Well, good morning, everybody, and welcome to our webinar this morning. The subject, of course, is cardiology, and we are very lucky to have two highly qualified cardiologists speaking to us this morning. Our first speaker is Nuala Summerfield, and she'll be with us from now until about 12 noon.
And after that, we moved to Kieran Burgelat. Now you're welcome to send in questions. You don't have any audio connection with us, but you can send in written questions to us, and we will deal with those in the breaks, as many of those as we can fit in.
And we'll also be throwing out some questions to you. So when those questions come up. We'll ask you to try and respond if you wish to, within about 30 seconds, something like that, we won't leave it running too long and then we'll just read out the results, to see what's come through.
So first of all, it's my real pleasure to introduce Nuala Summerfield. Nuala Summerfield runs the virtual vet specialist organisation. And qualified from the University of Edinburgh, and went on to do a residency in the University of Pennsylvania in the USA.
She's of course a recognised cardiology specialist and without further ado, I'll hand over to Nuala. Thank you very much and, and good morning everybody. So we're going to cover, how to perform and interpret cardiac diagnostics with confidence.
And so we'll be covering thoracic radiographs, echocardiography, so heart ultrasound and ECG. Obviously, technical expertise in performing and interpreting cardiac diagnosis is really important. And so what I want to do is to go through with you how to ensure an accurate diagnosis, so that we can then go on to talk about an optimal treatment plan.
We'll start with thoracic radiography. So when we do a chest X-ray of a cardiac patient, what questions do we need to answer? There are a few key things.
So, is there evidence of acquired or congenital cardiac disease? Obviously, the question about congenital will depend on the signalment of the patients. There is a young patient presenting to us.
Is there evidence of pericardial disease? Is the patient in obvious heart failure, or is the patient at risk of heart failure? And an important question is also, is radiology or is this a suitable test to answer these questions?
Remember that radiographs are not sensitive for assessing cardiovascular functions, so that's how well the heart muscle is contracting and relaxing. And we can't see the morphology of structures inside the heart, such as the wall thickness of the ventricles and the morphology of the valves. So we may need additional investigations such as heart ultrasound.
And ECG. Now, if we have dysneic patients, sometimes it's, it's not possible to get really good radiographs on those patients. We can consider an initial screening radiograph, potentially through one of these portable plastic oxygen tents.
Obviously, positioning will not be optimal, but it will allow us a sort of a preliminary view of heart size and whether the, whether there's evidence of congestive heart failure. We can do screening, radiographs, conscious or sedated, and I've put a dose there, of butrophenol that's generally well tolerated. But as I said, we may need to accept that these aren't the best radiographs because they're screening radiographs in unstable patients, and they can be repeated at a later date.
But they're really to give us initial information. But sometimes actually restraining a patient or sedating a patient for radiography, may not be as safe or as informative as doing a limited heart ultrasound, so an emergency heart ultrasound, which will come on to you later. So when we're taking thoracic radiographs in a patient that we suspect have heart disease, we need two views to assess the heart size.
So a DV, which should be straight, not rotated, and ideally inspiratory, and a lateral with the legs straight and pulled well forward, the chest supported, particularly in deep chested dogs, and again, ideally in spirity. Obviously, this is hard in a conscious patient. The heart sits within the mediastinum.
So the outline of the heart itself is not what we see on the radiograph. What we're seeing is the cardiac silhouette. So remember that the silhouette contains the heart, but also we have the pericardium around the heart.
And if we have contents within the pericardial sac, normal or abnormal, that is obviously going to affect the cardiac silhouette shape. It's normal to have some fat, but in very obese animals that we can certainly see an accumulation of fat within the pericardium that can, confuse heart size interpretation. Obviously, pericardial fluid is normal to have a small amount to help lubrication of the sack around the heart.
But with pathology, we can have a buildup of pericardial fluid, which will affect the shape of the cardiac silhouette that we see. The great vessels come out of the heart within the pericardial sac. And so the pericardial sac itself will contain the origin of those.
And then obviously, the heart apex, we can see better than the base because it's delineated by the air interface of the lung, but the base is harder to assess because of the overlying soft tissue. So as you said, we have the great vessels, the pulmonary veins, and lymph nodes. So if we look at this diagram here of, of cardiac anatomy, it gives you a rough idea of what chambers, what structures are aware on a lateral and a DV radiograph.
So if we look at this example here, this is really just to, to show when you have an enlarged cardiac silhouette, You can be posed with questions such as, well, is this true cardiomegaly, such as a dilated cardiomyopathy in this dog? Or is there something else going on within the pericardial sac? Maybe the heart size itself is normal, but there's pathology within the sac, whether it be fluid, sometimes if you've got herniation.
So, pericardial peritoneal diaphragmatic hernia, you can actually have got gut contents within the pericardial sack that can give the sack itself, an odd shape around the heart and make the overall cardiac silhouette look enlarged. My suspicion from these radiographs would be pericardial effusion. You can see here the very clear delineation of the cardiac silhouette.
And this is often seen if you have a large volume pericardial effusion. You can see there are no, I suppose no no edges to the pericardial sac. It's very circular.
And if you imagine the heart inside the sac, which is contracting, when you don't have pericardial effusion and the sac is adhered to the outside of the heart with only a very small amount of, of normal fluid, then you're going to see some movement artefact as the heart beats. But obviously, if you've got the heart beating within a very static fluid-filled sack, the edges of the cardiac silhouette can appear very, very well delineated as you can see here. So the cardiac silhouette assessment, when we're thinking about this, it's important to remember that the this cardiac silhouette can be highly variable between patients based on a number of things such as hydration, that's gonna affect the size of the heart.
The respiratory phase, also, as we said, changes in the cardiac silhouette can suggest underlying pathology. But radiographic assessment of heart size may be inaccurate. And echo is going to be the best way to truly assess the cardiac chamber sizes, individual heart chamber sizes.
And also remember that a normal heart size or a normal cardiac silhouette, I should say on radiographs does not exclude early heart disease. So if we look here at this lateral radiograph, this dog clearly has left atrial enlargement. OK.
So we can see here, we've got loss of the caudal cardiac waste. You've got elevation of the trachea up towards the, the, the spine. We have, splitting here of the, main stem bronchi.
You've got an increased height of the cardiac silhouette, so it's more than 2/3 of the height. Of the chest. And then you've got this sort of tenting here, which is where the left atrium sits in a dog.
When we look at the DV view, we again can see the bronchial splitting. I, I don't know how well you'll be able to see this, but you can see that here. And you get this cowboy sign.
And remember in a, in a dog, when we look at it a DV or a VD, the left atrium sits. It overlies the heart because as we saw on the lateral, it's, it's quite, dorsal. And so when we're, we're looking in a DV or VD view, it's overlying the cardiac silhouette.
When we see a bulge here, in the sort of 2 to 3 o'clock position, this would be left atrial appendage in a dog. So this dog has mitral valve disease, left atrial enlargement, but no congestive heart failure. So you can have patients that present with very loud murmurs from large volume mitral regurgitation.
But remember that the preclinical phase or asymptomatic phase of mitral valve disease can extend for, you know, prolonged period of time before the the animals experience cardiac decompensation. So here we have left atrial enlargement. We've got dorsal elevation of the trachea and the carina, and we've got straightening of the cordal border here.
But the lung fields are clear. We can see really well delineated the left atrium, left ventricular border, and here, . Around the sort of right heart, there's no evidence of any effusion or edoema.
Typically, obviously, dogs get edoema in the perihia region with congestive heart failure, but there's no other obvious pathology in this dog's lung. And again, here's the left atrial appendage in this 2 to 3 o'clock position. Left atrium and large left atrium overlies the cardiac silhouette.
Left ventricle, right ventricle, right atrium. This angiogram is is a contrast study. So contrast has been injected into the heart, into the left ventricle.
You can see the catheter here, the tip of the catheter in the left ventricle, injecting contrast. This dog has mitral regurgitation. So when the contrast is injected into the left ventricle, the normally the left ventricle would contract and blood would go out of the aorta and none would go backwards into the left atrium.
This dog has a very incompetent mitral valve. So when the left ventricle contract contracted, blood containing contrast was able to go retrograde into the left atrium so that we highlight the left atrium and you can see this enlarged left atrium, and it helps just to see where the various chambers are on the lateral radiograph. And here's another example of something to look for, particularly when we have dogs presenting with loud heart murmurs and they're coughing, and we want to to decide what the origin of the cough is.
Is it likely to be cardiogenic or is it likely to be related more to airway disease? And many older dogs will have concurrent bronchialacia as well as mitral valve disease. And here we can see left main stem bronchus compression.
Due to an enlarged left atrium. On these lateral radiographs, we can see two different types of cardiac silhouette shape. On the left here, this is more typical of a dilated cardiomyopathy.
But pericardial effusion would also be a possibility. We've got this very globoid heart. However, we do have evidence of sort of perihla dorsochordal infiltrating the lung, which would not be typical with pericardial effusion.
So Obviously, your physical examination findings, your signalment is so important when we're interpreting these diagnostics. We're looking at them as standalone images here. Clearly, you don't know what what patient they came from.
But, for example, if this came from a large or giant breed dog who's presenting with exercise intolerance, laboured breathing, you see this sort of large globoid heart with the characteristic pattern of pulmonary edoema. This would be very suggestive of something like dilated cardiomyopathy. This different shape here with the very pronounced left atrial enlargement is more typical.
Of mitral valve disease. Since they get, the dogs have primary valvular disease, so they have very large volumes of mitral regurgitation as they get into the end stages of the disease. Again, we've got some pulmonary infiltrates suggesting this dog may in left-sided heart failure, but you can see a very enlarged heart, predominantly left sided enlargement, straightening of the caudal border, and, and because This is a small barrel-chested dog.
When the heart enlarges, you can see how it becomes really space occupying within the small barrel shaped chest. So remember, when we're looking at these diagnostics, do think carefully about signalment, history, or physical exam findings, when you're, to help you to interpret these, diagnostics correctly. This would be same dog, but obviously, a DV view here and we can see again, globoid heart, more typical of dilated cardiomyopathy, doesn't have those very crisp edges that I showed you with the pericardial effusion case before.
This one's definitely got pulmonary infiltrate. So not typical of, of pericardial effusion. Your physical exam findings would help you obviously with that.
And here's a mitral valve case with this really big left atrial appendage and enlarged left atrium here, and again, a bit of pulmonary infiltrate. So depending on the type or stage of underlying heart disease, there may be only minimal and sometimes no obvious radiographic changes to the cardiac silhouette. Remember that dogs can present with other types of heart disease too, that may not cause, heart enlargement, at least in, in certain stages of the disease.
So with arrhythmias, we can see this in, in dogs and cats that have a erythmogenic right ventricular cardiomyopathy, particularly some boxer dogs may not have significant cardiac enlargement. With this disease, myocarditis, or inflammation of the heart muscle may not cause obvious heart enlargement on radiographs, but the dogs may, or cats may have significant arrhythmias. Infectious endocarditis, so, an infective inflammatory lesion of one of the valves in the earlier stages until there's been a lot of destruction of the valve and a lot of incompetence potentially of the valve and leakage across the valve.
But in the early stages, you may not see any change in heart size associated with that. These are going to be, this would be an echocardiographic diagnosis. And obviously the arrhythmias you would need to do ECGs to make those diagnoses.
Ruptured cordi tendons are one of the tendons supporting the mitral valve, if that ruptures again, until there's a significant amount of regurgitation associated with the rupture, for example, of a mitral valve cord tendon, you may not see significant heart enlargement. With pressure overload, so pulmonic stenosis, aortic stenosis, and in in cats with hypertrophic cardiomyopathy, remember that this is a concentric, myocardial hypertrophy. So that means that the heart muscle gets thicker at the expense of the lumen size.
So the heart doesn't always look larger on the ultra on the radiograph itself and it's more of a, an echocardiographic diagnosis. Pressure over Load. So we could also think of high blood pressure, systemic hypertension, can do this in in cats and hypertrophic cardiomyopathy in cats of its primary is a genetic issue rather than a pressure overload, but it it looks similar on ultrasound.
Heart muscle, myocardial neoplasia. This can be infiltrated into the heart muscle. Again, you may not see a change to the shape of the heart on the radiograph.
You really need a heart ultrasound for that. And then if you have small shunting defects such as atrial septal defect, ventricular septal defect, or patent ductus arteriosis, if the volume across the shunt is small, it may not cause any obvious change on radiographs in terms of heart size. Right ventricular enlargement, this can be easily overdiagnosed, so be careful with this.
The reason for this is that left-sided heart enlargement can cause, the right side to look enlarged. I'll show you some examples. And also there can be significant breed, influences on the shape of the chest.
So right-sided, hypertrophy can be challenging. On a lateral, when we're looking at right side enlargement, we're thinking about widening or rounding of the anterior border. Increase sternal contact.
This is slightly unreliable because again this can be breed related. Tracheal elevation, apical elevation from the sternum, and I'll show you some examples. And on the DV view, or a VD view, but typically a DV view, then, reverse D shape and rounding in the sort of 6 to 9 o'clock position.
So these radiographs are from a dog with pulmonic stenosis and right ventricular enlargement. If we look here, we can see this reverse D shape so the straightening of the left side and the rounding of the right side. So it's like a sort of backwards capital D.
And then if we look on the lateral view, you do see increased sternal contact here. But again, in some of these little barrel-chested dogs, You can see this even if they don't have significant right-sided enlargement on radiographs. But obviously, this dog is going to have a significant, sorry, left basil and murmur, consistent with pulmonic stenosis.
The history, the signalment will be suggestive, of congenital heart disease, and then the radiographs would help to confirm that. But it's difficult to make radiographic stand-alone diagnosis if you haven't seen the patient. Here's a dog who has severe sub aortic stenosis and left ventricular enlargement.
But again, this would be a pressure overload enlargement. So it's not a dilated left ventricle. It's a concentrically hypertrophied left ventricle, meaning that the lumen, the chamber size gets smaller, the heart walls get thicker.
In in response to the pressure overload. And this image here, which is again one of these contrast studies, helps to show what the radiograph is, is depicting here. So and if you can see there's a catheter coming in here through the carotid artery that's just going through the aortic valve and it's injecting contrast.
And as that contrast goes out through the, aortic outflow tract, you can see the sub valvular or the area below the valve is narrowed. This is sub aortic stenosis, and the contrast goes out into the aortic root where there's dilation. And then break his phallic trunk left subclavian, and then out into the well, you've got the aortic arch here.
And so you can then see what this is. This is this dilated aortic arch on the lateral view. And because you've got the apex of the left ventricle, because it's left ventricular concentric enlargement, the apex tips up so it can give this impression of increased sternal contact and the heart lying very horizontal.
And then you have this post-stenotic dilatation here of the aorta. So just be aware of that. But again, your signalment, your history.
This will be a young dog of a breed, such as a German Shepherd or a, golden retriever, a newfound and those types of, of dogs that are more prone to subbiotic stenosis boxes would be another one, that would be making you think, of this type of congenital defect. So how about in cats? Well, radiographic cardiac assessment in cats is, can be a bit challenging.
It's got poor sensitivity for predicting early heart disease. Really, we need ultrasound for this, because the relative change can be small. And this is because cats tend to get heart muscle disease and the most common form is the, the hypertrophic cardiomyopathy.
So the heart's getting thicker, as we said, at the expense of the chamber size. And therefore, the thickening is inwards and so we don't always see an obviously enlarged heart, at least in the early stages. And atrial enlargement is more difficult to identify in cats because the atria, the atrium sits more laterally on the radiograph.
So when we're looking at a lateral radiograph in a cat and we're looking for left atrial enlargement, we don't tend to see that tenting that you see in a dog in this position here. What you can see if you've got significant left atrial enlargement in cats is a bulge or a knuckle on the caudal border here. OK.
Because the atrium sits more laterally. It doesn't sit right up on top of the heart. Remember that the cat's heart is a bit more horizontally positioned, in the chest rather than the dogs.
Particularly deep-chested dogs can have very vertical hearts. Cats, and particularly as they get older, the heart seems to tip more forward and be more horizontal in the chest. So we're looking for, we see, this cat has an enlarged heart.
But we're looking for this knuckle here if we can see that on the caudal border to suggest left atrial enlargement. Now this cat actually had early hypertrophic cardiomyopathy on radiographs, but you can see the heart looks relatively normal here in terms of it being less than 2/3 of the width of the, the chest here. Whereas this cat had advanced hypertrophic cardiomyopathy, clearly, that's an enlarged heart with evidence of left atrial enlargement.
And in the cat, because the left atrium does sit more laterally, this would be the position. In a cat where we look for left atrial enlargement, whereas we said in a dog that tends to be more left atrial appendage because, excuse me, because the, the left atrium in the dog is more dorsally positioned. So remember again that thoracic radiography is not always straightforward to interpret because of things like chest confirmation, obesity, phase of respiration, exposure factors.
We can see here, this is the same dog in expiration and inspiration on a lateral view and certainly on expiration because there's less, less, thoracic volume. The heart looks relatively larger, the lungs are going to look more, There's more opacity because they're not fully inflated. So do be aware of that.
And breed is very important, as we said, deep-chested dogs. So sighthounds in particular have these very tall upright cardiac silhouettes. So mild enlargement in these dogs can be quite difficult to pick up.
So for example, a Doberman with early or preclinical dilated cardiomyopathy may have a heart that really looks quite normal on thoracic radiographs, but you really need an ultrasound to see how well that heart is actually able to contract. Then dogs with more of an intermediate chest shape, so golden retrievers, Labradors can have quite globular looking hearts. Athletic dogs.
So 11 breed that causes us quite a lot of problems is springer spaniels. Again, they can have these apparently very large globular hearts. But this dog, for example, had a normal heart on, echocardiography for the breed, believe it or not, this is a working, springer spaniel.
But when you look at that radiograph, it's not surprising that people would worry this dog had heart muscle disease. Again, it's not an inspiratory film, so that is going to be making the heart look bigger. But the, the globular shape can be really quite confusing.
And often we do need to follow these up with, with ultrasound to be sure. And then bowl-shaped chester dogs, so such as the bulldog, they have these round, cardiac silhouettes with increased sternal contact because of the chest shape. And sometimes they can have sternal abnormalities as well.
So do bear all of this in mind. Again, this is quite an expiratory film, which is going to be making the, the heart look bigger and not well positioned because the legs are, quite far back. So again, that's gonna make the lungs look more opaque.
Now many geriatric cats, as we said, can have these very lazy hearts. So we have increased sternal contact with a prominent aortic arch. So you can see here the heart's almost lying across the sternum, and then there's very obvious aortic arch.
Now this, this cat actually had calcification of the aortic arch, which is why you can see it so clearly. And but do be aware in older cats, they do have these very, these hearts that sit very close to the sternum, which is also where they can be quite challenging to get ultrasound pictures on because you don't have the same window that you do in a younger cat with a slightly more upright heart. Obesity can certainly affect the cardiac silhouette too.
So it's another thing to bear in mind. The fat within the pericardium can make the cardiac silhouette look larger than it really is. It can make the mediastinum look wide, which can be confusing, and it can increase the opacity of the lungs.
So you get this hazy interstitial pattern. So here we've got a very obese dog, probably the The exposure factors here could have been improved, but it's, it's an ex-spiritual, partially expiratory film as well, which isn't helping. But you can see we've got a widening of the mediastinum, and the heart looks as though it's filling more than 2/3 of the, sort of thoracic width or the cardiac silhouette's filling more than that.
But some of this is going to be fat within the pericardium. And again, you can see on this lateral view here. I've used the red arrows to show you the limitations of the actual cardiac silhouette and all of this down here is fat.
You can see this, this patient has a lot of fat here also below the liver in the abdomen. So we can use the vertebral heart score, which many of you will be familiar with, to allow us to quantitatively assess heart size, . It can be used as a guide to the change in heart size over time, and therefore repeated at different time points so you can compare within the same patient.
And that's really the most useful way of using the VHS is for comparison at different time points of the same patient. So let's say a mitral valve disease dog when you first pick a murmur up and then maybe 6 months or a year later and then another 6 months or a year later after that, to just see if the heart is increasing in size over time. The way that we, we, measure the vertebral heart score, I'll show you on a, on a diagram, but we measure from the ventral aspect of the carina to the cardiac apex.
And then we take the perpendicular measurement, at the widest point of the heart, and some of these two measurements together and compare them to the length of the vertebral bodies measured from the cranial end plate of T4. So I show that here. Here's our cardiac silhouette.
We're measuring from the carina to the apex, again, at the widest point of the heart, perpendicular to the long axis. So the short axis measurement should be a perpendicular to the long axis measurement. And then using, unfortunately, I apologise, you don't see very clearly, you can't really count the thoracic vertebrae very clearly here, but take it from me, this is the beginning of T4 or the cranial edge of T4, and we're counting back the number of vertebral bodies within each of those two measurements.
So the length measurement and the width measurement. We're gonna add them together. And here we get a vertebral heart score of 12.5, and canine normal is roughly less than 10.5, and feline normal would be on a lateral less than 8.
So you can see this dog has moderate heart enlargement. I put a reference here of a paper you can you can have a look at if, if this is something you'd like to read more about, but it just gives you a rough idea of, how typically we scale, or we look at the vertebral heart score and say whether the score refers to a mild, moderate or marked or extreme enlargement. What I would say is that more clinical studies have shown that specific breeds can really be outliers from what we call the normal VHS measurements.
And so what we say is the normal VHS range. As we said, for dogs and cats, but there are certainly dog breeds such as the boxer, Bulldog Cavalier. Obviously this is a dog we're commonly screening for heart disease, Labrador, Pug, Pomeranian, Whippet, who we know normally, can have VHS's when they have no heart disease that are outside of that normal range.
So do be aware of the breed specific VHS measurements that are being published and more will continue to be published. When we're assessing pulmonary vasculature, we should be ensuring that the pulmonary arteries and veins are of similar size. The veins are central on the DV and VD projection and ventral on a lateral projection.
And the diameter of the cranial low bar vessels should be less than approximal 3 of the 4th rib at the 4th intercostal space on a lateral view. DV views are better for assessing called low bar vessels, and the diameter of the vessels should be less than the width of the 9th rib as it crosses over. So if we look on our lateral view again, we've got the pulmonary or the cranial pulmonary artery, dorsal to the vein here.
So cranial pul pulmonary vein or cranial lobar vein, I should say, sorry, cranial lobar artery, cranial lobar vein, veins are ventral to the arteries on the lateral view, and they're central or medial to the arteries on a DV or VD view. Lung patterns can cause a lot of confusion. And it's helpful to, use a lung pattern interpretation to compile a differential list.
So when we're looking at lung patterns, we're thinking bronchial, interstitial, alveolar. Sometimes we can have, single patterns or sometimes they can be mixed, but it's helpful, I think, to, to try to decide what is, the predominant pattern. So when we think about bronchial patterns, it's this tram line and, and donuts, and this is caused by the thickening of the small airway walls.
So we get thickening of the, here's the, the, the bronchi or the bronchus here, and as the wall thickens, certainly on the, lateral and then on the, devial VD you see these little thickened doughnuts and you can see that here. On the lateral projection, we can see some of these end on thickened bronchial markings, and also here on, on this view, you can see them. The more you look, the more they kind of spring out to you.
Not typical for a patient with primary cardiac disease, but obviously they can have concurrent, they, you know, they might have cardiac disease and concurrent, pulmonary disease as well. This patient also has consolidation of the right middle lung lobe, which you can see obviously with pulmonary disease. Institial patterns.
So you have an increased opacity of the interstitium, but the alveolar air is still present, and you can still see the vessels. But it's almost like looking through a neck curtain. Everything becomes a little bit grey and hazy.
But do be aware, this can be caused also, artifactually by poor technique, poor ventilation. So if it's not a, a good inspiratory film, poor confirmation. So here's an interstitial pattern here so you can see it's almost like looking through a net curtain.
It's all a little bit hazy, . And again, on the lateral view, you can see that. Obviously, movement artefact can do that too, but the, the, the vertebral bodies are relatively well, delineated.
So that would certainly fit with an interstitial pattern. And then we have the alveolar pattern, which is a fluffy cotton wool-like appearance. And we get this unstructured soft tissue opacity that obscures the vessels.
And so you get air bronchograms due to the, The alveolar fluid flooding. And so what we can see here is you can't see the soft tissue blood vessels, but you can see obviously the, the air in the vessels overlying the flooded, alveoli here. So we've got the air in the bronchi here.
So these would be the air bronchograms. And again, another example here where we can see the air bronchograms. You can see those all through here.
And again, I don't know if you can see a nice example here of an air bronchogram. So, diagnosis of decompensated heart failure or congestive heart failure obviously requires The dog or cat to have characteristic clinical signs and supportive radiographic signs if possible. We're looking for evidence to support why the animal may have developed heart failure.
And so left atrial enlargement is important, if if we think this is left-sided congestive heart failure, pulmonary venous congestion, not always visible on radiographs, but it's certainly something we should be looking for. And obviously pulmonary edoema and in cats that, have left sided congestive heart failure, do you remember that cats can have pleural effusion with left sided congestive heart failure as well as or instead of pulmonary edoema. Whereas in dogs, pulmonary edoema is associated with left-sided heart failure.
And not typically pleural effusion. So here's a dog with severe left sided congestive heart failure. So we've got a very, very dense interstitial alveolar pattern here.
So you can definitely see some air bronchograms. It starts off in dogs in the perihila region moves dorso cordially to the peripheries. I don't see obvious pulmonary venous congestion here if I compare the pulmonary vein to the artery.
That's why I said it's not the most consistent finding, but certainly something that's important to look for. This dog is, is dysic, so it has a lot of air in its stomach. Here's another example of a dog, significant left atrial enlargement.
It's got an enlarged heart, so you can see that the height of the heart is more than 2/3 of the height of the thorax. And so the, the shape of the cardiac silhouette certainly makes you think there is primary heart disease there. Got, elevation of the trachea towards the spine here.
And although this might be a bit underexposed, there definitely is evidence of, of, an interstitial, and some air bronchograms. I don't know if you can see those if you look very closely, and again, definitely pulmonary infiltrate with some air bronchograms here and enlarged heart. And as we said, remembering dogs, pulmonary edoema is associated with left sided congestive heart failure, which we see here.
He's a large globoid heart in a dog with dilated cardiomyopathy, perihyla, verging into called a dorsal pulmonary edoema. And when we see a site, when we, when dogs develop right-sided congestive heart failure, they'll typically get ascites. They may develop some, pleural effusion as well, but ascites tends to be one of the first things that they develop with right-sided heart failure.
Most cats present to us in left-sided heart failure with pulmonary edoema and or pleural effusion. And here is a cat with an enlarged heart. We've got some evidence of sort of a patchy interstitial pattern.
And here's a cat presenting with very large volume pleural effusion, totally obscuring the cardiac silhouette. Do you remember in cats, when they present with left sided congestive heart failure, their interstitial alveolar opacities can be periher, like in a dog, but they can be very unevenly distributed and patchy or focal. So unlike a dog which has a characteristic perihila dis distribution to start with that can then spread out more peripherally as it becomes more severe.
Cats can have a pattern that can be quite difficult to differentiate from other lung pathologies, such as neoplasia or pneumonia. So you really again have to use your signalment history or physical examination findings. And if you can see the heart, obviously cardiac silhouette.
Size and shape is important too. So this is a very unusual looking pulmonary pattern. If this was a dog, we, we wouldn't be thinking, necessarily, cardiogenic pulmonary edoema, but this cat has an enlarged heart, we can see here.
But a very dense alveolar pattern here, and then you've almost sort of got a ventral, sort of mid ventral pattern here, but actually the periphery is quite clear. Here's another pattern, again, much more diffuse sort of patchy, peripheral pattern, and we've got some cranio ventral infiltrates too, but enlarged heart, so it does fit with the cat having primary cardiac disease. So the take home message really is that thoracic radiography is not always straightforward.
Beware of artefacts associated with technique and body confirmation. And do you think about what questions need answering and whether, thoracic radiographs are the right test to answer this question. Decompensated heart failure, so congestive heart failure is a radiographic diagnosis.
So if we can safely get radiographs in an animal that we assume to have congestive heart failure, at the time of presentation, that's really helpful as one of the diagnostic tests we need to do to confirm whether there is pulmonary edoema or pleural effusion present. But we must always interpret these in, in, association with other supportive clinical findings. So what we're going to do is, is move on to our next.
So Nuala, if I can just interrupt a second, thank you very much. I think that's been an amazing talk, very informative. And we just had one delegate just dropped a note to say they're really enjoying it.
They're finding the pace is quite fast. OK, I know you've got an awful lot to go through, but if you did feel able to just slow down slightly, I think they would appreciate it. OK, yes, I realise you've got a lot to go through.
Thank you and thank you for pointing that out. So my apologies if I have gone too fast. The other thing I would just urge our delegates, please do feel free to write in with some questions.
If you send your questions in and we, when we get a break, we will put those to Nuala and see if we can get some answers for you. OK? So Nuala, I'll hand back to you, sorry for the interruption.
No, not at all, thank you. So, what we'll do is we will move on and look at heart ultrasound or echocardiography. And we're going to focus on the straightforward, 2D and MO mode echocardiography, because this is available in a lot of practises.
And really we can make it, we can make diagnosis of, of the more common types of heart disease that we see using, 2DNM mode without needing to do complicated Doppler. If you have a case who that has congenital heart disease or, for example, pulmonary hypertension, These types of conditions do, we really do need to have Doppler assessment, but if we're looking at how well the heart contracts and what the appearance of the valve is, the mitral valve, for example, and how thick the heart muscle is, we can, we can make some initial, diagnosis of these animals to help guide our initial treatment using, ultrasound that a lot of people do have in practise. And it's just feeling more confident doing that.
So remember that heart ultrasound allows us to look inside the heart and to look at the proximal part of the great vessel, so the aorta and the pulmonary artery. And by looking at by using 2D and then M mode, which is motion mode, we can create dynamic images of the contracting heart. Now, when we use Doppler, this is colour flow and spectral Doppler.
This allows us then to look at blood flow through the heart, and to measure the speed of that blood flow and look at the direction of that blood flow. But many practises won't have access to that, but that shouldn't put you off doing initial scans on your patients to help you with your diagnosis of some of the more straightforward things that we, we do see in practise. So really important, I know this is very basic for some of you, but it's so important to prepare your patients properly, because otherwise, the image quality will be affected.
So I always recommend, obviously, RCona, but shave the hair where you're going to want to do your ultrasound to minimise the effects of air on sound transmission, cause obviously, ultrasound waves don't go through air. So we're gonna shave on the right between the 3rd to the 6th, and on the left from the 4th to the 7th intercostal spaces. And I clip from the costochondral junction to the sternum and apply the ultrasound gel if you can to the shaved area a few minutes before you start scanning.
It allows it to sort of soak into the skin and you get better contact. If you can gently restrain the animal in right lateral recumbency, ideally over one of these scanning tables, it has a cut out so that you can position the thorax, the cranial thorax over that cut out in the table so that the heart falls towards the right thoracic wall. So the dog's going to or cat is going to be lying in right lateral recumbency.
Heart falling towards the right thoracic wall, so downwards. And that way when you scan from under the table, the heart has fallen towards the probe and you get a good window. Ideally, if you have access to an ECG on your ultrasound machine, it's always good practise to attach the ECG for timing.
Now, clearly this, this dog is lying here for an ECG, but it's exactly the same positioning that we would lie, or we'd position the dog in over the cutout in the table for an, for an ultrasound. Keeping your patient as comfortable as possible is gonna mean they lie still more still for you. So a nice quiet room where you're not going to be disturbed with people walking in and out, a piece of vet bed, if you can, just helps to keep them more comfortable.
If you have an uncooperative or dysic patient, don't insist that they lie in lateral recumbency. You can do a screening ultrasound to, for example, assess left atrial size, look for pleural effusion, etc. Those can all be done from a standing, sitting or sternal position.
Much safer to do that than to struggle with a dissonate patient. Make sure that you're selecting the right probe to optimise your image quality. So higher frequency transducers will allow better resolution of structure.
So you get clearer images, but they don't penetrate very deeply. So you use a high frequency transducer in a small dog or a cat, and then a lower frequency transducer. Will allow you to penetrate more deeply, but you don't get sort of as crisp, clear images, but we have to use these for larger dogs, and then we get better Doppler readings when we're measuring blood flow.
There are 2 echo planes we're going to use longitudinal, so long axis views, which will image the heart from the apex to the base, and then the transverse or short axis views, which will image the plane across or image the heart across the width of the heart from left to right. So standard, what we call parasternal imaging, we're going to look at some long axis and some short axis section of the heart, and we're going to do this from the right side of the thorax, as we said, dog in right lateral recumbency. And there are standard views, that we look at.
But the most important ones I've, I've sort of ringed for you there, which would be #2, which is a short axis view of the ventricle, at the level of the, you've got the left ventricle here at the level of the papillary muscles. And so often this is called the mushroom view because you have the cap of the mushroom, the stem. And sort of all the stalk of the mushroom here, that's not a technical term, but it helps you to sort of pattern recognise what you're looking for.
In this view, you should be just below the cordi tendinna. Of the mitral valve and the right ventricle is a little sort of crescent shaped structure. And the second most sort of equally important view, but the other one we'll be looking at and focusing on is this one, which allows us to look at the aorta and the left atrium and to assess left atrial size relative to the aortic size or diameter.
So these two views, left ventricular short axis view, we do our modes from this view. And this left atrial aortic view we measure our left atrial size from. But if we start from the bottom here and work our way through here, we're looking right down at the cardiac apex.
So down here in short axis, you can see that we see just a little bit of the left ventricle and we hardly see any right ventricle. And the the ventricular shapes are different. The left ventricle is a cylindrical shape.
The right ventricle is always this sort of semi lunar shape. The left ventricular wall should normally be 2 to 3 times, as thick as the right ventricular free wall because the left ventricle is a high pressure chamber. So this is left ventricular free wall, interventricular septum, right ventricular free wall.
And then as we move dorsally, we, the papillary muscles start to be visible. As we said, this would be our kind of colloquial mushroom view and we can see the right ventricle here. And then as we move a little bit more dorsally, we start seeing the cord tendin attachments, which they attach onto the papillary muscles here, and they're going to attach onto the mitral valve, but we're just below the mitral valve.
We can't see the mitral valve yet. As we look a little more dorsally, so upwards, we start seeing the mitral valve, and that comes in, looks a bit like a fish mouth. You may hear people talk about a fish mouth for you as the valve opens and closes.
So you have the anterior mitral valve leaflet, posterior mitral valve leaflet, and starting to see a bit of the outflow tract to the left ventricle. Again, right, right ventricle here. And you can see these little, sort of blobs of muscle here.
These are the papillary muscles of the right side. And then as we look a bit more dorsally, as we said, aorta, so we've got right coronary, left coronary and non coronary cusp, left atrium. And then we've got the right side with the tricuspid valve showing right ventricle and pulmonic valve.
And if we look even more dorsally right up at the heart base up at the top here. We can see aorta. We're now passed or distal to the valve.
So it's just a tube. We have the right atrium, the right article or the right atrial appendage here, and then the pulmonary artery with the right and the left pulmonary artery branches. In the long axis views, we have the 4 chamber and the 5 chamber view, and we're gonna focus really on this 4 chamber view.
So we're looking at the left atrium, right atrium, tricuspid valve, mitral valve, cord tendiny, left ventricular free wall, papillary muscle, left ventricular chamber, interventricular septum, right ventricle, right ventricular free wall. So this is a long axis view through the heart. And if we look at a 5 chamber view, all that does is it just brings out the aorta so we can evaluate the aortic valve, and we'll often use colour flow across this colour flow Doppler to look at.
Blood flow or look for any obstruction. In terms of our imaging technique, all transducers or probes have a reference mark, and this reference mark can be a dot, a ridge. It can be coloured, illuminated, and it has two purposes.
Basically, it defines the plane that the sound waves leave the transducer and provides orientation for structures on the sector image. So the way that I always teach people to ultrasound is you cradle the transducer, hold the transducer in your hand with the reference mark under your thumb or index finger, depending on whether we're doing short axis or long axis views. We're going to position the probe or the transducer close to the sternum in cats and small dogs and a little way up from the sternum, in larger dogs.
So remember, they're lying on the right side. You're gonna feel for the apex beat on the right thorax, where you've got the hole cut out in the table, feel for the apex beat and place the transducer over where you feel the apex beat. And then you're going to, as I said, have your, if we start off with our short axis views, you'll have your thumb over the transducer mark.
And we're going to position that. If you imagine that the top of the probe. The bit that that touches the skin of the dog or cat is a clock face.
You're going to position the probe so that the transducer mark under your thumb is at 7 o'clock. So it's basically towards the downside elbow as the patient is lying in right lateral recumbency. Hold the probe perpendicular to the skin, and you should get a right parasternal short axis view of the left ventricle.
And then we can pan up and down through the heart to see the various views. And I know that It's difficult to teach somebody to sound through a lecture, really, you need some practical training, but it's really to sort of give you an introduction as to what you would be doing on those training courses or perhaps to give if you've been on a training course to give you a refresher. So the most clinically important measurement that we'll do in a lot of patients is assessing left atrial size.
This is really important for an emergency assessment. So you have an animal that presents, for example, a dys cat. It's really helpful to just look at left atrial size and be able to say, is this respiratory or is this cardiac by just assessing left atrial size, it can also help with prognostication.
So the way that we assess left atrial size is we're going to be looking at the diameter of the aorta, and we're going to relate that to the left atrial diameter. So when cats and dogs present in congestive heart failure, as we said, it's typically left-sided. So pulmonary edoema or pleural effusion in cats, develops because of the increase in left atrial pressure.
And therefore, if the left atrial pressures are high, and that's why the animals develop congestive heart failure, then it follows that the left atrium should be significantly enlarged in animals who do have left sided congestive heart failure. I wouldn't say it's 100% true, but it's almost always true. So really, what we're looking for is if we think this animal has conge left-sided congestive heart failure, we want to confirm that suspicion by being able to document left atrial enlargement.
So when we're assessing left atrial aortic ratio, we'll do this from a right paraternal short axis view, as we said, and we'll make our measurements of both the aorta and the left atrium, inner edge to inner edge, meaning that when we use our cursor on the machine, we'll measure from the inner edge to the inner edge. So we're not taking a lot of the sort of fat and, and some of the other, maybe soft tissue that sits around the outside of the structures. Remember when the aorta is closed, it makes this almost like Mercedes-Benz signs that can be quite helpful to look for, to help orientate yourself.
So here's a a right paraternal short axis view. Unfortunately, ultrasounds don't come pre-labeled, which would be nice if they, if they did. But here is the aorta.
We've got the right coronary cast, left coronary cusp, and non coronary cusp, and you can almost a bit of imagination, see where the Mercedes Benz would be here. And then here's our left atrium, this structure here. And this is a very enlarged left atrium, but we would be measuring from the middle of the right coronary cusp across to the commissure between the non coronary and left coronary cusp.
There are different ways to measure the aorta, but we'll stick to one simple one for now. And then we'll take that same line and we'll cross the left atrium, in term, in order to get a a comparative left atrial dimension. So here, this is actually a normal, a dog without heart disease.
And what we can see here is you've got our aorta. So we've gone across the aorta from the middle of this cusp to the commercial between these two cusps and then on that same plane. But again, inner edge to inner edge with our measurements, we've gone across the left atrium to measure the left atrial diameter.
Now, it's very important that you don't go diving off in here, which is the pulmonary vein. The pulmonary vein enters into the left atrium. And if your measurement goes down into here, you're going to falsely enlarge or, or increase the size of the left atrial measurements.
So what I've done is just extrapolated a line where I think the left atrial borders would be measured to that. So significant left atrial enlargement, as we said, will, will typically be present in cases of congestive heart failure. Normal sized, if we find a normal sized atrium, it makes heart failure unlikely in a patient presenting with respiratory distress.
In a normal cat, we can say that in a short axis view, such as here, left atrial to aortic ratio should be less than 1.5. So the left atrial dimension here should be less than 1.5 times the diameter of the aorta, and you can see here this is significantly enlarged.
This is the atrial appendage here. This is also very enlarged. But there is a large range of left atrial enlargement and obviously the, the larger the left atrium, the more significant that increase is likely to be.
And then in dogs, we can use roughly a similar type of ratio here. So we say up to 1.5 as a ratio.
So less than 1.6. And a wide, again, there's a wide variation in left atrial enlargement.
You can have mild left atrial enlargement, you can have severe left atrial enlargement. The most common disease that we see in dogs, acquired heart disease will be myxomatous mitral valve disease. This begins progressively, sorry, slowly, but it progresses over time.
So an animal may have no left atrial enlargement, but a small leak across the mitral valve to start with, and that will gradually, change as the mitral leak gets larger, left atrium will gradually increase. So this is something you can document over time. But many dogs will have left atrial enlargement once they get a significant amount of mitral regurgitation.
But remember, having left atrial enlargement does not mean you're in congestive heart failure. But if you have symptoms of congestive heart failure, you do expect to find left atrial enlargement, on your ultrasound. But remember, radiographs are really the sort of gold standard way to confirm that we do have evidence of, of pulmonary edoema.
Remember that diuretic therapy can affect left atrial size too. So in this patient here, this was pre-diuretic therapy. You can see here's the aorta.
Here's the, that's slightly changed. That should, that arrow obviously should be up here. So it changed as we save the presentation.
But you can see you've got left atrial enlargement here. And then after diuretic therapy, the left atrium is smaller. So do be aware of that too.
If you really volume deplete a patient with aggressive diuretic therapy, you can shrink the left atrium. Now, the other view obviously we're going to look at would be the left ventricular short axis view, as we said, to look at the heart muscle, and we can assess thickness of the heart muscle, but also how well that heart muscle is contracting. And so, here's the view we looked at the diagram earlier, where we have the left ventricle, the papillary muscles, the left ventricular free wall, interventricular septum, right ventricle, right ventricular free wall.
So this is a right paraternal short axis view through the left ventricle. And if we look at the, an image of this, this is from a cat with hypertrophic cardiomyopathy. What we can see is the heart muscle is contracting well.
Actually, hypertrophic cardiomyopathy is a, a diastolic or relaxation problem with the heart muscle because it becomes so thick that it, it just isn't able to relax properly. But what I want you to see is the heart is contracting and then to notice how, thick the wall is here, you can see it's slightly asymmetric. This part of the wall is not as thick as here.
And we've got these very thick papillary muscles as well. So you can see the chamber is almost obliterated or almost closed off when the heart contracts. We'll play that once more.
We've got very thick papillary muscles and very thick walls. If we look at it at a short axis view and a dog here, this is a dog with mitral valve disease, again has preserved systolic functions, the heart contracts well. Same view.
So we've got the left ventricular freewa, left ventricular chamber with the dog with advanced mitral valve disease, as they have a larger and larger mitral valve leak, they're going to get volume loading, so eccentric hypertrophy. Of the left ventricular chamber. So the left ventricular chamber is enlarged, but the heart muscle will appear to be contracting well and in fact, in some cases can seem almost hyperdynamic.
So I apologise these haven't looped very well, but I'll play them a few times. But you can see looking at that, that chamber may measure enlarged, but the motion, oops, I'm not sure what happened there. The motion of that heart muscle is not characteristic of a dilated cardiomyopathy dog.
It's contracting too well. Now this one here is a dog with dilated cardiomyopathy. So we can see in this particular patient we have right-sided enlargement too.
We also will, will watch the motion of the left ventricle here, but it's very poor systolic motion, systolic function. And again, I'll have to play it a few times because of the looping, but you can see very poor systolic function. The chamber size doesn't change very much.
The heart just appears to kind of wiggle, rather than really contract. So it's quite important not only to look at heart muscle thickness as in the cats with hypertrophic cardiomyopathy, but to look at the systolic function when we're deciding is this enlarged heart. A dilated heart, so dilated cardiomyopathy heart with poor systolic function, or is the heart enlarged because you've got a volume overload from a a large volume mitral regurgitation leak, but the heart muscle is still coping relatively well.
So I think at this point is a good time to take a 5-minute break, and we'll come back in 5 minutes and, and continue. So thank you very much, Nuala. Let's say, well, as you say, 5 minute break, we will not start before 10 past 11.
So I think what we'll do now is we'll go on to our long axis imaging techniques and These views help to complement what we're seeing on the short axis views. And so to obtain the right paraternal long axis 5 chamber view, which is the one where we can see the aorta, And the 5, when we say 5 chamber, basically it's because we can see left ventricle, right ventricle, little bit of the left atrial appendage, aorta and right atrium. So those would be our 5 chambers.
So what we'll do is, if we start from our short axis views, we had our reference mark under our thumb at 7 o'clock. And when I say a clock face, it would be as if you were holding the, the probe and looking down at the transducer head. So looking down on top of the probe, and you usually have that sort of little square or rectangular shape.
If you imagine that was a clock face, and that, that's how I'll refer to the, the various sort of time points on the clock. So, If you then rotate the transducer mark, so instead of being at 7 o'clock under your thumb, you'll probably need your other hand to help you do this. You're rotating it clockwise so that the transducer mark will now be under your index finger.
And pointing more towards 10 o'clock position. And you're going to still place the transducer head. On the, where you feel the right apex against your, your hand with the dog lying in right lateral cumbies.
So the same positioning and everything as before, all we're doing is twisting or rotating the probe, the, reference mark of the probe, 90 degrees clockwise to approximately 10 o'clock position so that we can go from the short axis to the long axis views. This definitely takes practise. Ultrasound is not something.
A heart ultrasound is not something that you learn overnight. You have to keep practising at it, because so many different confirmation, chest confirmations of dog, and then obviously, cats are their own, sort of entity in themselves when it comes to ultrasound. So I cannot, you know, stress enough, do practise, if you're interested in heart ultrasound, keep practising, go on courses, get tuition.
It's so important for the confidence that you need to not only get good images, but then feel confident to interpret them. Now with the short axis views, we have the pro perpendicular to the skin for the long axis views again, somewhat based on chest confirmation, but we often have to decrease the angle between the transducer and the skin of the patient to approximately 45 degrees. So it's not perpendicular, it's at an angle and point the probe face, so angle the the probe head cord dorsally so towards the lumbar spine.
For the 4 chamber view, which is, is the one we'll, we'll focus on a bit more today, all we do from there is in exactly the same position as you had for your five chamber view. You're just going to rotate the, the pro face or the reference mark. Very, very slightly more clockwise, so that it's now rather than 10 o'clock, it's now more at 11 o'clock, and you'll find the aorta disappears and you may need to angle the transducer slightly more cordially again, depending on the, chest con confirmation of the animal to maximise the, the full length of the left ventricle.
Now, if we're doing a triage ultrasound in a cat who's, for example, presenting with respiratory distress, and we just want to, to know is this likely to be cardiac or primary respiratory. A left atrial measurement can be really useful and we can use this right parasternal long axis view as well. As well as that short axis view I showed you, but we can also do this measurement in long axis, and we can take the measurement from a four-chamber view.
From the last frame before the mitral valve opens. And what we're going to do is measure here perpendicular to the mitral valve across the diameter of the left atrium in long axis. And there, there are, there are publications that suggests that, using a cutoff of saying that greater than 16.5 millimetres may help to differentiate.
A cat who's presenting with heart failure, dyspnea, rather than one who's dissonant from respiratory disease. So as long as your image is optimised, and this is why it's good probably to get, measurements from both short and long axis and to get the confidence, to, you know, practise and, and look at normal and abnormal because we don't just want to rely on measurements. If you oblique your image, or you measure from the wrong place or you you don't make the measurement, you know, in the in the right, sort of orientation, you can overestimate or underestimate these chamber sizes.
So measurements need to be interpreted, with caution. They do need to confirm what your subjective impression is first when you start to do the scan. If you think the left atrium looks enlarged, the measurement should confirm that.
If the left atrium looks normal to you, and you've done enough to feel confident with that. And you get a measurement that suggests left atrial enlargement, just make sure you're making that measurement correctly. We can also use the long axis for chamber view to assess how well the left ventricle is contracting.
So here is a, a normal, dog. We can see here that we've got, what happens is the heart or the, the ventricle sort of tapers towards the apex. So you can see this is left atrium, left ventricle, mitral valve, and the interventricular septum apex and left ventricular free wall here.
Now, if I compare that with the dog who's got dilated cardiomyopathy, where you can see even before the, the image starts moving, that we've got a very globoid ventricle. So this is left atrium, left ventricle mitral valve. Interventricular septum, freewall, and apex.
And you can see how rounded the left ventricular apex is. And if we look at the systolic function, you'll see that it's pretty poor systolic function. We'll go back and play that once more.
So that compliments what we saw in that short axis view of the very poor, systolic function with the dilated cardiomyopathy cases. Here we have the same 4 chamber, right parasternal long axis, 4 chamber view in a cat with hypertrophic cardiomyopathy. Remember we said in cats with HCM, the heart muscle has preserved systolic function.
It's more of a diastolic issue that they have, but the walls are thick. And so this is the free wall of the left ventricle interventricular septum. And this is the apex here, mitral valve, left atrium, left ventricle, right atrium, right ventricle, and tricuspid valve.
Because the right heart is in the near field, often we don't see that as clearly. But the key things I want you to notice are the thickness of, particularly the right ventricular free wall in this cat, and the fact the systolic function is relatively preserved. This is not a a case with poor systolic function.
I'll play that a few times, so apologies they're not looping as well as they could do. Here's our normal dog heart again, and here's a dog with advanced mitral valve disease. And in this 4 chamber view, we can see this disproportionately enlarged left atrium.
So very, very big left atrium. We've got bowing of the inter atrial septum towards the right atrium. Got left ventricle, right ventricle, interventricular septum, left ventricular freewa.
Here's the mitral valve. And in this particular dog, this dog has a very thick mitral valve. This is the anterior and the posterior mitral valve leaflet.
So it relates to this is the anterior and posterior mitral valve leaflet. And these are the cord attaching to the papillary muscle, but we're not seeing them here in this particular view because of our orientation. But this is a ruptured cord tendon, and in a moving image, this is a still, but in a moving image, you can see that flick backwards and forwards.
But even without colour flow, Doppler interrogation, if you have a small breed dog who has characteristic signalment and, and, physical exam findings, a loud murmur presenting with what you presume to be left sided congestive heart failure, pulmonary edoema, And maybe the dog suddenly decompensated and then you see this very thick valve, very big left atrium, and a ruptured cord tendon, you know, that, that's all very suggestive of advanced mitral valve disease, and left-sided congestive heart failure. So, moving on to M mode echocardiography, M mode is just a one dimensional image of the cardiac structures, and we typically obtain these from the the two-dimensional right paraternal short axis view of the left ventricle. So, I appreciate this is a lot of information to give you.
And really, these, webinars, I suppose, are a resource to come back to because if you're not doing ultrasound, regularly, and the same with ECGs and thoracic radiographs, if you don't feel comfortable necessarily with all of these diagnostics, trying to take it all in at once is probably too much. There is a lot of technical information, so come back to the webinars and, and go through these, these slides again. As you practise more and, and sort of improve your, your familiarity with it.
So what we do is we take our right paraternal short axis view through the left ventricle. This was that mushroom view I showed you before. And we're going to drop a cursor as, as sort of close to transecting that .
Left ventricle, if you like, as, as possible. So I want to be as as symmetrically as possible. So we have one, the, the cursor right down through the centre of it.
And that will mean that on our end mode, we will see any structure that this in mode cursor passes through, but only the structures that it passes through. So we'll see this bit of right ventricular freewall, this little bit of interventricular section, this part of the chamber and this part of the left ventricular free wall. We won't see.
Necessarily the papillary muscles unless they, as the heart moves come into that, single, one dimensional plane. And so what we see on an M mode is the depth and then we have obviously over time. So it's the sort of structures at various depths over time and how they move.
Now, again, if we have an ECG connected, this makes interpreting the air mode much easier in terms of the sys which, which phases cytoly and which are diastole. And if I show you, I'm gonna actually go forward and we'll come back to those slides. This is an M mode here.
So here's our right parasternal short axis view, and mode cursor through the left ventricle, interventricular septum, left ventricular free wall, left ventricular chamber. So here is our interventricular septum. That's right heart in the near field.
We don't see it particularly clearly as you can see here. Here's the depth that we're looking at an ultrasound down to 8 centimetres. That relates to this depth here.
And then this is over time because we're looking at this heart as it contracts over a number of cycles. So as it keeps beating, this sort of M mode graph, if you like, just, just keeps, we keep seeing the heart. Appearing.
So this is it in diastole. So the chamber, left ventricular chambers in is large. Then insistly, the walls contract and the chamber is small.
Diastole, the walls move apart, the chamber fillsyly, the walls contract. The chamber is smaller because blood's being ejected, diastole again, cystole, diastoleyly. So that goes along, you know, as, as, as long as you look through the mode image, you see this long sweep of of cardiac cycles.
What we've done here is we've measured left ventricular internal diameter and diastole, left ventricular internal diameter in systole. So these are what these measurements refer to. Then we can measure the interventricular septum in diastole.
And the interventricular septum in cystole, same for the left ventricular free wall in diastole and cystole. So, going back here, what we were saying is that we make our measurements from the lead. It's called leading edge to leading edge, which I'll show you again on that diagram.
And ideally, we should use measurements from at least a couple of cardiac cycles, ideally, say 3 to 5, because you're going to have changes in cardiac size, mild, but, potentially significant due to respiration, changes in cardiac filling if you have a sinus arrhythmia. And the routine measurements that we make as we looked at on the diagram are going to be left ventricular and interventricular, wall thickness in cytoly and diastole, and then the left ventricular chamber dimensions in systole and diastole. And then we can work out something called a fractional shortening, which gives us a rough indication of systolic function of the ventricle, and this is left ventricular internal diameter and diastole minus the diameter in systole, divided by the diameter and diastole times 100.
Thankfully, the machine will work that out for you once you've done your measurements. So here's leading edge, so top of, of the sort of endocardial surface to top of endocardial surface here, so leading edge to leading edge. Or we'll often say top of bright white line to top of bright white line cause these are the end right here is the endocardial surface.
And again, with our wall thicknesses, and here would be how the machine would work out fractional shortening as a percentage for you based on these. Left ventricular diameter measurements that you make. But as you can see, if you don't have a well aligned M mode, and you're making measurements from an M mode that hasn't been, you know, you haven't got a nice symmetrical mushroom shape and then you haven't dropped your cursor down through the centre of it, you can actually get measurements that are probably inaccurate.
So it's really important to try and get as good an image as possible. In terms of understanding what the dimensions, whether they're normal or abnormal, there are lots of published reference values that you can find in textbooks for that. Where possible, be aware of using breed values because, various breeds, have have their own specific values just like with, with the thoracic radiographs, as we said, some dogs have larger chambers than than others based on their, their breeds.
So for example, the springer spaniels, the sighthounds like the greyhounds, etc. And thank because obviously dogs vary in size, so we have tiny chihuahuas right up to huge Great Danes. Then the, you can often, if you can't find a breed value or breed specific value, you can actually, correlate to body weight.
Obviously, with cats, this is more difficult. But thankfully, our cat patients have a relatively small variation in body weight. So we tend to use a single reference range for each variable in cats, and again, you can find these in, in textbooks.
When we look at an M mode, it gives us an idea of systolic function. So again, you can see here the top image showing that there's quite active movement of the septum and the free wall, resulting in quite a a marked change between the diameter of the the ventricle and diastole and then in systole, and this would be associated with, for example, mitral valve disease where the systolic function is relatively well preserved or at least until the sort of end stages. But in dilated cardiomyopathy, because it's a primary muscle disease, you can see here that the septum and the free wall, the excursions are are very poor.
So there's not a lot of difference in size between diastole and cystole, in terms of the left ventricular chamber, and that's because obviously in in the in Sicily when the ventricle contracts, it's not really ejecting very much blood. In cats, it's a little more tricky when it comes to measuring heart wall thickness. Some of cats that have very thick walls, and if we're screening for hypertrophic cardiomyopathy, it may be difficult to get M modes in these cats because trying to drop an M mode cursor down between very hypertrophied papillary muscles might be challenging and also they can have asymmetric thickening of the heart muscle walls.
So sometimes we'll do the measurements from two dimensional images. So for example, here, this is a two dimensional image and this septum here is, you know, not, not necessarily thickened, but you can see it's obviously the free wall is much thicker than the interventricular septum. So this cat has asymmetric thickening.
Some cats have symmetric thickening, both the free wall and the septum, sorry, septum and freewall. Some have just one of those two walls are thickened, others. I said it can be regional.
You can just have sort of one area of ventricle that's thickened. Sometimes it's just the papillary muscles. So it may be, actually more useful to do two dimensional measurements as well.
So take home messages really are practise, practise, practise, when it comes to heart ultrasound. Make sure you know how to use your ultrasound machine, which probes you have and whether they're high or low frequency, so which patient size they're appropriate for. Try to look at in at as many normal animals as possible, so that you're going to find it easier to know what abnormal looks like.
And make sure that the measurements all make sense when you're interpreting your findings. So really, everything should just sort of be a piece of the puzzle. So your signalment history, physical examination findings, radiographs, if you've got them, then the ultrasound images, they should all be saying the same thing.
If one is wildly off, you need to really reassess it and, and see if you're going down the right track. And obviously analyse all the information together and it should fit together logically. Cardiac disease cardiology is a logical condition.
So that does actually make it much, much easier. As I said, left atrial enlargement should be present if you have an animal who's presenting with left-sided congestive heart failure. So those are the types of things to, to bear in mind.
OK, so what we're going to do is move on and look at some ECGs. I never know if this is the right one to end on because it's for some people. If I could just interrupt a moment.
Yes, of course. We've just had one or two questions come through. I don't know if you'd be prepared to answer those before moving on, of course.
So the first one is, referring to your first lecture, why is there dilation downstream of the subaortic valve stenosis? OK, so when you have, so I'm just trying to, to get the right slide to come up here. When you have an obstruction, And the the blood is having to accelerate to go past the obstruction.
Then post obstruction, it tends to become very, very turbulent. And so that can cause the, the muscular wall of the aorta to, to basically stretch and bulge out over time. So with the aortic stenosis, we have these fibrous ridges that develop below the aortic valve, and some of them can be extremely restrictive and tight.
So there's a huge amount of pressure that the ventricle has to generate to push the blood across that that stenosis. And then that pressure has to dissipate past the stenosis in the way that it does that it, as I said, it sort of swirls around within the root of the aorta. And because the aortic wall is muscular, it, it can stretch and, and, dilate over time.
Thank you very much for that. And just one other question, relating to your second talk that you've just finished. I ruptured cordder tendiny always end stage for therapy?
End stage. So, so if I understand the question correctly, there are some dogs who will rupture a cord or a corder, earlier on in the disease progression. Because when we think of mitral valve disease, we often just think of the valve being affected.
But actually, if you look at postmortem, the cordia often thickened and stiff as well. So not all dogs with mitral valve disease by any stretch will rupture cord tendon. Many will go through the whole stage of the disease, may go into congestive heart failure, may even die of congestive heart failure, but not rupture a cord.
Some dogs will rupture cords, and there's no way of knowing which dogs will, which dogs won't. It often will depend on which causes they rupture, how many they rupture, and I suppose When in their disease stage they rupture. So some dogs will rupture a minor cord, which is a smaller cord that doesn't support a leaflet edge.
It just supports sort of underside of the valve, so the valve can sort of buckle a bit, but the, the leaflet edges are still opposed. And if they rupture a minor chord, that may actually not really affect the amount of regurgitation too much that's happening. And so that, that may not cause the disease to progress too much.
If they rupture a major cord, these are the cords attached to the edge of the valve leaflets. Suddenly the edge of the valve leaflet can become very unstable. And actually what we call flail, so it can flick back into the left atrium and obviously is associated with a large increase in the amount of mitral regurgitation associated with that.
So it doesn't mean that you've reached the end of therapy. It just depends on whether you can stabilise a dog. Some dogs can be stabilised quite successfully with aggressive congestive heart failure, sort of emergency therapy, hospitalisation, intravenous therapy, and oxygen, typically.
But we can stabilise them again. Some dogs, if they have multiple cordia or a really major cordi and they're already very advanced and perhaps there's not a lot of cardiac reserve left, it can. The end stage, but it doesn't, it doesn't have to be.
And certainly, we know from published studies that dogs that do rupture cord tin, we used to think they had a much worse prognosis, but actually there was a study published or probably a good, maybe 10 years ago now anyway, but from, from France, it showed that, actually their prognosis is about the same. If they can be stabilised, they can do, they can do as well. Thank you very much, and if we can squeeze in one last question before you start your third presentation, where you have a cat or a small dog that won't lie still for ultrasonography, is it, what are your views on sedation, and would that affect the, the scan results?
So if you have one that won't lie still and particularly when you're starting off and you don't feel perhaps that confident or you know it's gonna take you longer, then absolutely you can sedate them. And I think as you get more confident, more quick, perhaps more targeted with what you're looking for, you may find that you need to sedate less and less. Just be very careful what you sedate with.
So again, the butrophol dose that I suggested before, that's a, a pretty safe drug to, to use if you've got a wiggly dog. There are certain drugs that will affect what you see on ultrasound, and not just ultrasound, but also then if you're doing other diagnostics such as, ECG. So using drugs like meatomidine are definitely going to, you know, affect what you're going to see in terms of slowing your heart rate down, which is going to increase the volume in the chamber because obviously, if you've, you've got more time between cardiac contractions, there's more time for filling.
Certainly, we, we did a study a while back looking at, sedating cats with severva fluorine that definitely seemed to affect their, their systolic function. So I would tend to sedate as sort of as minimally as you, as you need to in terms of the amount. So just take the edge off them, don't knock them out, and tend to stick to drugs more like butrophenol, or, say midazolam, ketamine, combi combination, something like that rather than using drugs like, Or rather than anaesthetizing or using drugs like meatomidine.
Thank you, Nuala. Thank you very much. Most helpful responses, I think for our delegates.
Now let you carry on with your next presentation. Thank you. OK.
So as I said, I apologise. I probably shouldn't have left ECGs to the end because they, for many people, they're a bit daunting and can be a little bit dry, but I hope to show you that they're not dry. And again, it is a resource to come back to you.
So I realised there is a lot of information in these In these talks, but I didn't feel it did you a service to skip things because then when you go back, there are bits missing. So we'll go through it and hopefully it won't be too fast a pace, but do you feel you can go back to it if you need to. So when we talk about an ECG, this is a complementary test in some patients.
We don't need to do them in all patients with cardiac disease, but certainly, in many patients, we will. And it's a complimentary test to the other diagnostics we've talked about. It gives us different information.
It's a transthoracic recording of the electrical activity of the heart muscle over a period of time. We obtain it obviously by attaching electrodes to the skin and the ECG amplifies these little tiny electrical signals from the heart muscle that are detected at the skin surface so that we, we can see our ECG. Obviously, it's going to, it's a gold standard for diagnosing the source and the frequency of the abnormal rhythm.
And it tells us health status of the heart muscle, but also it can tell us about physiological factors. So things, you know, think about if you, if your patient is very stressed or very hot or very cold, electrolyte disturbances, all these things can affect the ECG. But it has important limitations.
So it does not give us any information about how well the heart's contracting. We need to look inside the heart with an ultrasound to see that. It doesn't tell us about heart valves or the lining of the heart, the endocardium.
Again, we'd need an ultrasound to look to look at those. It doesn't tell us, obviously about whether there's congestive heart failure there. We can have clues such as loss of sinus arrhythmia or sinus tachycardia, but it's absolutely not diagnostic for congestive heart failure.
We need a thoracic radiograph to confirm that. And it will be affected by body confirmation and body size. We record ECGs in patients obviously that we detect abnormal heart rhythms in, but also in patients that have heart murmurs as heart disease.
We can have structural heart disease as well as concurrent electrical heart disease. In patients where we're seeing abnormalities on thoracic radiographs, so cardiomegaly. If we have a patient who's collapsing or, or fainting, and we want to know if there's an arrhythmic, cause.
Drug effects or toxicities, electrolyte disturbances, so potassium obviously is a, is a key one and for monitoring. So anaesthetic monitoring, ICU monitoring. We're going to position our patient in the standard position, which is the same as for a heart ultrasound in right lateral recumbency.
And same with the cat in an ideal world, it's right lateralcumbency, but we do know that we can get good ECGs in patients who are internal, and there are some published reference ranges for for cats internal. But just like in dogs, if you have an uncooperative or particularly dissonate cat who's got a chest full of pleural effusion, do not try to restrain them for ECG and lateral recumbency because they're typically very unstable. So it's much better to just do your ECG with the patient in, in a sternal position.
Maybe on flow by oxygen. And all we want is a rhythm strip. And we can get a rhythm strip in any position.
OK? So don't, don't, worry about trying to get them into a standard position. Whenever we're focused on the arrhythmia, you could, you could get that, you could make the diagnosis of the arrhythmia with the animal in pretty much any position.
So attaching the electrodes, traditionally people have used crocodile clips, which are quick and easy to apply, but they're quite traumatic if you've ever put them on your own skin. So I would always advise to flatten and file the jaws of the crocodile clip, as I've shown you in the image to make them less traumatic cause they're going to be better tolerated and your patients will lie still. Or you can use these, little specialised clips.
There are others as well on the market. These ones are called comfy clips, and they're very well tolerated. And will fit to most ultra so most DCG machines.
Attach the clips directly to the skin and moisten the skin, and the electrode with either commercial gel or spirit. I like these are limb leads, so you don't want to place them on the torso or on the the sort of body of the dog because you'll pick up respiratory artefact. And you don't want them, as I said, on the actual chest or on the abdomen, so they need to be on the limbs.
Now, I position them just below the, elbows and just below the stifles because again, the skin is looser just below the joint and it's well tolerated. Same, exactly the same in a cat. In terms of sedation for an ECG, I really try to avoid sedating because we know that certain drugs can affect what we see on the ECG, and if you're using comfortable, electrodes, you're gently handling the, the animal, not making them lie in lateral recumbency if they don't want to, quiet examination rooms so you don't have people walking in and out.
And as I said, avoid using drugs such as meatomidine, which will profoundly affect your ECG. So think of that when you're thinking of your sedation protocol. Do bear in mind all the tests you might want to do because you may think, well, the meatomidine is fine for the radiographs, but it will affect your ECG.
So if you think you might want an ECG, don't use that, that drug. Uncooperative or disic patients, as we said, you absolutely can get your ECG with the clips in exactly the same place, but in a standing or sternal position. To remind you about the cardiac conduction system, remember that the normal impulse comes from the sinoatrial node, the SA node, travels through the atrial muscle cells, then converges at the AV node.
Then goes down into the ventricle, initially into the bundle of hiss, then it goes into the right and left bundle branches, then into the Pikinji fibres in in each ventricle, and then throughout the ventricular myocardium. And so this little video here shows you how the impulse as it travels through the heart, causes the characteristic PQRST. So we'll wait till it starts again and then we'll run through and show.
Or explain what it's showing. So first of all, you have your sinus node and the impulse arises from the sinus node, spreads through the atrium and causes the P wave. Then it converges and travels through the AV node and travels through the ventricle, and as it travels through the ventricle, you get the QRS complex.
And then the T wave is the recovery or the electrical repolarization of the ventricle. So when you see a P wave, you're not seeing the impulse, you're not seeing the sinus node impulse. How do I describe this?
You're not actually seeing the impulse leaving the sinus node. What you're seeing is that it depolarizing the atrial muscle. And then the QRS is the depolarizing of the ventricular muscle and the T wave is the repolarization of the ventricular muscle.
When we talk about ECG leads, when we do a timing lead, so this is just for example, one that we're running during anaesthesia or during ICU monitoring, it's often lead to. But we'll go through the six leads just so you understand what they are, even if you, you know, you're not using them routinely. When we talk about the limb leads, as we said, we, we talked about where we're going to attach our limb leads to.
But those limb leads, so we've got right arm, left arm and left leg, and then obviously we, we have an earth lead on the other leg as well. But those three leads, right arm, left, left arm, left leg, make a triangle. This is called Eindhoven's triangle.
And so the lead one. And you can remember the lead by the number of L's in the combination. So lead one, right arm, left arm, left arm has one L in it, so that's lead 1.
Right arm, left leg, two L's, left leg, that's lead 2. And then left arm, left leg, that's 3 L's, that's lead 3. So that's how you remember which which lead is which.
But lead 1 goes between the right arm and the left arm. Lead 2, as we said, right arm, left leg, and lead 3, left arm, left leg. And if you look at the direction that lead 2 is in, you can see that that is most in line with how the electrical activity travels through the heart.
Because if you're looking at the average direction of electrical activity through the heart, it's going to rise in the right atrium and travel out through the ventricles. And because the left ventricle is the, the biggest, most sort of muscular ventricle. You know, the sort of average, direction is, is out through the, the left ventricle if you're summing all the little electrical impulses together.
So this is why you get the biggest positive deflection normally in lead two, and that's why we use that lead for our timing leads. But so if you just wanted a rhythm strip, we'll often just do a lead two. But if we're measuring all three leads, one thing you should notice is that it's normal for the QRS complex to be positive in leads 12, and leads 3.
But the biggest positive deflection is in lead 2. And then AVR, AVL and AVF are what we call the augmented unipolar, limb leads. And so basically the machine just uses that Einhoven's triangle in a slightly different combination to measure another three leads.
And the reason if you think about having these 6 leads, it's like when you look at a sculpture, you don't just look at it from one dimension in a gallery, you would walk around it and look at it from different dimensions. And that's what the leads are allowing us to do. We're looking at the heart from different Dimensions to see if we pick up anything abnormal.
But when you measure these leads, it's normal to have a negative deflection, you know, the predominant deflection of the QRS being mainly negative in AVR. Often it will be a bit positive and a bit negative in AVL, so what we call isoelectric, so they kind of cancel each other out. And mainly positive.
There's big predominant positive deflection AVF. OK. So even if that's what you take home from these six leads that you know, it's a way of looking at the heart from different directions and that the, the leads should be positive in 123, and AVF, typically negative in AVR and a little bit of both in AVL.
Now, when we look at our ECG paper, it can be a bit confusing to know how to interpret it, but basically, Again, it's like a graph with amplitude in millivolts and time in seconds. OK, so we've got our vertical axis and our horizontal axis and the millivolt marker on the ECG will tell us what the amplitude setting is, and we'll go through this in more detail so that we can actually, if we wanted to measure the height of the complexes, we know. How to do that because we know what the setting is, but we're measuring this in millivolts and we're measuring this dimension in time.
And again, depending on what we set the machine to, we can either run the ECG at 50 millimetres per second, which basically the paper runs through the machine faster and so it spreads out our complexes, or we can run it at 25 millimetres per second, which tends to, well, it runs the paper slower so that the complexes are closer together. For cats, we tend to and for faster heart rates, definitely opt for the 50 millimetres per second. Let me show you that in a little bit more detail.
So when we're choosing the paper speed, What I'm showing you here is this is the same dog, but we've just run the ECG at two different speeds. So if I run the paper speed at 25 millimetres per second, this is just a matter of pressing a button on your ECG machine to run it at 25 millimetres per second. The distance between these two R waves here.
Is 24 millimetres if you were to measure it. If I run the paper speed at 50 millimetres per second, it just stretches everything out because the paper runs through the machine faster. So it follows that the distance between the R waves is going to be double.
What it is at 25 millimetres per second, so 48 millimetres per second. The reason this is important is for when you're measuring heart rate, you really need to know what speed you ran the paper at so that you can accurately work out the heart rate. When we're picking the sensitivity, or deciding how to record the ECG with the sensitivity, standard sensitivity, so if you don't alter it, it will measure you the ECG machine will measure it 10 millimetres or 1 centimetre for 1 millivolt.
And you often have these little millivolt markers here which you can actually look at if you don't know what sensitivity is. And it'll show you 10 little tiny boxes, each one of these is a millimetre. So 10 tiny boxes vertically is equal to 1 millivolt.
So here we can measure our wave and it's 15 millimetres, so we know it's 1.5 millivolts. If we have really big complexes and they're all overlapping each other, we can actually ask the machine to measure half sensitivity.
So it means that 1 millivolt is now equal to 5 millimetres. And so if we measure our our wave here, it'll be 7.5 millimetres tall, but we know because we're at halftime, half sensitivity, that's still equivalent to 1.5 millivolts.
And exactly the same for twice sensitivity. Often cats have very small complexes. We might want to run their ECGs at 20 millimetres per millivolt.
Again, shown by the millivolt marker. And we measure our wave here. It'll measure at 30 millimetres, but we know because we're at twice sensitivity that it's equivalent to 1.5 millivolts.
So again, important not only to know the paper speed, but to know the sensitivity or amplitude setting if you want to be measuring heights of complexes. Now some ECGs will measure single leads only, one after the other. OK?
Other ECGs will allow you to measure 3 leads at a time, and others will allow you to do all 6. So this would be lead 123, AVR, AVL, and AVF. In an ideal world, this is the best way to look at an ECG cause we can glance and say yes, positive in lead one, big deflection, positive deflection 2, positive in 3, negative in AVR.
Positive in AVF and a little bit of both in AVL. So this is what we call a normal mean electrical axis, or it just means that the electro activity is travelling through the heart in the normal fashion. If you think about that little, video I showed you earlier, how it travels through the heart.
If it travels through the heart in that normal way, then that's what the ECG should look like. So how do you read an ECG? Well, first of all, we need to know what the heart rate is.
And in order to know what the heart rate is, as we said, we have to know the paper speed. And there are a number of ways to calculate heart rate. One of the simplest one is to use, but it has to be a big pen, so it's a big pen method because the cap with the cap on from the cap tip to the end is equivalent here to 15 centimetres in length.
So obviously you could just use a ruler with 15 centimetres and you measure your R to R intervals here. So it's not our waves, it's intervals, which is the the R to our interval here, and you count the number of R to our intervals in that 15 centimetre length, because at, depending on the paper speed at 50 millimetres per second, that's equivalent to 3 seconds in duration. We know that there are 60 seconds in a minute, so 60 divided by 3 would give you 20, so it would be 20 times the number of our to our intervals.
In this 15 centimetre length that would give you the number of our to our intervals in a minute. OK? And so it would be if this was at 25 millimetres per second, it would be 15 centimetres is equal to 6 seconds.
We know we would have to multiply that number of R2 intervals by 10 to find out the number of R2R intervals in a minute to work out our heart rate per minute. So for example, this is 50 millimetres per second. We have 8 R to our intervals in this strip here.
So we can see 1234567, and then half on each end. So it's 8 times 20. This gives us a heart rate of 160 beats per minute.
There are other ways to do it, such as using ECG rulers, but obviously this works if you have a very regular heart rhythm. If the heart rhythm is varying. Then you can't use just that instantaneous heart rate and expect it to be relevant for the entire trace.
And make sure you use the side of the ruler that is relevant to the paper speed that you've measured at. The instantaneous rate method, again, is exactly the same as the ruler. Basically, you're going to measure the number of millimetres between your R2R intervals and it's exactly what the ruler is doing for you.
And then you're using a factor here, so it's 3000 divided by the number of millimetres between the R2R intervals. If it's 50 millimetres per 2nd and 1500. If it's 25 millimetres per second, and it'll work out an instantaneous heart rate for you.
So if you don't have a ruler, you can come back and, and, look at this method, but it's only for regular heart rates. So measuring intervals, we need to know the paper speed and the amplitude. And as we said, the intervals here that we can measure a PR interval, which beginning of the P to the beginning of the QRS complex.
We call it a PR. Some people call it PQ interval. The QRS, which is the beginning of the QRS complex to the end of the QRS complex, you can measure the R wave.
And you can measure the, The, the sort of T wave, but often we don't tend to measure ST and T individually. Often people will measure PR interval, QRS complex, R wave height, and you might do your sort of QT interval, so beginning of the QRS to the end of the T wave. I haven't gone into all the intervals and .
Amplitudes and what they mean because to be fair, we don't tend to use those to measure heart, chamber sizes very much anymore. They used to be relied on much more for assessing heart size, but now because radiographs and heart ultrasound are so available and much more accurate, we're really, and I would really want to sort of just emphasise that I would advise you to use the ECG more for rhythm. Diagnosis rather than trying to interpret heart size from it.
But if you want to know more about that, there's plenty of information in textbooks, but it's probably beyond the scope of this talk. So when we look at the heart rhythm here, we're going to decide, is it a normal or an abnormal heart rhythm. And so one way to start reading the ECG is to say, is there a P wave for every QRS complex?
And is there a QRS complex for every P? So here we can see there's a P for this QX, a P for this QRS complex. Here's a big abnormal looking QRS complex with no P in front of it.
P for QRS, PQRS P QRS, that's just baseline, artefact PQRS. Here's one that doesn't have a P wave in front of it. So these are curses without Ps in front of them.
And here we've got a PQRS. That's a T wave. Here we've got a P wave without any QST after it, P wave without any curS complex after it.
PQRS. This is the T wave, P QRS T wave, PQS T wave, and here's a P, not followed by a QRS. T complex.
So those are important questions to ask yourself when you're looking at an ECG if there's an abnormal rhythm. And then we want to look at, whether the conduction looks super ventricular. So is it coming from the top of the heart?
Or is it coming from the ventricle? And if it's nice and narrow and normal looking, this would suggest it's super ventricular. OK, so even if it's, we can see here, this is a regular rhythm, then this is an irregular or an early complex that comes in.
But this is likely to be a premature complex or early complex coming from the top of the heart because it's narrow. It looks the same as the sinus complexes. Therefore, it's travelled, in the same route as the sinus complex.
Whereas this one here, here's a normal sinus complex PT. Then we have this wide bizarre abnormal complex without a P in front of it. This will have arisen in the ventricle.
It's also premature, but it looks totally different to the sinus complexes, so it's arisen from a different location. When we're looking at the timing, we want to say if it's premature or if it's escape or late. And a premature complex as we said, is early relative to the preceding R to our interval.
So if that's a normal R to our interval, this one is a short R to our interval. So this is a premature complex. That's a normal R to our interval, that's a short R to our interval.
So that's a premature complex, often followed by a pause afterwards. Here, these are our normal R to our intervals, but now we've got a long pause before the next one. So this is an escape complex.
It comes in after a pause. Here, this, if we take those as what the typical R to our intervals were before the pause, we've now got a long pause, then we have an abnormal looking complex, but this is an escape complex. So this is a ventricular escape complex.
So we're just gonna just have a look at some rhythms and really with ECGs it's pattern recognition. You've got to keep coming back and looking at normals and abnormals and just training your mind as to to what or training your brain as to what they look like. So here's normal sinus rhythm in a dog, PQRST.
P QRST. These two waves look a bit strange, but T waves can be very pointy like this. They can be positive, negative.
But basically, we do have a P for every QRS. And this is a normal cat. So we've got a small P wave, small QRS, often very small complexes, but there is a P for every QRS complex.
Sinus arrhythmia is normal in dogs, not normal finding in a clinic in cats because obviously, cats tend to be more stressed in clinics, so the sinus arrhythmia will disappear in most cats. You would hear it at home if you snuck up on your cat and listened with a stethoscope, most likely. The heart rate increases with inspiration and slows down with expiration.
So you can see it's increasing, and then it slows down and then it increases and slows down. Easier to hear and to see if you listen over a longer period. So those were normal rhythms.
And then if we look at some abnormal rhythms, we'll start with sinus bradycardia. This is a normal sinus rhythm, but it's at a slow rate. It's an inappropriately slow rate, so we'll have a P for every QRS.
And a cures for every P. And often this is physiologic, so increased vagal tone. An animal who perhaps has, has, increased intracranial pressure, intraocular pressure is very cold.
Those things can slow down heart rate. Sinus tachycardia looks like a normal sinus rhythm, but it's just faster, often physiologic again, increased sympathetic tone. Atrial premature complex is our normal sinus rhythm in the background, and then we have a complex which is narrow.
But it's coming in early relative to the preceding R to our interval. So it's going to be a premature complex. It does have an ectopic or an ape associated with it, but it's hidden in the preceding T wave.
And again, for a cat, it looks, it's exactly the same as a dog, but often with cats, the rate is overall rate is faster and the complexes are smaller. I think for the interest of time, I'm just going to show you these, but I said, please do come back and have a look at them. Atrial tachycardia is a rapid, a narrow complex rhythm.
OK. So it's the complexes, the cures is a narrow, upright. They look like sinus complexes, but the rate is so fast that you can't really see the P waves cause they're hidden in the T waves.
Atrial fibrillation is a very common rhythm, in large breed dogs with dilated cardiomyopathy. You'll often see this. It's an irregularly irregular rhythm.
So it's the kind of rhythm that, you'll sometimes hear people say, it sounds like tennis shoes and the tumble dryer. It's, it's just really chaotic and hard to predict when the next, contraction is coming. And we do find it in cats, but it's, it's not common in cats because you have to have a certain heart size to sustain it.
So it's typically in cats associated with very severe advanced heart disease and atrial enlargement. Obviously in in dogs, we can see it without the presence of underlying heart disease, but more commonly seen in large and giant breed dogs with dilated cardiomyopathy. And then we have our block, so remember AV block, so 1st, 2nd and 3rd degree.
1st degree AV block is just a prolongation of the PR interval, but every P conducts. 2nd degree, intermittently P waves don't conduct, but some do. And 3rd degree block means there's no conduction between the P's and the QRS's.
So the pes are marching through here independently. There's one superimposed here, and the QRS is an escape rhythm in the background that's totally independent. And then we can have situations where there is conduction, but it's so intermittent, so 2nd degree block can be very, very high grade.
Essentially, it's like 3rd degree block. The rate would be so slow, but that this is not 3rd degree block because there is intermittent conduction. But you can see here there are a lot of pieces that are blocking.
So this would be an example of 2nd degree block, but very, very high grade. I'm going to move on through some of these slides. Just lastly, to show you a few examples of ventricular arrhythmias before we stop.
I said, this is really pattern recognition. You have to come back and look at these multiple times to get comfortable with them. With VPCs or ventricular premature complexes, wide, bizarre, premature complex, and it's premature when we look at the timing relative to the preceding R to our interval.
Exactly the same in a cat. In terms of the morphology and these VPCs can be positive or they can be negative depending on where they come from in the ventricle, but they have no P wave in front of them. This is an example of VPCs.
Every second complex, this is a sinus complex, it's a cat, so it's a very small complex. This is sinus ventricular, sinus ventricular. When it's alternating like this, we call it ventricular by Germany.
Ventricular tachycardia is simply just a string of VPCs one after the other, either sustained or or for long periods that occasionally breaks. So here's the dog with ventricular tachycardia, then negative VPCs one after the other, two sinus complexes break through, and then he goes back into VTA, and again, a cat with ventricular tachycardia. Be aware of something called purring artefact that you might see in some cats, just an interesting thing to show you here.
Here's a cat with a normal heart rate, but intermittently we see this baseline artefact. This is not an arrhythmia. This is just something that you see, it's an interference from purring.
So, we've come to the end. Thank you for your attention and I do appreciate there's a lot of information there, but I hope that you have found that useful, and it's a resource to, as I said, to go back to and, and to give you some sort of support and guidance when you're doing your cardiac diagnostics. Nuala, thank you.
That has been an absolutely amazing set of presentations. I mean, you've taken us through radiology, ultrasound, and ECGs in the most clear, thorough and authoritative way I've ever heard those things described. So thank you very much indeed.
I know all our delegates will have benefited from that very greatly. I think probably the most telling comment is one that's come through saying, brilliant, for the first time ever, I really understand ECGs, which I think says, you know, says it all, really. We took a few questions earlier, and I'm afraid in the interest of time, well, we probably can't take any more questions from you now, and we'll move on to Kieran Borgelet's presentation.
But thank you very much indeed, and a reminder to everybody. That the presentations and the notes will all be available on the website. So thank you very much indeed, Nuala.
I really appreciate that.
