going to rise so much that it's also going to shift septum and now look the septum gets shifted from the right ventricle towards the left ventricle look how tiny that space is now in the left ventricle now what you're going to do is is you're going to impair filling into the left ventricle

so there's a reduction right ventricular filling and there is a septal shift from the which side from the right ventricle to the left ventricle both of these things will then massively reduce left ventricular filling if you reduce the left ventricular filling you're going to reduce the stroke volume and then reduce the cardiac output so these patients will have a very low cardiac output and then that precipitates a low blood pressure so what you're going to see out of these patients is that they are going to have a very very low blood pressure so we call

this hypotension right sometimes this hypotension can be low enough that you don't perfuse organs and that is called Shock so that's what we can see is we can see potentially very low blood pressure that could progress to shock what are ways that your body tries to compensate for a low cardiac output it constricts the vessels so it tries to increase your svr but it may try to increase your heart rate so one of the other reflexive reactions here is this may try to create a reflex reaction and one of the reflex reactions here is to

increase the patient's heart rate so they will have low blood pressure they'll have tachycardia you know what else if blood can't get into the right side of the heart where does it go I already told you this it'll back up into the jugular veins because what's increased your central venous pressure If central venous pressure is increased what is that going to do to your jugular veins then it's going to plump those suckers up and so what we will see is is we see a increase in the drug of the venous pressure or jug of the

venous distension so if I see jugular venous extension I see shock features of hypotension and tachycardia and one other finding which is super common look how much fluid could be around this if you have a big big big effusion there it may be hard to listen and auscultate and hear heart sounds so one of the other findings is muffled heart sounds and if I have a patient who has these three particular findings which is what we're going to Mark these here one jvd two muffled heart sounds three features of shock such as hypotension this is

classic of cardiac tamponade you know what they call this these three findings it's called a Triad we call these Becks Triad now in true like reality this is probably not as common but for your boards super high yield okay that's one finding the next thing that also will seal the diagnosis of cardiac tamponade and help you as if you see this feature of pulses paradoxis you can see this in other disorders but this is going to be classic in cardiac tamponade what happens here is let's say here we have a normal heart and then we

have a heart that gets progressed to tamponade so here we're going to say that they have the progression into tamponade so tamponade has developed in this normal part so now they are fluid all up in their pericardium whether this is serious fluid whether this is blood it doesn't really matter the concept is the same the concept is is that this fluid is compressing the right heart and impairing the filling process right that is being inhibited now if we look at this concept when a patient decides to breathe you have respirophhasic changes in their blood pressure

so here's an arterial line so you have a patient who has an arterial line and you're monitoring their blood pressure here in a normal patient whenever they expire so this is an expiration this is an inspiration and this is another expiration what do you notice you notice a small little decrease in their systolic blood pressure during inspiration a tiny little change it should generally be less than 10 millimeter mercury decrease in systolic blood pressure during I'm going to abbreviate this inspiration that's normal okay so this would be a normal scenario in tamponade however what do

you notice well they're compressing their right heart right so whenever they try to take a deep breath in what happens they're trying to suck blood into the right heart but they have a reduced filling and on top of that not only do they have reduced right ventricular filling but what did I say happens to the septum it shifts so now you shift their septum and reduce left ventricular filling so they're supposed to be getting blood into their heart during inspiration but are they getting blood into their heart during inspiration no not enough and so whenever

they go through systole and try to push blood out they don't push out enough so there's systolic blood pressure drops so in this scenario you see expiration you see inspiration and again you see expiration what do you notice the differences between here huge drop in the systolic blood pressure during inspiration because of a reduction in RV filling and septal shifting reducing the left ventricular feeling and cardiac output so this has to be greater than a 10 millimeter mercury drop in the systolic blood pressure during inspiration and this is classic of tamponade all right so with

that being said we now have an understanding here of all the different types of pericardial diseases and how they could potentially present and progress now what I want to do is I want to take some time and go through the diagnostic approach all right how do we approach pericardial diseases giving these findings well first thing is acute pericarditis you need at least two or more out of the four findings to make this diagnosis one pleuritic chest pain two a friction rub three classic EKG changes the classic EKG changes is usually there's diffuse ST segment elevation

that's present and usually it's in this kind of like concave or smiley face type of appearance that's one thing sometimes you can see these like little hooks there as well that also can be potentially suggestive of more of a pericarditis picture but again diffuse ST segment elevations and here's the classic thing PR segment depression if you see that the pr segments are depressed below the isoelectric line that's classic especially if combined with st elevations Perler to chest pain and friction rub classically seen with acute pericarditis so there's three out of the four what's the fourth

finding it's an echo and if the echocardiogram shows the pericardial effusion you have clinched the diagnosis of acute pericarditis all you need is at least two or more out of the four findings again pleuritic chest pain friction rub classic EKG changes and a pericardial effusion and you've made the diagnosis constricted pericarditis again look for right heart failure KU small sign and a pericardial knock ECG sometimes because the actual pericardium is so thick it Alters the electrical waves that are moving from the heart to the pericardium to the chest to the electrode and so the voltages

can be low but that's not super helpful what would be helpful if you get an echo and you see a thick pericardium there you see that septum bouncing from the right side to the left side that's also classic of constrictive periditis and then abrupt drops in ventricular filling during inspiration that's usually the classic signs of constricted peritis sometimes though you may need a cardiac CT or MRI to really clinch the diagnosis to throw that very very thickened pericardium and then sometimes catheterization may also be helpful here we'll talk about how that's really important especially with

differentiating between restrictive cardiomyopathy the next one is pericardial effusion pericardial effusions if you have a lot of fluid that's present within the pericardium and it's causing the actual Apex to move in fluid from kind of like left to right during the cardiac cycle then it'll cause alterations in the amplitude of the QRS complex because imagine the heart the electrode is like right here and then all of a sudden when the heart is moving in this fluid the Apex where usually you're having that constant Vector Down lead two going towards like the Apex that's moving off

of that that kind of like axis and so because that'll cause alterations in the QRS complexes and again if you see that that's one thing you see a pericardial effusion which is this fluid here within the pericardial cavity that could also be helpful in making the diagnosis of pericardial effusion the last one is cardiac tamponade again you're going to see the same concept you need a pericardial effusion and you're going to see that electrical alternates maybe low QRS voltages but the echo is super classic it's a pericardial Fusion for one but you need the next

thing to make the diagnosis you need a chamber collapse so here's the right atrium here's the right ventricle you need these to collapse during diastole that is the key feature all right so we've made the kind of like diagnostic approaches done for cardiac tamponade for constrictive pericarditis acute pericarditis and pericardial effusion really quickly with constricted pericardites because they love to test you for this on the exam is how do we differentiate these two on physical exam they're both going to have features of right heart failure but they'll also have cusumal sign one of the big

differences those constricted Paradise is a pericardial knock restrictive cardiomyopathy does not echocardiogram you have a thick pericardium you'll have a septal bounce you'll have abrupt drop in ventricular filling restrictive you're going to have biatral enlargement and diastolic dysfunction for the cardiac CT or MRI you'll see a thick pericardium restrictocratic cardiomyopathy it's a normal pericardium and then a cardiac cath what happens is in constrictive pericarditis the septum intraventricular the septum is healthy so it'll Bounce from left to right left to right which will cause discordance of the ventricular pressures the in diastolic pressures in the left

and right ventricle whereas restrictive cardiomyopathy the septum is stiff rigid it's filled with infiltrates and it will not move and therefore there will not be this discordance of end diastolic pressures that occur all right how do we treat pericardial diseases well first thing is if it's acute it's all about the pain really that's the big thing that you're trying to treat but treat the underlying cause so one of the big things is most common cause of acute pericarditis is viral so cocci B virus so NSAIDs will help to reduce the inflammation there and colchicine will

help to again help to have a little bit of a prevention as well aspirin and colchicine would be the best if the cause is due to post MI and here's the biggest thing that can really trip you up with this on the exam uremia it's not doing any of these it's dialyzing these patients whether it's starting them on dialysis or giving them more frequent dialysis sessions that is super helpful and again treating acute pericarditis because if it's uremia these above measures won't help you it's dialyzing them because the uremia is causing these complications constricted pericarditis

again with this one it's usually a pericardyectomy so the pericardium is so fibrotic rigid there's nothing that you can really do you can try to treat the underlying causes from preventing the progression but you got to cut out that disease pericardium pericardial Fusion you don't really do anything it's just observation maybe get a Serial kind of transthoracic ultra echocardiogram in a couple months and then again if it's continuing to get bigger or you've figured out the underlying cause again then you can try and treat those but if it does not improve sometimes you can do

a pericardial window I would say this is for recurrent fusions that are usually neoplastic and origin so there's some type of neoplasia that's usually causing this and then designed to use the pericardial windows that the pericardial fluid doesn't collect collect collect collect and cause the patient to go into cardiac tamponade but if the patient does develop tamponade what is the treatment it's always stabilizing the hemodynamics because this can cause a patient to go into obstructive shock so give them IV fluids start them on vasopressors if need be but the best thing that you can do

for these patients is if it is again if it even if it is it says here non-hemopericardium even if it is a hemopericardium regardless you want to try to do a pericardiocentesis pull the fluid off because what you're going to do is you're going to help to make the diagnosis because if the blood pressure improves and they come out of the shock state again you've made the diagnosis oh it's cardiac tamponade Plus on top of that you've treated them therapeutically um if the patient does have a hemopericardium you can still do a pericardiocentesis but it's

not going to be enough because it'll likely re-accumulate and that's where this next step comes in if it is a hemopericardium you can do a pericardiocentesis first but you're probably going to have to go in and actually fix the underlying issue did the aortic dissection cause this did a free wall rupture cause this they develop trauma to the chest that caused this I got to go fix those things so it doesn't actually reaccumulate all right my friends that covers pericardial diseases I hope it made sense I hope that you guys enjoyed it and as always

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