Hi everybody, I'm going to do a really short video here on infectious inflammatory disease of the heart just to give you a good overview of what that entails. Pericarditis we'll start with. If you remember, the pericardium is what holds the heart in place.
It's stretchy, but only to a point. The pericardial cavity is filled with serous fluid. This provides cushion and protection for the heart.
Pericarditis is simply an inflammation of the pericardium, but of the whole pericardium, including the epicardium. It's not really divided. It doesn't just affect one or the other, but it affects the entire pericardium, which includes the pericardium on the outside, the pericardial cavity, and the epicardium. So it includes the whole thing.
There's a number of etiologies that can lead to pericarditis. There are viral TB, rheumatological disorders can lead to a pericarditis. Uremia, you can just have an idiopathic pericarditis. And rarely you will have cancer of nearby structures that can cause pericarditis. So the manifestation, the big three manifestations of pericarditis.
One is pleuritic chest pain. So really, what is pleuritic chest pain? It is pain that's worse with inspiration.
But another thing you can do to tell if this is really pleuritic is that if you have the individual lean forward and it improves, then that's indicative of a pleuritic chest pain. Because what happens is when you lean forward, you take the pressure off the heart. You will often hear a pericardial friction rub, which is best heard at the left sternal border. And I think one way to tell about this, if you hold your breath, it doesn't eliminate this rub. It's still there.
It's a scratchy, squeaky sound. It sounds like a continual murmur. Your EKG will show some nonspecific ST elevation. And you'll also see some, sometimes you'll see PR segment depression.
And this is a picture of an EKG. If you look at this, you see ST elevation all over the place and multiple leaves. It's very nonspecific.
And this is a telltale sign of pericarditis. So what do you do for it? You want to, of course, treat whatever that underlying cause may be, which we're going to talk about in a minute. But for any kind, colchicine and NSAIDs are your go-to.
And actually... Both of them together work best if you can give them together. If you can't, if you can't give colchicine because they're having terrible diarrhea, then just give the NSAIDs. If you can't give the NSAIDs because of renal function, then just give the colchicine. But if you can give both, that is the most effective form of treatment.
Alternately, you can, of course, get prednisone for this. There are many, there's some subtypes of pericarditis. There's the serous pericarditis. Uh, and so this is, remember that's serous fluid in the pericardium anyway.
Um, but this is when it gets outside of that, fills up that pericardial space and you have an effusion. And so when you have an effusion, uh, but it doesn't have any bacteria, anything in it, it's a serous effusion. Uh, we would, this is usually from a viral illness.
You can also have fibrinous pericarditis. Um, and that's when you get this fibrinous exudate in that pericardial cavity or fusion. This usually occurs post-MI trauma or cardiac surgery.
When somebody gets a post-MI, that's called Dressler syndrome. They often do give colchicine post-cardiac surgery to prevent this. And lastly, there's purulent pericarditis, which is bacterial in nature, usually secondary to hematogenesis spread or post-operatively.
It'll spread from some other infected area in the body. Of course, this does require antibiotics and sometimes drainage as well. Constrictive pericarditis.
If you, you know, if something is inflamed enough, it just keeps being inflamed, then it will scar. So the pericardium is one of these. If you inflame both sides of it, then it will just kind of meld together and will scar.
The fibrous pericardium is made again a fibro elastic material and it's supposed to stretch and accommodate the expanding ventricles during diastole It kind of separates the heart and the pericardial cavity from the rest of the mediastinum, but it gives room for that ventricle to relax during diastole. When it's scarred, it ceases to be elastic and becomes more like concrete. This prevents that ventricle from really relaxing like it should, and it impairs that filling that occurs during diastole. So what you will end up getting is they will not be able to fill up appropriately.
And so they'll get symptoms of diastolic heart failure or heart failure with preserved EF. So you'll see some of the JVD. You will see dyspnea on exertion.
You will see edema. But you'll also hear a pericardial knock, which is the sound of the ventricle striking that thickened pericardium. So this is when you have, you know, when this has gone on too long, that inflammatory.
process just keeps going that you can end up getting a constrictive pericarditis. Let's talk about pericardial effusions. The pericardial cavity normally has 15 to 50 mLs of fluid.
When somebody has an effusion of that pericardium, this, you know, over time you have an increased accumulation of this fluid and it causes that pericardium to stretch out. And so as that stretches out and that fluid gets in the way, you will, you know, you will not be able to hear that friction rub anymore, even though you may have heard it earlier during pericarditis, maybe without an effusion. But now with an effusion, you won't be able to hear it.
The heart sounds, because of all that fluid between the chest wall and the heart, the heart sounds are going to sound very distant. You can identify this on a chest x-ray. But you can also get it as an echocardiogram. There's several things that can cause a pericardial effusion. It can be hemorrhagic from surgery gone awry, from a hematoma, from some kind of trauma.
It can be a malignant pericardial effusion. It can be exudative from a TB or bacteria that we talked about earlier. It can also be transudated, which is when you just have extra fluid from either CHF, myxedema, nephrotic syndrome.
And really the only way to determine, okay, what is this, is by evaluating the pericardial fluid, which you'll have to do in a pericardial synthesis where you'll take some of the fluid out. Tamponade. So that fibrous pericardium, you know, again, made of that material, but it can stretch, but only a little bit.
And it is supposed to have, you know, it's supposed to take the shape to allow for diastolic filling. It'll kind of change shapes and then get formed to that newer, larger shape. If given enough time, it'll stretch out. conform to the new larger shape.
That means that the small pericardial fusions and large fusions that accumulate slowly over time can be accommodated by this fibrous pericardium. It can stretch over time, take that shape. So if you just have a small fusion or you have a fusion that comes up very gradually, then this fibrous pericardium will adjust to accommodate that.
If a pericardial effusion accumulates rapidly, so there's no time for that fibrous pericardium to stretch out and to accommodate, or if it's a very large volume, the effusion can then begin to impair your ventricular filling. The heart changes shape when it contracts, getting smaller so that it can expel the blood. It is then supposed to relax.
to fill for the next beat, expanding to its normal ventricular volume. And what happens in tamponade is the ventricles contract without difficulty, decreasing their volume. But the pericardial pressure is so high that the right ventricle, the left ventricle, and the pericardial effusion are all competing for space. So in tamponade, The effusion takes up the space of that decreased volume as the heart contracts.
The heart contracts, that pericardial fusion takes up that space. And then it prevents the heart from relaxing and filling up again, prevents that diastolic filling. And so if the heart can't fill, then it can't empty.
And so what you'll see are some of the main symptoms of Beck's triad. You'll see hypertension, sudden hypertension, usually sudden JVD, and of course those distant heart sounds. Um, you diagnose this, um, um, by, if you have time, you don't often have time.
It happens so fast. Um, but if you did, you would diagnose this by Poulsus paradoxus, which becomes exaggerated. Um, there just isn't enough room for both ventricles.
So they compete for that space. Uh, normally during inhalation, the right ventricle receives more preload and more venous return. Um, This increases that right ventricle volume.
But because there's no extra room in the pericardial space to expand into the right ventricle, then it expands into the left ventricle space. And that means a smaller left ventricle, which means a smaller left end diastolic pressure in that ventricle. And this leads to less stroke volume and less cardiac output. output on the next beat.
That being nudged by the right ventricle happens normally, but then there's an additional compromise of the left ventricular venous return caused by the bowing of that right ventricle into the left. So the finding that you will have is an exaggerated Pulitzer's paradoxus or a change in systolic blood pressure more than 10. 10 points or less than a greater than a 10 point change or a decrease of 10 points would define this hemodynamic consequence of tamponade. And that's a way that you diagnose it. So normally the variation in blood pressure between inhale and exhale will be 10 points or less and that's a decrease in 10 points between your inhalation and your exhalation and this is typically would be somebody using an ICU and having continuous monitoring so it's possible to do it manual it's just not very difficult to do the but in tamponade you'll have an exaggerated Pulse's Paradoxus in which we'll have more than 10 points decrease between inhalation and exhalation And that is just because of this effusion kind of taking the place of where the heart should be and not allowing it to fully expand and then contract much.
We're going to talk briefly about endocarditis. Endocarditis basically is inflammation of the endocardium. The endocardium lines the heart chambers and also lines the bowels. This is always secondary to vegetation or a bowel, which can occur quickly, which we'll talk about, or over time.
So infective endocarditis starts with some type of injury, usually secondary to some turbulent flow. some injury to the endothelium, the endothelium breaks and then clotting begins. So it could be some form of injury. This exposes the basement membrane of that endothelium.
And then you begin to have that whole process that we know take place where the healing process, where the platelets arrive, they adhere and aggregate at the site of the injury and form that temporary platelet plug. And then you have your clotting factors, which use the platelet plug to form a more permanent and stable fibrin thrombus. And this enables to the repair of the endopilium and eventually the removal of that thrombus. Now, if that same process occurs with organisms circulating in the blood as well, then when the platelets try to form their platelet plug, the organisms become trapped in it. and the platelets can't do their job quite as well as they're supposed to.
A fibrin thrombus attempts to form. But it serves only to really secure that organism inside it. So the immune system notices this and leukocytes attempt to fight the organisms.
But rather than a really clean fibrin thrombus we would normally have from a clean platelet plug and it resolves, the combination of the white blood cells, the platelets, the fibrin, and that organism forms this vegetation, which does not go away. It grows and that vegetation there with that organism inside of it, the vegetation kind of shields the organisms from our immune cells. And it allows those organisms to multiply and then to embolize.
So people then will have a bloodstream infection or bacteremia, which is constantly supplied with these new organisms that are being shed from this vegetation. So as vegetation spreads, there's more and more endothelial cells are claimed. Infective endocarditis, we will often see this in drug users.
The tricuspid valve is the most common site for this. And that's because, of course. In this instance, the bacteria is enduring usually through the skin that has not been cleaned prior to injection.
And when it comes in, of course, into your right atrium and then through the tricuspid valve, that's where the vegetation will begin to occur. I'm going to show you a little bit difference in the presentation of acute infective endocarditis and subacute endocarditis. A diagnosis of this is made by an echocardiogram.
But It really needs to be a transesophageal echocardiogram. They're much better at recognizing this vegetation. The treatment, regardless of the kind, is at least six weeks of antibiotics. Occasionally, surgery will be required. If it's a very large vegetation, if they have severe CHF secondary to some valvular destruction or the chordae tendina have ruptured, if it's a fungal infection, failure of antibiotics, or if they're...
embolization of this vegetation has occurred. You will see some prophylaxis of individuals who either had endocarditis or they had a prosthetic valve repair. They will require amoxicillin prior to dental or colon procedures. So in the acute form of this, I of course have an acute presentation. These are caused by really highly virulent organisms.
They're destructive. They eat up the valves that can cause a chordae tendineae to be damaged. And these can affect previously normal heart valves.
They often present with really large vegetations. The organisms are typically pretty easy to culture and to identify. And staph aureus, which is from your skin, is the most common.
The patient will present usually with high spiking favors. They'll have... positive blood cultures, evidence of valve destruction.
The bacteria gets into the valves and it erodes the valve leaflets and the chordae tendineae. And this will result in a new regurgitant murmur. So they'll have some regurgitation of whatever valve it's attacking. Again, bacteremia will be there. The new regurgitant murmur and evidence of bacteremia are really enough to...
to diagnose acute infective endocarditis. This of course can be found with an echocardiogram which you then can then can visual visualize the vegetation. If the vegetations get large enough they will immobilize and so as this is an acute disease you're not getting a lot of micro embolizations or little small ones you're getting big ones. And these can actually compromise arterial supply to distant organs.
You often see some really large ones originating with the mitral aortic valves. And they can go to any organ. If they originate in the tricuspid valve, they will then go to the lungs.
And these will have... They will have... elevation of their inflammatory markers as well. Treatment remains the same.
And subacute endocarditis, it presents insidiously because the infection is with different types of bacteria. These are less virulent organisms. They typically require a previously damaged heart valve to attack or a prosthetic valve, some congenital defect, maybe rheumatic disease, or they've previously had endocarditis. They'll present with smaller vegetations. The organisms are often difficult to culture, but they are also less likely to cause valve destruction or embolization.
Often repeated cultures will be required to identify the organism. And they will also have positive inflammatory markers. They will...
Embolization can occur in subacute infective endocarditis, but it's not in the same way. It typically consists of microembolization and immune complex vasculitis. Those are kind of these kind of result in some of the physical findings you may see. Microembolizations include splinter hemorrhages where you have these linear hemorrhages at the nails.
Janway lesions, which are painless areas of hemorrhage on the palms and the soles of the feet. Immune complex vasculitis lesions are Osler nodes, which are vasculitis on the tips of the fingers and the pads of the fingers. Those are painful.
And Rothspot, which are retinal hemorrhages that you'll see small irregular red areas with a central white dot that's showing you there. So those are some of it. kind of unusual findings that you do see with a more subacute infective endocarditis that's happened slowly over time.
So your patient presentation, gradual onset of symptoms, they may or may not have a fever, but it will be real vague. You know, they may get a fever one day and not have one the next. It just comes and goes. So not as with an acute infective endocarditis, they'll really have a, you know, they'll have a fever.
So a spike of fever will be significant. They'll present with some really nonspecific symptoms like weight loss and fatigue. They can have anemia of chronic disease.
So it's a little bit harder presentation. Again, the treatment really is the same, but it sometimes takes a little bit longer to diagnose the subacute presentation. Lastly, there are a form of non-bacterial thrombotic endocarditis. where there's no organs present. The vegetation is, instead of being an organism, it's a platelet fibrin aggregate and immune complexes.
This usually occurs on the mitral valve and it's often associated with some perineoplastic syndrome, somebody who's had cancer in a hypercoagulable state. These can embolize. So if they are found and diagnosed, that patient will require anticoagulants.
All right. And that is all. Thank you.