Thank you very much for the introduction, Anthony. Hello, everybody. I hope you're very excited to know a little bit more about the diagnosis and management of pericardial disease.

It's something that I wanted to talk about because it's something I see quite a lot, in the emergency-based practise that I work at and, and have, you know, worked at for the last sort of 10 years. And I think being able to at least diagnose and pericardis and tease these patients really is important. General practitioner skill.

So, OK, let's start out with the introduction. So, as I've said, it's a reasonably common emergency requiring immediate stabilisation, recognition and pericardiocentesis. And pericardial effusions have an overall prevalence of about 0.43% in, dogs examined at university teaching hospitals, and, they make up about 7% of all referral cases of dogs with clinical signs of cardiovascular disease.

So it's quite a lot. It's most common in dogs, as I'm sure you'll all know, due to sanguinous or sero sanguinous effusions, leading ultimately to signs of cardiac tamponade, and it's that in particular that makes these patients a cardiovascular emergency. So, the prognosis varies greatly in dogs and is based on the underlying diagnosis, and we say it is poor to guarded for patients with hemangiosarcoma with median survival times of approximately 1 to 4 months, and good to excellent for patients with idiopathic.

Pericarditis, and with survival times of up to 4 years being quoted. With regards to cats, fortunately we're not gonna have to talk about them too much, because they don't really get pericardial tamponade. I've seen two cases in the last 10 years.

But they do, however, get pericardial effusions. However, those effusions are never normally large enough to require drainage. So we'll touch on the cats just once or twice more, but generally everything that I'm going through today.

Pertains to dogs. So, a little bit about anatomy, I'm sorry to have to, you know, draw all this information back up from when you were at university, but it is pretty basic, and it's worth knowing about. So the pericardium consists of two tough fibrous layers, OK, which obviously surround the heart.

The outer fibrous pericardium is composed of collagen and elastin. Whilst the inner serous pericardium is composed of a single layer of mesothelial cells. So this serous pericardium lines the inside of the fibrous pericardium and is referred to as the parietal layer.

This parietal layer continues on the inside of the pericardial sac and then when the pericardial sac attaches to the base of the heart, this lining of mesothelial cells reflects back on itself at the base of the heart and covers the outside of the myocardium and can otherwise be referred to as the epicardium or the visceral layer of the serous pericardium. OK, so it just helps highlight that it's one continuous layer. Of lining that that lines the inside of the pericardial sac and the outside of the heart, if that makes sense.

So the two layers therefore of this serous pericardium create a potential space which is referred to as the pericardial cavity. And this is usually filled with a small volume, about 1 to 15 millilitres of lubricating pericardial fluid. The fluid itself is an ultrafiltrate of plasma and is produced by the visceral mesothelial cells.

And the pericardial fluid should be continuously being produced, pardon me, and drained accordingly via the lymphatic system into the mediastinum, and the right side of the heart, OK? The function of the pericardium itself is quite important, it does quite a few things. So the fluid that's within it reduces resistance during motion of the heart as it beats normally within the chest cavity.

The pericardiosac itself really helps maintain the shape of the heart as well. It acts as a buffer, a physical buffer, for the heart from external impact to protect it. And it also very importantly, acts as a barrier against infection and neoplasia, particularly from the lungs.

OK. So we obviously know about the ability for infectious organisms to translocate through the pulmonary parenya into the plural space and establish our pyothorax, you know, cats in particular. And you know, the, the job of the pericardium is to help prevent disease processes like that from affecting the heart itself, OK.

So now on to pathophysiology of pericardial effusions and pericardial tamponade. And I find this quite interesting because of, of the, the, the way that it's quite a unique process within this area of the body, whether you agree. Well, we'll see.

The, the process begins with irreversible fluid accumulation within the pericardial sac. Which ultimately is enough to exceed the volume of the pericardial space. The rate of the pericardial stretch, which is the stretching of the pericardial sac to help accommodate that extra fluid volume, but also the rate of pericardial drainage, OK.

So in the early stages, a small volume of fluid starts to fill the pericardial reserve and the pericardial pressure begins to rise. As the pressure rises in the pericardial sac, it first equalises with the right side of the heart, OK, at around 4 to 8 millimetres of mercury diastolic. So the right side of the heart has much lower filling pressures than the left side because it only has to pump blood to the lungs, whereas obviously the, the, the left side of the heart has to pump blood around the whole body.

So, as we get on to talking a bit more about the clinical signs that we see with pericardial disease, they particularly relate to disorder of the right side of the heart, OK? So we get this pressure rising in the pericardial sacer within that fluid that's accumulating in there at first, . Equalises with the right side of the heart.

As the pericardial pressure increases further, it becomes higher than the diastolic pressures on the right side of the heart. And as a result, it causes physical compression leading to collapse of the right side of the heart, OK? So, this causes two significant problems.

It significantly reduces the, the diastolic fill of the right side of the heart, which causes a big drop in the venous return, OK? It also then increases the central venous pressure, so the pressure within the caudal and cranial vena cava that that are draining into the right side of the heart. OK, so pressure starts to rise in those greater vessels.

Now why is that drop in Venus return such a problem? Well, due to the Frank Starling mechanism, a drop in Venus return to the right side of the heart results in an underloaded ventricle. And an underloaded ventricle, then will produce a smaller forward or stroke volume, OK.

So that decrease in venous return to the right side of the heart can reduce cardiac output by up to 21% because of this Frank Starling mechanism. So even though at this point, The pericardial fusion is not really directly affecting the left side of the heart, it's indirectly affecting the left side of the heart by underloading the right ventricle, if that makes sense. So in the later stages of cardiac tamponade.

The pericardial pressures become even more increased and eventually when they do become high enough, they can overcome the left atrial. And left ventricular pressures causing further collapse of those chambers and a further decrease in cardiac output and coronary blood flow. Now that's really quite uncommon to get to those sort of stages because the filling pressures on the left side of the heart are very high, and the left side of the heart has a very, very thick wall compared to the right, which again helps resist, collapse of that, that side of the heart.

But that decrease in cardiac output becomes really, really severe at that point and, your coronary blood flow, which supplies the myocardium. Obviously with this oxygenation comes out of the base of the aorta and actually occurs in diastole. So as pulsatile blood leaves the left ventricle through the aorta to go around the systemic circulatory system in the diastole, yeah, we get blood flow moving through the coronary arteries, to the myocardium.

So we do get a drop in coronary blood flow, but fortunately, as our heart is sort of not able to contract very well within this pericardial fusion, fortunately, the myocardium doesn't need too much blood flow at that point, and it tends to not affect, myocardial function too much. It doesn't tend to cause too much ischemia. So we also get the activation of the Renin angiotensin aldosterone system or the RAS.

And this happens as a sort of compensatory response to the drop in cardiac output, as we get in any patient who has heart failure signs. And this process leads to fluid retention within the kidneys because of sodium reabsorption. And because of, ADH binding to the collecting duct causing free water reabsorption, which also in combination with the elevated central venous pressure that we mentioned, a couple of slides back, ultimately precipitates in the development of pleural effusions and ascites in our patients.

OK. So we'll talk about that a bit more, when we go into clinical signs, but it's important to remember that, you know, when these guys, Develop congestive signs, they are congestive signs of pleural effusion, and cites and not pulmonary edoema. We also get a significant increase in the sympathetic tone as well, which causes tachycardia, and we get peripheral vasoconstriction as well of our arterios.

And that happens in an attempt to increase the systemic vascular resistance. in a bid to maintain, arterial blood pressure. OK.

So our arterial blood pressure is essentially determined by cardiac output multiplied by, the systemic vascular resistance. If our cardiac output has dropped because of the tamponade, what our body does is increases that systemic vascular resistance, to help maintain mean arterial pressures, so. So finally, the cardiac tamponade, if left untreated, will eventually overwhelm all compensatory mechanisms and lead to a state of obstructive shock and eventually cardiac arrest.

The final thing to sort of mention about the pathophysiology within the pericardial sac is that the fluid within it. Exhibits, this interesting relationship between the amount of volume of fluid that's in there and, and the pressure, that that fluid creates. And this occurs in two distinct phases, as my pretty awful hand-drawn, depiction shows on the right, whereby, In the early phase of fluid accumulation below this line here, what we see is that pericardial fluid volume increases quite significantly.

We don't get any significant increases in pericardial pressure, just a small increase up until this point, and that's essentially because of the pericardial stretch that's able to accommodate that fluid. However, in the late phase of fluid accumulation, we see that just small increases in fluid volume within the pericardial space lead to significant increases in pericardial pressure, OK, which is what leads to our tamponade. And this diagram helps to sort of explain the reason why when we are draining our patients who are in pericardial tamponade, generally, you only need to actually drain off the 1st 3rd of the fluid, to be able to relieve the tamponade and restore near normal heart function.

Now that doesn't mean that in every case, we say, only drain the 1st 3rd of the pericardial effusion. But what it means is that if you've got a case that you're really struggling to drain, it may be that actually as long as you've got about 1/3 of that fluid out of there, you've probably improved the tampona enough for that patient to be able to be left overnight. With monitoring and be referred on somewhere else the next day or have a second drainage attempted by yourself in clinic, OK?

So that was talking about pericardial stretch and how much fluid the pericardium can accommodate. There are a few things we need to be aware of that will affect how much the pericardium can stretch. So the first one is crinicity, and what we know is that generally the slower the effusion develops, the more time the pericardium has to stretch to therefore accommodate it, OK?

So we find that more chronic, slower pericardial effusions are often bigger at the time of diagnosis, because the heart, the pericardium, sorry, has had a chance to stretch to accommodate it. Whereas, effusions that have developed much more quickly, you know, tend to be smaller at diagnosis because the pericardium hasn't had a chance, a chance to stretch, and we'll come on to the two different reasons why, the effusion may develop at different speeds in just a few more slides. There are other diseases as well that can reduce the compliance of the pericardial sac.

And these include our primary malignancies of the pericardial sac, which is pericardial mesothelioma. We'll talk about that in a few more slides. Scarring of the pericardial sac following any sort of surgery, and chronic inflammation affecting the pericardial sac as well.

So we can see that in patients who've had multiple pericardiocentesis, for instance, that leads to inflammation of the pericardial sac. But another, disease process that I suppose springs to mind is patients, who've had a chronic kyothorax. The yothorax does, really initiate a, a process of chronic inflammation within the pericardial sac, and often when a patient goes for surgical referral for a yothorax, they often do do a pericardectomy to help prevent the development of chronic inflammation and fibrosis in the pericardial sac long term.

OK, good. So we're just going to move on to talk a little bit more about the aetiology now of pericardial effusions, primarily within dogs as I say, cos that's who we're gonna be seeing this disease in by far most commonly. So hemorrhagic effusions are the most common cause of effusions within dogs.

And what that means is that the fluid that we drain from the pericardial space appears really dark red in colour, like a fine burgundy wine, I suppose we'd say. And what we know is that when we get that pericardial fluid out of the patient and we're draining it into a kidney dish, that pericardial fluid, even though it can look like blood, it should never clot like blood. If it is clotting like blood as you're draining it out, then that veterinary surge is unfortunately probably in the heart, draining the ventricular lumen rather than being in the pericardial space.

So that's always something to be aware of when. You, you're performing pericardiocentesis. I've never seen this firsthand, drainage of the heart rather than the pericardial space, but I have heard of it anecdotally in practise, OK?

Generally, the hemorrhagic effusions that we see in dogs are caused by either, neoplastic disease or idiopathic sterile inflammatory disease. So let's go through each of those in a little bit more detail. Starting with the neoplastic pericardial effusions.

Well, we tend to see these more commonly in the older patients. So generally, those dogs that are over 7 years of age at presentation are more likely to have neoplasia as their cause of refusion than than idiopathic disease, but it certainly isn't an absolute cut off by any means. The incidence of cardiac tumours in general has been reported with an incidence rate of perhaps about 0.2%.

And something that's quite interesting when you look at some of the retrospective studies of pericardial disease is that dogs with a history of collapse, were more likely to present with a mass on echocardiography. And, the dogs that didn't have a mass at echocardiography, either the ones that had idiopathic disease were less likely to present, with a history of collapse. And that's possibly.

Because the patients who have neoplastic causes of their pericardial effusions, they tend to develop quite quickly. And as a result of that, I think the pericardial sac likely doesn't have a huge amount of time to stretch and accommodate it and cause other clinical signs before the tamponade occurs. So of all the neoplastic pericardial effusions, by far the most common one that we see is the hemangiosarcoma.

And this represents about 70% of cardiac masses in several retrospective studies looking at pericardial disease. But it is fortunately uncommon in cats. The next most common tumours that we then see are mesothelioma of the pericardial sac, chemoectommas, lymphoma, and ectopic thyroid carcinomas.

So we're gonna go through each of these in a touch more detail. So Hemangiosarcomas are a nasty tumour as we all know, and they're unfortunately common in pericardial disease and they tend to quite commonly affect the same areas of the heart and that typically tends to be the right atrium or the right aricular appendage of the heart. Hemangiosarcomas are very vascular tumours.

They are a vascular primary vascular tumour, and they are therefore at risk of rupture leading to hemorrhagic effusions, just as these guys do in the abdomen, when we see patients who present with hemo abdomen and splenic rupture because of HSAs. So HSAs commonly do involve the spleen, and I think it's always sensible in a patient that we suspect of having, a cardiac, hemiosarcom. It's very sensible, to scan the spleen to look for, for metastatic spread or even for a primary, and bear in mind that we may have concurrent hemoabdomen in these guys as well.

So German shepherds are overrepresented for all common, all forms of Hemangiosarcomas, so we see lots and lots of German shepherds with heme abdomens because of ruptured splenic HSAs, but I think it's very much the same in pericardial effusions. And when I see a German Shepherd with a pericardial effusion, it is generally a HSA until proven otherwise. And I can't remember a German Shepherd that I've treated with a pericardial effusion that didn't have a characteristic, right atrial mass on echocardiography.

The image to the right is just a postmortem here, of a HSA on the right side of the heart, just showing how, sort of vascular, in nature it is and how friable you can imagine that tissue is as well, quite commonly leading to rupture. HSAs are highly metastatic malignant neoplasms, as we know, and they commonly metastasize to the liver, lungs, and kidneys. So when we are, you know, screening patients for HSAs, it's very sensible, to image all of these areas.

Survival times are short in patients with hemangiosarcomas, with the median survival time. Meaning about as low as 26 days for dogs with right atrial hemaosarcomas with a neoplastic pericardial effusion. OK, so it's a pretty much a game over type diagnosis in most patients that present in first opinion practise.

Sadly, survival times may still be lower than 2 months from diagnosis, even with pericardectomy. So we talk about surgical interventions towards the end of the lecture. And actually, patients who do undergo pericardectomy, alone may actually have no increased survival time over those that just undergo pericardiocentesis.

In selected cases, however, surgical debulking of a right aricular mass followed by chemotherapy may improve our life expectancy, although reported median survival times are still less than 6 months. Chemodectoma is the next most common form of neoplasia that causes pericardial effusions, and it is itself the most common form of heart-based tumour. So, these tend to arise from chemoreceptor cells at the base of the aorta.

And chemodectomas are quite slow growing masses that actually have quite a low metastatic potential indeed. And therefore, these guys, unlike HSAs actually may be treated effectively with surgery. Chemodectommas are most commonly seen in brachycephalic dogs, and we think that may be associated with, brachycephalic obstructive airway syndrome in these patients, almost causing a state of chronic hypoxia that causes neoplastic proliferation of these chemoreceptors at the base of the aorta.

So certainly, you know, I picked these up. Quite commonly in brachycephalic dogs as a cause of their pericardial effusion, but also, I pick up lots of these guys as an incidental finding in dogs that are undergoing, for instance, CT of the thorax for something else, and you pick them up as an incidental finding when they've not got a pericardial effusion associated with it, you know, and those tumours can sit there for months to years and cause very little problems unless they incite a pericardial effusion. Pericardial effusions caused by chemodectomas not treated surgically have similar survival times to patients with sarcomas.

However, those patients that do undergo pericardectomy, do have a significant increase in survival time, extending survival times from less than 2 months, to approximately 2 years. OK. So these guys certainly are, surgical candidates.

Just moving on to pericardial mesothelioma, these are tumours that can be very hard to diagnose, OK, and can often be mistakenly treated as idiopathic pericarditis. So pericardial mesothelioma can cause the slightest thickening. Of the pericardial sac, and that can be completely missed even on advanced imaging with CT contrast, it, they're very rarely if ever diagnosed echocardiographically, and ultimately these guys are normally diagnosed, Following surgical pericardectomy, where the pericardial sac is stripped from the heart and always sent off for histopathology, and some of those patients that you think, you know, an initial diagnosis or idiopathic cases actually end up coming back as pericardial mesothelioma, from the lab.

So, they are tricky ones to diagnose indeed. Then we see patients with stage 5 lymphoma. So stage 5 lymphoma is lymphoma that either affects your blood, so the leukemic lymphoma or your bone marrow or it involves any extra lymphoreticular sites.

So anything out of your out of your lymphoreticular system, which certainly includes the heart and the pericardial sac. So you can see these in dogs and cats. I've diagnosed a couple in cats, and just recently one in a dog, .

And these can be treated with multimodal chemotherapy, sort of standard multi-drug protocols, however, they do unfortunately carry a long term prognosis that is quite poor. Other forms of neoplasia include various different heart-based tumours, including malignant histiocytosis and metastatic carcinomas as well. So this was just a little, echocardiogram from a patient that I was investigating.

That didn't have a pericardial effusion but did have signs of right side and congestive heart failure because of rhythmogenic right ventricular cardiomyopathy. But he was a brachycephalic dog and we picked up, this incidental mass, here at the base of his aorta. So this is the left ventricle.

The heart, this is the right ventricle, the right atrium. This here is the left ventricular outflow tract in the aorta and this big thing here, is, is a suspected chemodectoma that was sat at the base of this dog's heart and actually not causing any, clinical problems in this patient, OK? Well, skip to the next slide.

OK, good. So if we've not got neoplastic causes of our pericardial effusion, by far the most common cause would then be idiopathic or benign pericarditis, and this is the one that we want to diagnose if at all possible, it's by far the more treatable. So this is most common in younger.

Medium to large breed dogs, OK, so if they're young, large breed dogs, they're probably more likely to have neopathic forms. If they're smaller, older dogs, they're more likely probably to have neoplastic forms. And we commonly see this in golden retrievers, Labrador retrievers, Saint Bernards.

And Newfoundlands, although any breed of any size may be affected. The median age of presentation is about 6 to 7 years, and we seem to see that males are significantly overrepresented with this form of disease. So with these patients, we get a mild sterile pericardial inflammation of unknown cause, hence the idiopathic, which leads to perivascular fibrosis and focal haemorrhage from the pericardium.

And this leads to a fusion being produced by the mesothelial cells within that pericardium. This may be a recurrent process in which fibrosis of the pericardium, you know, starts to affect the stretch, and this can lead to what we call a constrictive, pericardial disease, which is really quite an unusual sort of form of pericardial disease and really quite hard to. Echocardiographically, but it is essentially the end stage fibrosis of the pericardial sac, meaning that not only does it lose its stretch, but it actually starts to constrict tightly around the heart like a band significantly affecting its diastolic function.

And certainly constrictive pericardial disease, really needs, surgical intervention. So patients with idiopathic pericarditis and pericardial tamponade are more likely to present with ascites than patients with neoplastic effusions and also to present with a larger volume of pericardial effusion than patients with neoplastic effusions. That's looking at a couple of retrospective studies, .

And generally, that can be of some use. So you've got that patient in front of you and you're trying to differentiate whether they've got idiopathic or neoplastic causes. If they've got a SITS, perhaps it's more likely to be idiopathic.

And that's because the disease process with idiopathic pericarditis is much more slow in its development. And that basically means that we get stretching of the pericardial sac, and a sort of more slow development of tamponade, and right sided congestive heart failure signs, which kind of gives us, well, that patient time to develop ascites in its abdomen, OK? Whereas those patients with the neoplastic effusions, often that tamponade occurs so quickly, that they go into significant cardiovascular collapse before they can develop, significant ascites.

OK? So the prognosis with this form of disease is variable, as some patients need a single drainage for cure, whereas other patients need multiple drainages for cure, and some of those guys, the effusions keep coming back and don't resolve with pericardiocentesis alone. So we say among echo negative dogs, which means dogs that we don't see, a tumour, an echocardiography, about 64% have relapse and fusion.

So it's a good sort of take home message to be able to advise clients, look, I can drain your dogs, pericardial effusion today, and if we don't think it's neoplastic, then, you know, there's a 1/3 chance that it'll be cured from that single drainage, but 2/3 of the time we're going to have to be thinking about what we're going to do if it reoccurs, repeat drainages and or surgery. So effusions in echo negative dogs that do not resolve with multiple drainages, may be treated sur surgically, as I say, we'll come on to that later on. So we get much better survival times in patients with idiopathic, pericarditis than neoplastic, with median survival times of about 1000 days, being reported.

Other causes of pericardial effusions, some of these are things that we should just be aware of, but they are really quite uncommon. So left atrial rupture is one that's important to be aware of, and I've seen a couple of cases of those in the last few years, and that occurs secondary to significant enlargement of the left atrium in patients with really advanced mitral valve disease, and essentially we get a little tear of the left atrial wall which causes blood. To leave the left atrium and go directly into the pericardial sac, leading to rapid development of pericardial effusion and tamponade.

Now these are about the only form of pericardial effusion that you should not drain as they are continuous and will continue to develop and you will essentially exsanguinate that patient. Sometimes, you'll see these patients when you're doing an echocardiography and they've, they've had a bleed and it's formed a clot and you can see a big fat thrombus sometimes sat on the outside of the heart adhered to where the tear is, . Coagulopathy is a cause of pericardial effusions, but normally it's quite an obvious cause to, to diagnose because generally the patients will have other signs of bleeding di diathesses.

So bleeding is the GI tracts, the urinary bladder from mucous membranes, etc. Etc. Penetrations can be seen as well.

So we've seen a few stabbings that have led to low volume pericardial effusions. In dogs in particular, but you'll also see them, with overzealous, thoracocentesis and pericardiocentesis leading to iatrogenic, damage of the heart. Septic pericarditis is a very, very rare form of pericardial disease in dogs in particular, but is most commonly associated with.

Migrating, foreign bodies such as grass horns that migrate through the pulmonary tissue, enter the pericardial sac, and set up bacterial infection in there, although we can sometimes see hematogenous spread of fastidious organisms to the pericardial space from other areas of the body as well. In cats, with wet or effusive FIP, it's quite common, to see pericardial effusions, and that effusion would be what we class as a non-septic exudate, but it's very uncommon for those effusions to be big enough to cause tamerard. Where we do see a lot of pericardial effusions in cats is those with congestive heart failure.

Cats with congestive heart failure have reduced lymphatic drainage of the pericardial space, and as a result they do develop often sort of mild pericardial effusions and congestive heart failure that doesn't warrant any specific therapy, unto itself and certainly doesn't require drainage. Hypoalbuinemia again can lead to development of third spacing of fluid, whether that be plural space, abdominal cavity or pericardial space, but again, that's quite an uncommon form. OK, so let's go on to the clinical signs of this disorder.

Initially, the clinical signs are very vague and non-specific as these effusions sort of slowly develop. One thing that we do sometimes anecdotally hear about is patients having some degree of PUPD. However, in the build up to, an episode of tamponade, but it's not, not that common.

But as the tamponade really does start to develop and affect our, cardiac output, we get the classical signs associated with. Heart failure of weakness, exercise intolerance, progressive lethargy, weight loss. Abdominal distention, your scis.

And sometimes we might get syncope, cough, and collapse, although generally, you know, those three things are more commonly associated with left-sided cardiac failure and the vast majority of the signs we see in our patients are primarily right-sided congestive heart failure. So what are we going to pick up on our physical exam? So we will see muffled heart sounds very commonly, and particularly on the right side of the thorax, and that might be because of the pericardial effusion itself, muffling our heart sounds, but it might also be because of a concurrent pleural effusion, which we often get in patients with, with right-sided congestive heart failure, which will muffle our heart sounds.

I said earlier, we commonly are seeing tachycardia in these patients. And tachypnea as well. And the tachypnea is often due to pleural effusion, because of the, as I say, diastolic right-sided, collapse.

Something that I always look out for, and it's something that I think is really, really quite commonly overlooked on our physical examinations, are looking for evidence of distention of the jugular. So whenever I'm checking my patients, I'll clip a little bit of hair around the jugular for the long head, but with the short hair, you can just spray a little bit of spirit on that area. And if you lift the head up and look at the jugular, it should be raised in patients that have congestive, sorry, it should be distended.

And without you having to raise it in patients with right-sided congestive heart failure because of elevated central venous pressures. So that's something that's really, really, really useful to look out for. You may also see jugular pulsation as well as a sign of heart right-sided heart failure.

So you generally see the lower third of the jugular pulsing away. And that's quite commonly seen in patients with right-sided heart failure and concurrent tricuspid regurgitation. Another cool test that you can do as well if you're suspicious of right-sided heart failure, but the jugular's not that distended, is the hepatojugular reflux.

So you stand at the head end of the pet with them stood. Up and have a look at the jugular vein whilst one of your colleagues really quite firmly presses on the cranial abdomen in the area of the liver as its jugular reflux name suggests. And what you tend to see is that as they push really hard on the cranial abdomen, you see that the jugular vein becomes raised and distended, OK?

And if you see that, that's apatic jugular reflux and that indicates right sided heart failure, OK? Ascites as I've said, is very common, so we're gonna check for that by blotting the abdomen and just looking for distention. And we'll also generally see some reduction in femoral pulse quality, particularly more advanced tamponade, and also pulsus paradoxus.

Now this is a, I think it's quite a subtle, physical examination finding, but when you do see it again, it can be highly indicative, of, cardiac tamponade. And basically, it's a reduction in pulse pressure when the patient breathes in, OK, so you get this phasic increase and decrease in pulse pressure during the patient's respiration. We might see pale mucous membranes and reduced capillary refill time, indicative of poor peripheral perfusion because of the low cardiac output.

And bear in mind as well, even though this is a cardiovascular disorder, we don't tend to hear heart murmurs, OK, because this is not a primary, disease of the myocardium itself or of the the valvular apparatus, but it's a pericardial disease, so, you very infrequently have murmurs. So just going a bit more onto diagnosis, we've done our physical examination and we're highly suspicious that we would be perhaps in this patient with a very acitic abdomen with distended jugular veins that they've got. Pericardial effusion and tamponade.

What's the next step? Well, for me, it would always be what we'd call a point of care thoracic ultrasound. So we come on to that just in a couple of slides.

But I think now within the sort of, realm of emergency and critical care. We are more and more using ultrasonography for investigation of thoracic emergencies instead of radiography, because that can be performed generally in the conscious patient with them happily stood up or sat up in sternal position, whatever makes them more comfortable. Rather than radiography, which needs a lot more generally chemical or physical restraint.

So what are we looking out for on our radiographs? Well, enlargement of the cardiac silhouette, and it's often very globoid or rounded on both views. We're gonna check for er sorry, plural effusions.

We're gonna look for distension of the caudal vena cava. . Remember, pulmonary edema's not that common, because that's a sign of left-sided heart failure.

And these guys can be quite tricky, and they can mimic patients who've got congestive heart failure because of DCM because those guys again are often young, large breed dogs with big round hearts and effusions on, on radiography. And we may also see metastatic lung disease in patients with hemangiosarcoma. So here's just a couple of radiographs.

Just to highlight how significant the cardiomegaly is in this patient, the heart should never fill more than 2/3 of the thorax at this level, on a, on a DV view, and that certainly is, is getting towards 80, 90%. It's very rounded, you can't see individual chamber enlargement, very much the same thing here as well, in this, OK. Electrocardiography.

You open the textbooks and it says electrical alterns, you know, this, this is highly indicative of a pericardial effusion. This is where you see varying amplitudes of your QRS complexes. So we go from tall to small, tall to small.

And, and that's representative of the fact that the heart is swinging back and forth in the pericardial, fluid. So obviously the voltage that you're measuring from your leads is gonna, alter as that heart moves to and away from the different leads. .

So yeah, you certainly can see this in patients with pericardial effusions, but you do see it with other disorders as well. And I certainly think that this is really quite uncommon er that I see this even in patients in really quite large pericardial effusions. Other things that you sometimes see are just generally small amplitude QRS complexes, obviously tachycardia, as I said, VPCs may be seen as well, although they're probably more common post-drainage.

So echocardiography, as I say, this is really the, the best way in my opinion, of diagnosing these patients with pericardial effusions, and this is exactly how I would do it. A point of care, really quite simple ultrasound unit here. We've got a patient who is sat internal recumbency, and they could be on flow by oxygen, minimal restraint, certainly no chemical restraint.

And you know what, a lot of dogs, you don't even need to clip the fur off the side of the thorax. You just spray a load of spirit, on that side of the chest, bang a load of ultrasound gel on here, pop your probe on, and you will get a really good image of that patient's heart, pericardial effusion, pericardio sac, and pleural effusion. So, this is definitely the, the, the way I think we should be diagnosing these problems.

Then if you're quite confident with your thoracic ultrasonography, you might want to also, sorry about that, you also might want to look for evidence of any neoplasia of the heart because at this point, if we're doing, . About to do a pericardiocentesis, if we can diagnose cardiac neoplasia, that kind of changes the whole prognosis, and the treatment plan and and where the owners might then want to go with their pets, so, . That's how we generally quite commonly diagnose cardiac neoplasia.

And one thing to bear in mind is that masses of the heart are much easier to see on ultrasound when there is a pericardial effusion present. So if you do have somebody who's in the area or in your practise who does do echocardiography, it's a great idea to maybe try and get them to quickly scan the patient before you drain that effusion, cause, the effusion gives nice contrast, to, to a lot of pericardial masses to spot them more easily. I also like to use ultrasound.

During pericardiocentesis to guide what I'm doing. So these are a couple of videos that I hope will play nicely of pericardial effusions. So this is the heart in its long axis.

You've got the left ventricle here, the right ventricle here. What you'll see up here is the right atrium and you'll notice that the right side of the heart is collapsing in diastole because of this, . Pericardial effusion here, so pericardial effusion, here's the pericardial sac and the right side of the heart here is undergoing dioid collapse, you can see that right atrium there collapsing, OK, this is, A short axis view of the heart, and we've got the left ventricle here, very rounded chamber with two papillary muscles, and then we've got the, the right ventricle wrapped around that.

And what you see in this patient is again, we've got a pericardial effusion. You'll see the pericardial sac here. You'll even see a bit of pleural effusion on the other side of the pericardial sac.

But watch what keeps bobbing in and out of the image here in this area. So pleural effusion, pericardial sac, pericardial effusion, collapse of the right ventricle, but this here, as we found higher up, during the echocardiographic study, was a right atrial hemangiosarcoma. Attached to the, to, well, this German shepherd's right atrium.

So you can imagine that, you know, that's actually not a particularly hard type of cardiac neoplasia to diagnose echocardiographically, OK, so you should give them a go, but they're not all that easy. So echocardiography, it's, it's, you know, certainly, a good way to screen for cardiac neoplasia. However, the accuracy of presumptive diagnosis, of the type of, cardiac neoplasia, based on its appearancecardiographically is, was only moderate when, when we look at postmortem, in some of these cases in a retrospective study.

And cardiac tumours that, that in this study were considered to look unusual on an echocardiogram actually were found to be quite common forms of cardiac neoplasia. So what can we, you know, sort of make from, take home from that? Well, we can generally diagnose neoplasia with echocardiography, but perhaps not the type of neoplasia based on its echocardiographic appearance.

So what other ways have we got of imaging patients? Well, cardiac MRI is frequently used in people with pericardial effusion to screen for neoplasia. However, in one study in dogs, it did not improve the diagnosis of cardiac tumours when compared with TTE, which is transthoracic echocardiography.

OK, so no better than echo. But it did yield useful information regarding the extent, anatomical location and potential tumour type. With multi-detector CT, a series of 11 cases, looked at this and again found that CT did not improve the detection of cardiac masses in dogs with pericardial effusion over echocardiography.

However, it was very useful in screening for pulmonary metastasis and extra cardiac lesions, OK? A fusion analysis, we're gonna talk about pericardiocentesis at any point. But bear in mind as we're doing our pericardiocentesis, we need to collect samples in plane tubes for culture and sensitivity and EDTA tubes for cytology.

However, the diagnostic utility of cytological analysis of pericardial effusions is very variable, and often fluid analysis is not able to definitively diagnose our cause, so it cannot, the vast majority of cases, differentiate idiopathic from neoplastic causes. And that's because most of the neoplastic causes, their cells do not readily exfoliate into the pericardial effusion. The exception to that, however, is lymphoma, where you very commonly see, neoplastic cells in the fusion, and also in infectious diseases where you see, inflammatory infiltrates that are consistent with infectious disease.

So there's been some studies looking at other things that we can check with the pericardial fluid and one study found that neoplastic pericardial effusion values for lactate, hematocrit, and urea nitrogen was significantly higher compared to idiopathic cases, whereas values for pH bicarbonate and chloride was significantly lower. So. Unfortunately, even though there were significant differences between groups, there was too much overlap to allow us to draw any meaningful cutoffs from these studies, OK.

So essentially, a fusion analysis is not, not of any significant use. Perhaps troponin, is of some use. A series of 37 dogs, the pericardial effusions found that lo and behold, those are the fusions had higher serum concentrations than normal dogs, as you'd probably expect.

But actually dogs with hemangiosarcoma had significantly higher concentrations of troponin than did those with idiopathic effusions. So, we've got 10 minutes to quickly go through how we're going to drain these guys. Well, all patients with tamponade need to undergo pericardiocentesis, and as we said earlier, a significant percentage of patients, will need repeated pericardiocentesis, about 50%, will need several drainages.

There is some, . Sort of, people who condone the use of prednisolone as an anti-inflammatory in patients with idiopathic pericarditis because it's an inflammatory disease. However, I don't think there's any studies backing use that up and and I use it.

So how are we gonna perform pericardiocentesis? OK, it's important to get this right, and fortunately there aren't too many things I have to remember. I've got some images and I've got a video as well to show you this being done.

So I position my patient's internal recumbency with oxygen supplementation administered throughout, as flow by using a mask. We need an IV placed in all our patients with a crash kit on standby, because they can, at any point potentially go into cardiorespiratory arrest. I've only had that twice happen in the last 10 years, but it's never a nice thing when it does happen.

. Chemical restraint is not always necessary. Some of these patients are so collapsed, you can perform pericardiocentesis with no chemical restraint whatsoever. But I tend to find it is uncomfortable to some degree, and that most benefit from at least butorphenol, not so much as an analgesic, but more because of its sedative effects.

And I use anything from 0.2 to 0.5 migs per gig titrated to affect IV, plus or minus ACP if you absolutely need to give more chemical restraint.

To be able to drain them, but what we definitely don't ever want to be doing is anaesthetizing our patients with pericardial effusions. So we'll get our nurse to clip and aseptically prepare the right side of the chest, and we often perform, an intercostal nerve block, the 5th to 6th rib space with lidocaine. Talking about that is sort of beyond the scope of, of what we're gonna do today, but it's something that I think .

We should be, you know, familiar with as a technique, because it really does help reduce the amount of sedation we need to give these patients to perform the procedure because it keeps them much more comfortable when we're introducing that quite thick drain through the intercostal muscles, and in our practise, it's, it's the nurses who tend to perform this procedure. As the vets are preparing, their kits. So we need to drape the site, and we've got several options of what kind of equipment we're going to use to perform the pericardiocentesis.

So I tend to favour theseeldinger pericardiocentesis kits. One here. There's a couple of different companies that do them.

I don't think I could probably mention their names on this webinar, but they cost about 50, 60 pounds, and it's everything you'll need to perform pericardiocentesis. You've got a scalpel even, guide wire, a dilator, the drain, your needle. It's all you need in that kit.

And certainly having used IV catheters before, I find that these drains will drain all of the effusion. And much more quickly than if you're messing around with an IV catheter that's constantly sliding out of the pericardial space or kinking and and I certainly would recommend getting a couple of these in stock if you are seeing. Pericardial effusions regularly, commonly.

I have used the technique before as well of using an IV catheter and threading a cat urinary catheter through the inside of that lumen, to help, facilitate drainage, but I very frequently ever have used a pigtail catheter kit. So, I'll talk through it perhaps as we go through the pictures rather than all this text. So this was a dog that I did at my last practise and we've got the patient internal, oxygen flow by, we are performing an intercostal nerve block here with local anaesthetic.

And where we're draping off the patient, and then I like to use the ultrasound probe to identify where I'm going to go with my needle and watch the needle as I introduce it to pericardial space. Now that definitely is not essential. If you don't have ultrasound, if you go in at the 5th and 6th, rib spaces, you will not miss a pericardial effusion.

There's a nice notch there where there's no lung tissue. And you have direct access into the pericardial space, and these guys have bigger fusions and you don't need to worry, you know, about damaging the heart going in blind if you don't have ultrasound. But if you do, I still tend to use the 5th or 6th rib space, but sometimes I'll slide my probe around and just find a place where there seems to be the most effusion for me to pop a needle into.

So we've taken our needle out of the kit and we've, we've made a little stab incision. In the skin with our scalpel blade, very, very small, that does cause some dogs to react a little bit, so you can instil a little bit of lidocaine just subcut there before you do that. Then we pass our long needle through the intercostal muscles and into the pericardial space.

Then we see our pericardial effusion starting to drain out and as we go into the pericardial space with our needle, you feel a little pop, . As that needle just pops through the pericardial sac and sits in the pericardial space. We don't then advance any further because the next thing that you might feel is something flicking against the end of your needle, and that's the outside of the heart.

We'd want to avoid that. So we go in on the right side of the heart as well, sorry, the right side of the thorax rather than the left because you have very few coronary arteries on the right side of the heart when compared to the left. So there's less chance of of damaging.

Coronary vessels. We then thread our guide wire through this needle into the pericardial sac, as you can see here, if your kit's got one, you'll thread a dilator over this needle to er sorry, over the wire to dilate the hole that you've made through the intercostal muscles into the pericardial sac. You'll then remove the dilator and thread your pericardial drain over your guide wire all the way into the pericardial sac and then remove your guide wire and you're left with something like this, you can close your clamp, attach your three-way stopcock.

As shown here and start to drain that effusion, and this dog, we managed to get about 1 liter.5 of pericardial effusion out, it was a huge, huge volume of effusion. So I'll quickly show you this video, it's just a couple of minutes, I've been in real time doing a pericardial drainage, so I'm finding the space that I want.

I've already made my little stab incision through the skin, with a scalpel. So we've got the, the long needle here going through our little stab incision in the skin through the intercostal muscles. And then there's a little pop as we go through the pericardial sac.

And we get our pericardial fusion draining out of the catheter, so we remove this stylet and leave the catheter in place and then we feed our guide wire. Through that catheter into the pericardial space. OK, remove our catheter.

We don't have a dilator with this kit. So we immediately thread our pericardial drain over this guide wire. Which is nicely sat inside the pericardial sac.

And this part they tend to react as well a little bit, you have to give them a bit of a push just to pop that pericardial. Drain through the intercostal muscles into the pericardial space. So sometimes they do react a little tiny bit there, OK.

This dog was chemically restrained with just butorphenol, given IV we performed a intercostal nerve block as well. So threaded that catheter in. We now removed the guide wire.

That our three-way stopcock and syringe. And then we start draining our fusion. If you are pulling back on your syringe and you're not getting any fluid back, never apply more than 2 mLs of, negative pressure, because more than 2 mLs of negative pressure if that drain is sat against the heart or if it was, you know, in the plural space, is enough pressure to actually damage, the tissue that it's sat against.

OK? So I hope that just shows how relatively quick and easy pericardial drainage can be. A little bit about monitoring throughout the procedure, so this is where we need to make sure our nurses have a patient on an ECG throughout.

What we're looking for are two things. One of them are VPCs, so these wide bizarre complexes, and often we see those when the heart is not happy. So that's generally if our needle or catheter is touching or damaging the heart.

So I always say to the nurses, if you see any of these guys, let me know cause I'm doing something wrong and I need to adjust what I'm doing. I also asked the nurses to monitor the heart rate as well throughout these patients are tachycardic when you start doing the effusion, drainage, but as you drain that 1st 1/3 of fluid and relieve the tamerard, you should start to see heart races, heart rates, sorry, decreasing down to more normal level. The signs of right-sided heart failure, the effusions tend to rapidly resolve once you've relieve the tamponade, and they do not need any diuretic therapy.

OK? That patient does not have chronic congestive heart failure, so they don't need a post-drainage diuretics. We need to monitor demeanour cardiovascular parameters including respiration rate and effort and abdominal distension throughout their stay.

And as I say, we tend to use intermittent or continuous ECGs post-operatively as well, because, ventricular ectopy can be seen postoperatively, as well, although it's very infrequently severe enough to need any medical therapy. We hospitalised for a minimum of 24 hours and attend to check their echo the following day to make sure there's no return of the effusion before they're discharged. This is important, and if at any point you're worried that the effusion has, has redeveloped during their stay in the hospital, you need to get the probe back on that thorax.

I've seen patients with neoplastic pericardial effusions that are drain every drop, and within 4 to 6 hours, they've fully, reoccurred and back in tamperard and obviously those patients really don't do well. I then tend to arrange weekly echocardiograms thereafter. To follow them up.

So that's this patient postoperatively being monitored. So tiny bit on surgical options. So if we are draining repeated effusions and they are recurring, we can look at surgery.

I think subtotal pericardectomy is generally the most commonly performed. Reported, mortality rates have been as high as 13% in some studies, but generally, by performing subtotal pericardectomy, we can provide a favourable long-term prognosis. So, In one study, dogs that had suspected idiopathic pericarditis that underwent pericardectomy had median survival times of 1200 days compared to 500 days for those that didn't undergo surgery.

One option that's probably not commonly performed is balloon pericardiootomy, which is basically the introduction of a, balloon dilating catheter across the pericardial sac using fluoroscopic guidance, and this balloon is then dilated, to rupture a little hole in the pericardial sac, i.e. A pericardiootomy.

This was looked at in a retrospective study. Of dogs with a recurrent pericardial effusions, most of which had, heart-based neoplasia as their cause. There were no dogs that experienced serious complications with the procedure, and it was considered successful in 4 of 6 dogs.

With one dog being alive, without recurrence of the effusion one year after the procedure, 3 dogs dying of unrelated disease without recurrence of the pericardial tamponade at 5, 19, and 32 months. But two dogs, however, out of these 6 did have recurrence of tamponade at 9 weeks and 6 months, OK. Thoracoscopic partial pericardectomy, this is essentially, removing as much as the pericardic sac as you can do, with, thoracoscopic, technique.

And there are a couple of studies, looking at this technique. Some of the complications, you know, do involve phrenic nerve transection, lung laceration, and intraoperative, bleeding. But of, the patients in this study that had the idiopathic pericardial effusions, two of these dogs remained alive at 585 days and 1200 days postoperatively, which is pretty good.

And in another study, they looked at, survival times in dogs with idiopathic pericardial effusions, and they were a median of 600 days, which is significantly longer than those, who had a thrachoscopic partial pericardectomy with neoplasia, which is more like 30 days. Complications, however, were reported in, 26% of the cases. And then just to finally wrap up, I know it's been quite quick, but bear in mind that this is, meant to be aimed at general practitioners.

And, and, you know, thoracic surgery is probably not that high in your list of things to do, next week. But certainly the options are, are there for referral, should you be stuck with a patient that's had recurrent fusions. But one option to consider would be chemotherapy.

So there's a retrospective study that looked at dogs with right atrial masses and pericardial effusions. And they received a single agent doo protocol and had median survival times of 140 days. This is a longer survival time, interestingly enough, compared to dogs that were treated with pericardiocentesis alone, or, in dogs with right atrial masses, that had resection, alone, and it was actually a comparable survival, mean survival time.

To another study in which patients with right atrial mass had resection and adjuvant chemotherapy. So following this study, there was the idea that perhaps doxorubicin-based chemotherapy alone appears to be a viable alternative, for owners who don't want, surgical intervention, for dogs who have, right atrial masses. So, I know it was a bit of a whistle stop tour of pericardial effusions, but there's really quite a lot to get through, so perhaps there are gonna be a few questions at the end, but thank you all for listening.

Thank you so much James, that was fascinating. Always happy also for you to er talk about names of suppliers, so that's fine if we, if anybody wants to know who they they were from before. Just a chance for people to get questions together.

We've got . Sue's saying she's apologising for being a bit late. We didn't notice because we were able to slink into the virtual lecture theatre without us seeing Sue, but she's looking forward to the recording, which, as usual, should be up within the next 24, 48 hours.

Are there any other questions? Just, perhaps a few thoughts. Are people seeing pericardial effusion, how many of those sort of cases are you seeing a year on, on the whole, so perhaps if people just put in a number that they're seeing, or any interesting cases that they've had.

So Paulette is just asking, do we know why males are overrepresented? No idea, I'm afraid. No it looks, yeah, I mean it's, it's, you know, it's, it's idiopathic, pericarditis.

I think we, we, we don't understand the pathophysiology of the disease process itself, so yeah, I wouldn't be sure as to why males are more likely to get it. John's saying my good friend John Gaye's on and he's saying very rare that he sees these. So again, I mean, how many of these would you be seeing in it?

In a, in a sort of year, are you seeing them quite commonly or? Yeah, I mean, one thing that that springs to mind is that I think this is significantly underdiagnosed. Yeah, and particularly in clinics that don't have ultrasound or that don't regularly reach for that ultrasound in patients with suspected cardiovascular disease.

I certainly know that one of my colleagues who works at the RSPCA I won't name which clinic, but it's a busy RSPCA hospital. And prior to them having ultrasound, they saw very few pericardial effusions. They then got ultrasound, started doing these point of care scans, and they started seeing a case a week.

So the last practise I worked at, we covered for 40 clinics out of hours, and we practised at covers for 40 clinics out of hours now, and I would say probably 1 a week. Yeah. It's, it's one of those things if it's not on your differential list, surprise, surprise, you don't see it, do you?

Absolutely, absolutely. But I think with the pericardial effusions, that constellation of clinical signs that constitute right-sided heart failure are not caused by that many of the disorders. So if you are quite keen at checking.

For pulsus paradoxus, checking for jugular distention, thinking about why a patient might have ascites, and a pleural effusion, and you know perhaps we'll pick up more than than you think. Mark's saying he's just had a case and he drained the pericardium. Well done, er, ascites has gone, but I did use diuretics, but the pleural effusion is still present after a week, any suggestions?

OK, one thing that we sometimes see is that when you're performing pericardiocentesis. When I started out and I was a bit inexperienced, I would be in and out with my catheter several times, probably moving it around a bit more than I should do, and you often create like a little window in the pericardial sac. And actually some pericardial effusions as we're draining them, will drain into the plural space.

So some of those patients maybe, as you've done the pericardiocentesis, some of that fluid is sat in the, the, the plural space and is waiting to sort of be reabsorbed. I think that's probably a common reason why. It may also be that, you know, in some patients with malignancy, the malignancy may also actually involve, the plural space.

You know, in which case you're gonna get recurrence of that diffusion. I had a case the last month, it was a lymphoma dog that did the same thing actually. We've got another question, are there any significant arrhythmias associated with pericardial effusion or generally not beside the odd VPC?

Yeah, good question, . So as I say, ECG changes generally are decreased amplitude of the QRS complex, electrical alternans, but what I tend to see, particularly post drainage, is that VPCs are common and quite often those individual VPCs become couplets, which is 2 in a row, or triplets, which is 3 in a row, or salvos, or you end up seeing a whole host of VPCs marching across your lead to trace. And when you see that, it's quite important to, Think about the heart rate in that patient who has a series of VPCs because when their heart rates get over 180 beats per minute, we class that as ventricular tachycardia, and that requires therapy with lidocaine, whereas when we've got a series of VPCs in a row and the heart rate is less than about 160 to 180 beats per minute, that's called an accelerated idioventricular rhythm, and that does not require therapy, it just requires monitoring.

And by maintaining that patient's analgesia, by maintaining their oxygenation, just checking their electrolyte levels causes hypokalemia will make you more likely to develop an arrhythmia. You know, these changes on an ECG that can look really scary actually suddenly become not such a big worry and quite treatable. So yeah, I would say VTA, VPCs, and accelerated idioventricular rhythm are the most common ones.

Brilliant. I think that's all the questions. Speak now or forever hold your peace, just remember, do go over and have a look at the virtual congress.

I think the link is, in the chat box. If not, obviously just go over to the webinar vet.com and look for virtual congress on the tabs, and you'll be able to go and see the, the.

The timetable isn't quite right yet, so that there is a few more things needing to go on, and it's not quite as it should look. But it, it is showing you, you know, the things that you'll be getting for free. And, you know, if you've got any friends, colleagues who, who might be interested, we can do you a, a discounted ticket for them.

So, you know, if you need to get in touch, just email me, Antony at the webinar vet.com and I'll try and get that sorted out for you. I don't think there's any more questions, James, that was really interesting.

I mean, it's, it, it's one of those lovely ones, I think, you know, when you, . Do a webinar on something that perhaps we, we think is a bit rare and then suddenly the, the, the penny drops. Mhm.

Maybe I had a case like that 3 weeks ago that I wasn't really thinking about and so it it's so useful just to come in with one or two things that perhaps will just improve the way we do general practise. So thank you so much for the. For the webinar today, it was really clear and great videos as well, we love the videos of those in future, absolutely, yeah, they're really good, thanks so much James, speak to everyone soon at another webinar, bye bye.

Yeah, take care, bye bye. Thanks, bye.