Transcription
[Music] I'm going to talk about the role of Echo and pericardial diseases. So my objectives for today are: we'll talk about first the anatomy of the pericardium, the function of the pericardium, and then I'll go over some of the pericardial syndromes and mostly talk about acute pericarditis, pericardial effusion, and tamponade constriction restriction. And then, uh, we'll go over some other subtypes as well.
Um, so for my, uh, slides, I went over those two guidelines. So the first one is the ASC guidelines from, uh, 2013, and the second one is the 2015 ESC guidelines for the diagnosis and management of pericardial diseases.
Um, the first thing is the anatomy of the pericardium. So the normal pericardial, uh, thickness is less than two, uh, is one to 2 mm in thickness. It has two layers. There is an outer layer called the fibrous pericardium, and then there is an inner layer called the serous pericardium. And the serous pericardial layer itself has two parts. So the parietal layer covers the fibrous pericardium, and the visceral layer covers the heart, proximal great vessels, and variable amount of the epicardial fat.
Um, the reflection of the serous pericardium, so this layer, the, the reflection of the serous pericardium between the arteries and veins form sinuses and recesses, and I'll, I'll show you a couple of pictures for that. And then the pericardial fluid is drained by the lymphatic system and by the pericardial veins, which ultimately drain into the innominate veins. The pericardium also has extensive, uh, nerve autonomic innervation.
So those two images, the one on the left side shows you the layers of the pericardium. So this thick one is the fibrous layer, and then these are the, um, serous layer. So the, the, and the one attached to the fibrous pericardium is the parietal, and the one attached to the myocardium is the visceral layer of the serous pericardium. And this area in between is the, it's a small pericardial, um, space. And this, then you have the myocardium and then the chambers. On the right side, you have two. So these, I, I pointed towards this potential, uh, empty space, and this one reflects the superior aortic recess, which is between the ascending aorta and the SVC. And there is another one in the called the inferior aortic recess, uh, which is between the aorta and the right atrium.
And in terms of sinuses, the one over here on the left side, this is a, te, um, I couldn't find a good TTE, but this is the transverse sinus, which is a potential space between the ascending aorta and the left atrium. And this is the oblique sinus, which is posterior to the, post to the posterior wall of the left atrium.
So what are the functions of the pericardium? The mesothelium produces 25 to 50 cc of pericardial fluid, which has many functions. It works as an anti-inflammatory; it has antigen-presenting properties; and it has, um, f anti-enzymes and has pericine function. And it facilitates the sliding of the pericardial layers. It also provides mechanical protection and it limits the cardiac chamber distension. Uh, it also exerts a hemodynamic effect on the atria and ventricles, and it promotes the diastolic coupling or interdependence between the ventricles, uh, especially, I'll talk about this more in tamponade and constrictive pericarditis.
So pericarditis, very briefly, it's an inflammation of the pericardium. There are so many causes; it's a long list. You can have, um, it can be infection-related, autoimmune; it can be, um, malignancy-related. But in general, they can be either primary pericardial process or secondary to other etiologies, like, for example, a systemic illness like in lupus arthritis. Um, most common causes are idiopathic and viral infections, and majority of these cases are self-limited. And in terms of symptoms, if patients have, um, symptoms less than three months, we call it acute pericarditis, and if it's chronic, more than we call it chronic if it was more than three months.
So how does the echo help you with acute pericarditis? So echo, in general, is a very safe and easily readily available, uh, tool. It's, you can use it as the first imaging modality for pericarditis, and you can find, although it may be normal, there are a lot of things that you can find with pericarditis. So you can have a bright pericardium; you can find, you can see a pericardial fluid; for septal bounds, um, or even it shows you actually a physiology of tamponade. And then the other thing you need to look at with acute pericarditis is the LV wall motion. If you have a, a wall motion abnormality or LV dysfunction, always think about myopericarditis, and because those, those patients in general they have, um, elevated heart elevated troponin and, um, they will need further investigations like cardiac MRI, for example, to look for the extent of myocardial injury and involvement.
This slide shows, um, few findings in pericarditis. So on this one over here, I, I, this is a long, long peristal, long axis, and this is peristal short axis. What I want to show you here is the bright thick pericardium and po, so this is the, um, so this is the thick, so bright pericardial layer, and then, and, and it, and you can also see it over here. So inflamed pericardium. The one over here shows you, you can see all these walls over here are moving nicely, but this wall is down. So this person will need some other form of imaging modalities. And the one over here shows you a, the some fibrous strands in the pericardium, and you can see this in chronic pericarditis, um, in patients who have, for example, uremic pericarditis or in general, it's not very specific, but it tells you in general there's some, some sort of inflammation happening. And this one, I wanted to show you that you can also have masses in the pericardium that can cause, uh, pericarditis and effusion and tamponade.
So when do, when do we consider multimodality imaging? So when would, would you do CT scan or cardiac MRI? Um, if you have patients who have inconclusive Echo findings, or if a patient fails to respond to anti-inflammatory therapy, or if they have atypical presentation, let's say subacute pericarditis, or if you have suspicion of constriction, if someone has trauma, or if you think about other causes, like, for example, pancreatitis, infection, those patients will need further imaging. This is an MRI, but this is beyond the lecture itself. I just wanted to show you the, uh, so this is a T2, which shows stick, sorry, inflamed pericardium, and then this is the late gadolinium, which shows you inflamed myocardium.
The next thing I want to talk about is the pericardial effusion and tamponade. The normal amount of pericardial fluid is less than 50 cc. Um, if the, we call a pericardial effusion small if the size was less than 1 cm in diastole; it's moderate if it's 1 to 2 cm; if large, we call it large if it's, uh, more than 2 cm. And some in the Echo manual, they actually have another category. So if it's more than 2 and a half cm, they call it very large. Uh, the size of the, very, this is a very important, um, point to make: the size of the pericardial effusion correlates poorly with its hemodynamic, and this is what I'm trying to, I'll try to explain this over here. So what you see here is, uh, the pericardial pressure-volume relationship. And as you can see in normal pericardium, normal pericardium, the, pericardium is able to accommodate up to a certain amount of pericardial fluid, after which a small change without causing like big change in pressure. But after a certain point, even if you add the same amount of volume in the pericardium, it can result in a very high pressure change. If you, you get a steep rise in the, um, pericardial, uh, space pressure, causing, and at that point is when the patient has tamponade and becomes clinically unstable. Sorry.
Um, contrast this to patients who have chronic pericardium, and the reason why this happens that the pericardium is not, uh, remodeled in patients who have chronic pericardium. You can see, to begin with, it is able to accommodate a higher volume of, um, fluid in the pericardium before it reaches the pericardial stretch point and result in, uh, tamponade. So the tamponade physiology is somewhat similar to constriction, but the reason behind, um, the compression and, and abnormal pressure transmission is in particular pericardial in tamponade is related to pericardial fluid, while in contrast in constriction, it's because of fibrous tissue. I'll go over the hemodynamics of constriction after, but what you see here is basically when the, there is a cumulation of the pericardial space, results in inhibition of, cells, sorry, um, it prevents diastolic filling of cardiac chambers, which happens on the extent of both chambers. So if, if you get more filling on the right side, it reduces the filling on the left side, which reduces the cardiac output. And this is actually what we call clinically, uh, pulsus paradoxus. I'll go over this again later, uh, in the slides.
So what are the echo findings of tamponade? So with tamponade, there are a lot, so many signs, but they're not very specific. So you need more than one, like you need more than one, uh, sign to be able to, to diagnose p, uh, tamponade. So you can see pericardial effusion early; they, s collapse of the RV; collapse of the RA; dilated IVC with minimal or no collapse during inspiration; and then ventricular, you can also see ventricular interdependence and swing, ventricular interdependence, which basically causes clinically, um, pulsus paradoxus. And then also swinging of the heart in the pericardial space, which we see on ECG reflected as a, um, electrical alternans. And then, uh, there's also this is also very, very important part of the assessment of pericardial tamponade. So you, you'll have to, f to see, um, respiratory variation in the, um, tricuspid inflow and the mitral valve and flows, and I'll show you more pictures of, of this.
These two pictures just to show you the anatomy of and where to find the pericardial fluid. So this is descending aorta, and anything anterior to it will is the pericardial space. So this is pericardial fluid, and you can actually see some of it up here. And anything on the other side or sometimes we say below the, the descending aorta is pleural effusion. So this whole area is in the pleural space. Want to show you this, um, okay, okay. So what I wanted to show in this picture on, in the back is, um, ventricular interdependence. I can, okay, no. So what you see here is early collapse of the, uh, during the, the, um, inter, so the free wall in the, um, diast, so in diastole, because the, the RV normally expands to the outside, there should be no collapse during diastole, but with, in patients who have tamponade, you can see that during diastole the RV, um, uh, collapses toward to towards the, um, chamber. And this is a, um, oops, this is what you see here. So there is an RV collapse during diastole, but also it should, this picture shows, um, an RA collapse. Okay. So the, the other thing I wanted, I talked about was the ventricular interdependence, and the reason why it happens is because the ventricle, the right side and the left side with tamponade are not able to really expand on the outside. The right side filling has to comp, to, to accommodate this increase in right-sided filling. So the only way you can do that is by shifting the, um, interventricular septum towards the left side, and this is what, what you see in demonstrated here. So with inspiration, you get more filling of the right side, and to accommodate this volume, it shifts the septum towards the left ventricle. And then with expiration, there will be more filling of the left side, which compromises the right side. So the filling of one chamber happens on the expense of the other one. And this one is just to show you, um, IVC plethora. So as you can see, basically here, the IVC is not, is very large, and it's non-collapsable. This is why you would typically say RV pressure of 15.
This slide talks about the mitral inflow. So this, this is a PW across the, um, mitral valve. So what, what you see here is on the left side with inspiration, the pressure, the velocities go down. So with, this is during inspiration, and this is during expiration. So with expiration, you have higher velocities; with inspiration, you have lower velocities because the RV fills more. And this change for the mitral valve has, have to be more than 30%, and the way you calculate it is you go with expiratory, you would say, um, 124 - 99/124. So expiratory minus inspiratory over expiratory, and it has to be more than 30% for the mitral valve, and it needs to be more than 60% for the tricuspid valve. So as you can see here, with inspiration, the E velocities are higher; with expiration, it goes down. And this is also, you can also do that for the LVOT, and what you see here with inspiration and expiration is a drop with inspiration and increase with output with expiration. And this is what you find clinically if you do, um, if you look for, if you do blood pressure measurement, you, you, you, you can find, um, pulsus paradoxus. And in order for you to call it that, you need a drop in blood pressure, systolic blood pressure, more than 10 mm mercury with inspiration.
The ultrasound is not, not only helpful for diagnosis, but it also helps you for in terms of, um, therapy. So if you want to do pericardiocentesis, ultrasound guidance is very important pre, during, and after, because it can also help you tell when to, uh, take out the drain. Um, it also reduces the risk of major complications, and so which makes sense. So if you go and blind subcostally, the risk of major complications are 25, 5 to 25%; it goes down to 3% with ultrasound guidance.
Uh, this is another entity that I wanted to talk about. I didn't, I'm not going to talk about it in detail, uh, details. I left you the article here, so you can go over it if you want, but in general, low-pressure tamponade tends to happen in patients who have chronic pericardial effusion, whom if they have any reason for decreased intracardiac pressure, they go into tamponade. So if they are over-diuresed, have, if they have acute blood loss, and under, if they undergo dialysis, they can have, um, they can go into tamponade because they have higher pressures on the outside in the pericardium.
Um, there are other ones that I didn't, I'm not going to talk about in details either, but so one of them called, so the tamponade in pulmonary hypertension and postoperative effusion-related tamponade. And the reason why I wanted to bring these up is that they don't really have the classic findings of tamponade. So, and for example, pulmonary hypertension, because the right-sided pressures are high, patient can, can be in tamponade, but the, you won't find RA collapse, RV collapse because the pressures in, in, in inside the, um, chambers is elevated. And in the case of postoperative, if you generated tamponade because it can be localized, let's say to close to the right atrium or right ventricle, you won't really see the classic findings and the collapse of all chambers except that one, but it will have a hemodynamic effect on the, um, patient.
The second thing I wanted to talk about is the constriction, is constrictive pericarditis. It is somewhat similar to tamponade, but the reason behind that is not fluid but thick fibrous, um, pericardium. And what you see here is it, the chambers look relatively fine, but the patient has issues with, um, hemodynamics and filling because of the constrictive pericarditis. And this is an old study that looked into, um, the cause, causes of restrictive constrictive pericarditis, and it's good to say most of them were idiopathic, cardiac surgery pericarditis. But it's good to say it's that in the developing countries, infections are higher up is, is higher in the list, and most of them are because of TB, while in developed countries, you can have the idiopathic etiology, cardiac surgery, and radiation are more common.
So how do you make the diagnosis? You can do it through multiple imagings. Echo is also helpful here, and I show you the, I'll show you, I'll go through the Mayo Clinic criteria after, and you can make the diagnosis with confidence without even having to do right heart, like a heart cath, but sometimes it's, it's very difficult to reach the diagnosis of constriction. Sometimes it's mixed with restriction. So in these cases, you need to, sometimes you have, you end up having to do surgical exploration to be able to diagnose the patient appropriately.
Um, so this, I, I know I stressed a lot on the importance of, um, pericardial thickness, but I wanted to show you that in this study done back in 2003, they have patients who have surgically proven constrictive pericarditis, 18% of those patients had normal thickness of the pericardium, but they had actually constrictive pericarditis. So a normal pericardium does not rule out constrictive pericarditis.
So what's the physiology of constrictive pericarditis? Again, it is a thick stiff pericardium, which works as an insulator. So prevents the cardiac chambers from seeing the outside changes in the intrathoracic cavity. So which is normally, within inspiration, intrathoracic pressure drops, and, um, this will be reflected in the cardiac chambers. But in constriction, drop with inspiration, um, the filling of the RV is more favored over the filling of the LV because of the lower pulmonary vein-left atrial pressure gradient. And when this happens, just like what happens with, um, tamponade, the right side fills on the expense of the left side, causing ventricular interdependence. And then the flow velocities on the, uh, right sides will increase while the flow velocities on the left side will decrease with inspiration, and the opposite happens with expiration. This is a video from Mayo Clinic which shows these phenomena. So with inspiration, you can see the pressure on the left side drops, and the gradient between the pulmonary vein-left atrium drops, and the right-sided filling is increased. So this results in lower left-sided pressures and then, um, higher, uh, right-sided, tricuspid valve and hepatic vein pressure. And then the opposite, they'll show you also the opposite, which that, um, which happens with the expiration. So with expiration, more blood forces towards the left side, more filling of the left side, higher, um, velocities on the left side, and lower velocities on the right side.
I have some Doppler images to show you. Um, this, this is again ventricular interdependence. So more filling, um, septum shifts towards the septum shifts towards the LV on expiration, more filling with the left side, shift septum shifts towards the RV. Um, similar concept, right-sided pressures go up with inspiration, and then they go, sorry, this is a mitral, so this is the left-sided pressures go down with inspiration, and they go up with expiration. And then the opposite happens with the right-sided pressure. So they go up with inspiration; they go down with inspiration. Note that these numbers are different for constriction and tamponade. So with constriction, you need more than 40% change, while, while it was more than 60% for tamponade, and you need drop more than 25% in the left side compared to the 30% for tamponade.
Tissue Doppler is important as well, because not only helps you with the, the diagnosis, but also helps you differentiate restriction from constriction. So what you see here, because the lateral walls are constricted by the thick pericardium, they will not be able to move as, um, freely as they should be. And then the lateral e' will be lower than the medial e', which is not what you see normally. So normally the lateral walls have higher, um, e', while the, the medial one has a lower e', and this is called annulus reversus. So higher e' medially, lower e' laterally. And this is also hepatic vein Doppler. I just wanted to show you the flow reversal during expiration, as I said, right-sided, they go lower during expiration. This is also not be, this is beyond the lecture too, but I just wanted, I thought this looked really nice. So, uh, with inspiration, look at septal, so with inspiration, the septum moves towards the LV, and with expiration moves toward RV.
Um, so this is, so this is Mayo Clinic criteria for constrictive pericarditis. And what it looked at, they looked, um, into patients who have surgically proven constrictive pericarditis and looked into people who have severe TR because they can have similarities, and then also the, as well as, um, they, sorry, they looked into three, very multiple Echo findings, and they found that three of them were independently associated with constrictive pericarditis. So if you have, um, respiratory ventricular septal shift and medial e' different sources, they say different numbers, but in general 8 to 9 cm/second, and, and or if you have hepatic vein ratio in expiration more than 0.79, if you have the first one with one of the other two, you have an 87% sensitivity and 91% specificity for the diagnosis of constrictive carditis, and you don't really, you can make the diagnosis confidently without the need for heart cath. Um, if you, if you have all three, the specificity goes even higher, but this is on the expense of the sensitivity. So the sensitivity drops down to like 64%. And this is the same thing, but in, in, um, flowchart. So you can see here if you, it's on this side. So this, you have septal motion; if yes, if it's more than eight medial e', constrictive pericarditis. And if, if you also have another one, you can make a definite diagnosis of constriction.
So this slide talks about another kind. So effusive constrictive pericarditis is basically people who, who have, um, they present with, um, pericardial effusion, tamponade physiology, and then you drain them, and you remove the, uh, fluids from the pericardium and equalize the pressure, and then they still have, um, persistent diastolic filling abnormalities which go with restriction. So you can say that those patients are treated; you can retrospectively, um, diagnose them with restrictive pericarditis after removing the pericardial fluid.
Next thing I wanted to talk about is the constriction versus restriction. So an important point to make here is that with constriction, it's a pericardial disease, whereas, and, and, um, restriction, it's a myocardial disease. With, so the tissue Doppler velocities are also very helpful in these cases because it shows you a very low tissue Doppler velocity in restrictive, restrict in restriction, sorry, because it's a muscle issue. So the myocardium is affected, while in pure constrictive pericarditis, they have normal myocardium. So they will, the, um, the med, the, um, medial e' will be elevated because the annulus is moving freely and it's not restricted because it's not a muscle issue. And this is a video to show that. So over here, this, this is the normal finding. So you have higher lateral e' than medial e' because it's able to move, high, that normally moves more freely. And restriction, this, you can see that it's barely moving, and then the tissue Doppler is also very low, while in constriction, these ones are, um, constricted by the pericardium, while the medial e', you can see that it's, it's even bouncing outside the box; it's higher than the normal, um, a', medium e', sorry. And this is what they call, um, and this is what they call, um, annulus reversus.
So I wanted to make sure, like, to make a statement here: constrictive pericarditis and restriction, uh, may imitate each other, and it becomes very hard sometimes to differentiate between them. And in those cases, sometimes you, you have the only way you can establish diagnosis is after exp, like exploratory, um, thoracotomy. This is a, um, a table that you can see. There are a lot of similarities between constriction and restriction, but there are also some findings that you find in constriction but not restriction, like, for example, the septal bounds. The septal bounds is not the same as interdependence, um, and it's, I have a picture to show you after. And then you can, you get more respiratory variation with constriction but not restriction. You get the, um, pulmonary venous flow velocities are higher with restrict constriction but not with restriction; it's absent. And then the mitral ring tissue Doppler are very important. This is what we just talked about.
Um, in this slide, I wanted to show, so this is an M-mode through the RV interventricular septum, left ventricle, and then the posterior wall and the other structures. So what you see here, you, you see two things: you see ventricular interdependence. So this is interdependence, and what it does, these are changes with inspiration and expiration, while these jiggly movements here are the septal bounds, and you see them with constriction because the sudden movement because of higher pressures and the constriction itself.
Um, there are other pericardial, there are other findings in pericardial Echo that you can see with, but they're not really specifically pericardial, so I didn't really go over them, maybe in part two.
And then, fun fact, I want to, sh to talk about is, so the very first time, um, Echo was actually used was for detection of pericardial effusion. It was the first clinical application of Echo, but using A-mode. I don't think we use this anymore.
But it was back in 1963, and this is the first time sepal bouns was um described by Dr. Candalla in 1978.
And this is a very rich slide, but it's a summary of what you find in the tampana in terms of tissue dopplers and velocities.
And this is another slide for constriction.
Then these are my references.
Thank you very much.