Hello, welcome to this webinar lecture on common cardiac diseases in the dog and cat. So we're going to start along by going through the pathophysiology of some common cardiac diseases. We're going to cover mitral valve disease, dilated cardiomyopathy, aortic stenosis, pulmonic stenosis, and then hypertrophic cardiomyopathy and hypertrophic obstructive cardiomyopathy.
Within that, I'm also going to go over some treatment aims along with nursing considerations and suggestions for each of these disease processes. So we're gonna start with a bit of basic stuff first. We're gonna go through the, just the flow through the heart, just to make sure we're all understanding our cardiac anatomy and where everything is going to, and then it makes it a little easier to link into those disease processes then.
So we're gonna start with the oxygen poor blood first, which is going to come in. Into the right atrium. Through the caudal and and cranial vena cava, here, we're going to flow through the tricuspid valve into the right ventricle, and then we're gonna go out through the pulmonic valve and the pulmonary artery and off to the lungs for oxygenation.
Conversely, then we've got the oxygen-rich blood coming in through the pulmonary veins into the left atrium, and then through the mitral valve into the left ventricle, and then leaving the left ventricle via the aortic valve out to the aorta and along then to the rest of the body. Going to be using a lot of echo pictures as we go through this lecture so that you can really visualise each disease process. So we want to start off with a normal picture first.
And this is the left sided 4 chamber view, and we've got the left atrium here with the mitral valve, and then we've got a nice bullet shaped left ventricle septum in the middle, and then we've got the right atrium at the top of the screen there with the tricuspid valve and then the right ventricle. So to start off, it's good to start, I think, start about talking with the the staging of heart disease. Now this is the ACVIM stages of myxomatous mitral valve disease in dogs, and it's been widely adopted through the veterinary world as a really good way of grading the heart disease processes that your patient is going through.
So we start with a grade A, and these are breeds that are predisposed to heart disease. So we're thinking breeds like the Cavalier King Charles Spaniel, the cocker spaniel, Maine Coon cats, also, Dobermans, Great Danes, you know those breeds of dog and cat that you would think as maybe very susceptible to having heart disease. Those are all a stage A simply by being the breed that they are.
Then we move on to a stage B1. Now these are patients that likely have a heart murmur. They're often patients that we are referred to us in our practise as having auscultated a heart murmur at a vaccine check or even a first or second vaccine, if they're a puppy or a kitten.
And it's usually their routine checks that bring up in their GP practise, the fact that they've heard a heart murmur and then they're referred on for, for a cardiac workup to find the cause of the murmur. When we do go on an echocardiograph, a B1 patient, we don't see any cardiac remodelling. So there's no chamber size enlargement, and there's no, not necessarily any sort of any sort of major signs or a component of structural changes within the heart, but we can identify the cause of the heart murmur.
So a heart murmur is a turbulent blood flow within the heart. So by using colour flow Doppler, We can actually look at each of those areas within the heart and identify where that murmur is coming from. But there's no structural changes along with that.
Then we move on to a stage B2. So this is where our patient most definitely has a heart murmur now, but there is evidence of cardiac remodelling on echo. So we can see chamber enlargement sizes, we can often see cardiac myocardium changes as well, and there there's those structural changes that are appreciative, and the flow of blood is usually disrupted in more than a minimal way.
We don't always see clinical signs reported by the owners. We don't often hear of clinical signs reported by the owners, even at a B2 stage. Sometimes it takes a progression along the pathway to an advanced B2, but owners may report something like slight exercise intolerance, maybe showing a little easier to tyre than they would do, maybe a bit of inappropriate panting.
Little things like that. So, sometimes there's these very minimal, clinical signs reported by owners, but, not always. Then as we go further down the staging, we then come into stage C.
So stage C is when there are signs of congestive heart failure. So a patient has a congestive heart failure episode, be that left sided or right sided, but they meet those criteria for being in congestive heart failure. So usually they have if it's a left-sided failure that's increased respiratory rate and effort, and also, quite severe exercise intolerance, maybe in a regular heart rhythm as well.
Maybe some effusions identified, etc. So that's when they enter a stage C is when they are, classified as being in heart failure. And then we do obviously have those quite significant clinical signs of heart failure as well.
Stage D is the last stage, and this is when congestive heart failure signs are actually refractory to treatment. So basically, the drugs don't work anymore. We're giving them those usual standard quad therapy for, for heart failure, but it's not actually hitting the mark anymore.
It's not keeping our patients stable. Sometimes then we need to think a little bit outside the box and tweak the medications, and maybe think about different medications that we can swap in in order to try and stabilise the patient again, but then they are, they are in that stage D. So the stage that we're really interested in, to be honest, in a cardiac referral setting is the stage B2, because this is when we want to start treatment for any heart disease process that we've identified, particularly mitral valve disease in dogs.
Now it's the EPIC study, it's the big study that came along, some time ago, now it's had a part 1 and a part 2. And this is proven that with a mitral valve disease in dogs, if we identify them as they become into a B2 stage, if we start treatment, Then we can actually prolong the time in which it takes them to reach stage C. So it's a really, really crucial moment, and we try and, and hope and pray that we get referrals through for our canine patients where we can actually catch them entering their B2 state so that we can start that treatment at the very opportune moment and make sure that we are medicating these patients as appropriately as possible to make sure that they Stay out of heart failure for as long as possible, extend that time in B2 stage and give them the longest, best quality of life possible.
OK, so let's talk a little bit more then about that mitral valve disease. So this is where the mitral valve is, becomes thickened and ineffective at doing its job, which is stopping black back flow of blood from the left ventricle into the left atrium. So because we get that leak in the blood flow, so instead it's going backwards through the, through the mitral valve there, in, in Sicily.
So when the left ventricle contracts, all the blood should be leading out the aorta, and most of it does, but some of it will go backwards into the left atrium again. So because of that, we get a left sided apical murmurs, that's the one that you can hear sort of left armpit region in your, in your patients. And that's that's a good signifying if we identify that left sided apical murmur, then we can extrapolate that that is most likely to come from a leaky mitral valve.
As the disease progresses, we get reduced cardiac output. The more that leak comes back into the left atrium, we get a reduced cardiac output, and the body puts into play its normal compensatory measures. So we're talking by the constriction, raising the heart rate, increasing contractility, those normal measures that we expect our patients in order to maintain blood pressure.
All this then gives an increased workload onto our heart and an increased oxygen consumption rate for our cardiac myocardium. And then that can lead us then as the disease progresses even further into left atrial enlargement and left ventricular dilation. So we end up with a lot of blood sloshing in between the left atrium and the left ventricle, going back and forth from the atria to the ventricle and instead of really sort of going through and leaving the heart as it's supposed to.
So we end up with that atrial enlargement and the left ventricular dilation as well. And we then get the volume overload of that left side as that blood is continuing just to jump back and forth instead of actually going through and leaving the heart. Eventually, as we get through into stages Cs and D's with mitral valve disease, we end up with left ventricular wall thinning and a much reduced contractility, and we end up with a dilated cardiomyopathy phenotype, which basically means that the mitral valve disease has progressed so much that our heart actually looks like it's got DCM instead of mitral valve.
So when we see a patient that, presents in heart failure and we, we do the echocardiography and we, we find a heart that looks like it's a DCM you're never quite sure whether or not it comes from a, an advanced mitral valve disease or whether it is a primary DCM. Sometimes looking at the, the actual structure of the mitral valve leaflets can help, make that diagnosis, but the cardiologists do have, do have a nose for it, and very often they, they, they can make a a very good educated guess as to which one is, is going for that there. We then give rise to arrhythmias as well, so as that disease progresses, we get that unhappy cardiac myocardium as the cardiac output is reducing, as the chambers are enlarging, the contractility isn't so great, we can then predispose out into arrhythmias.
So very often arrhyth anti rhythmic therapy is part of our treatment plan as well. So the end then is left congestive heart failure with our pulmonary edoema and sometimes we also see plural or pericardial effusions as well. So here's some echo pictures for you, some video loops of a mitral valve B1 stage.
I just need to take off my laser pointer, there we go. So this is a standard left apical view, much like the normal echo picture that I showed you before. So we've got our left atrium here and the mitral valve, flippy flapping, and a left ventricle there.
And it's maybe not as bullet shaped as it could be, but it's still doing a good job, isn't it? It's contracting nicely. We've got our right side at the top of the picture there.
So it's not doing too bad, is it? And then when we have the colour on the colour flow Doppler, you can see that you've got this lovely flash of green colour flow which is the leak coming back through the mitral valve. And so our colour flow is very, very helpful.
We can identify on the standard. That our mitral valve leaflets are maybe a bit thickened, maybe not quite closing as snugly as and succinctly as they could do. And when we put the colour on, we can then see that regurgitant fraction of blood coming back into the left atrium and identify the cause of our murmur.
As we progress then, this is a mitral valve stage C case and you can appreciate the very large left atrium here that's much larger than it should be. Our mitral valve through here and a very rounded left ventricle. There's also a little bit of a fusion here as well, and then you can also see the green turbulent blood flow of that leak coming back through.
So treatment aims for this condition, we really want to maintain our heart rate and our blood pressure. We want to improve contractility and reduce systemic vascular resistance as the disease progresses along those stages. If our patient is exercise intolerant, then obviously we want to improve that for them as well.
You know, we want to make sure that our canine patients can run about and exercise as they would like to. And we're talking, talked before about delaying the onset of stage C, so making sure our treatment plans are. Enacted right at the, the crunch time and the opportune moment is the most helpful.
We can also think about surgical suitability for our mitral valve disease patients as they go into stage C. They are actually eligible for either a mitral valve repair procedure or even the tier procedure, which is the edge to edge clamp repair, which is done in the UK as well at a couple of centres. So you, if your, if your client is keen and you have the funds available, then you can contact these centres and see if your patient is suitable for, for having the surgical stability done.
Nursing considerations for these patients, I'm going to talk a lot about similar nursing considerations for, for all of the cardiac diseases, really, and age and comorbidities are definitely one of the ones that we consider for every single type of heart disease. It really does make a difference, the age of your patient and then whether They do have any coexisting disease processes going on. So as our patients get older, this is very often when we are noticing heart murmurs, when we are evidencing mitral valve disease, and then they also come hand in hand sometimes with those endocrine diseases like hyperthyroidism.
And also Cushing's and Addison's as well. Kidney disease is also impacted. The kidneys are very, very delicate structures, aren't they?
Bless them. They don't like to be uninterrupted with their perfusion or anything. So when we have got cardiac output issues, the kidneys are the first ones to throw their hands up and have a hissy fit.
So definitely kidney disease is one of those ones where we need to identify and make sure that that is stable along with any heart considerations. The stage of the disease, obviously I've, I've spoken about this before, it is really, really important if we know if there are B1 stage or if there are B2 stage or if they're straight into stage C and they're showing signs of heart failure. We ideally in a cardiac referral setting, we want to see them before they get to their heart failure.
Stage. So the best time to have those conversations with clients about potential referral for cardiac workup is before their pet is showing any clinical signs of heart disease. We want to see them when you've heard that heart murmur.
And they've not got exercise intolerance and they've not got respiratory compromise and they've, they're, they're not showing any kind of, syncopal signs or anything like that. So the best time for us to get that referral is when that heart murmur is identified because then hopefully we can get them at that B1 or even B2 stage and start that medication. The temper for medication obviously is really important and client buy in obviously is really important as well, so it's working with our clients with all those tips and tricks that we know as nurses to help with the medication because medication for heart disease, it's daily and it's for the rest of their life.
They, they don't retract back along the heart disease stages. Once you're a B2, you're always a B2. Once you're a C, you're always a C, and they won't come off these medications.
So, getting your patient to accept that and getting your client in a routine that they can perform those medication times and, and deal with that is really, really important, something we can really be involved in with as nurses. One of the great things that owners can do at home for their pets, particularly with mitral valve disease, but with other heart disease processes as well, is monitoring the sleeping respiratory rates. They can do this via the Cardali app, it's very, very helpful, it's very easy to use, it's widely available and downloadable, it's free for use.
And it really prompts owners into being able to use their phone to record when their patient is having a respiratory cycle, and then it can calculate that rate for them. It produces a graft and that's an emailable graft as well, so they can send it to us at the practise, which is great because we can keep tabs on that resting respiratory rate, really closely. So we want that to be under 30 breaths per minute, ideally.
When, obviously every patient is slightly different. So it's really helpful when owners know what their pet's normal is, and then they're very aware of when that resting respiratory rate starts to creep up towards the 30 and over the 30 consistently, and then they can give us a ring and request a recheck, and then we can hopefully identify when those stage progression is happening. Nutrition is really important and I'm not going to, sort of speak about any specific diets, but definitely making sure that we have those omega 3 fatty acids and alcarnitine supplements in there.
They again, these are widely available over the internet, they don't need to be sourced from a veterinary. Practise you can get your clients to to get them online and source them online, but it's been shown that the particularly the omega 3 fatty acids and the L carnitine can really help heart health. So it's definitely something to look into see the stock on your shelves as a practise or to find a brand name that that your vets like and then you can offer that out to your clients.
And as ever with patients with heart disease, avoiding tachycardia and stressful situations is again really, really helpful. The old cliche adage of stress is a killer, yes, it can be, particularly with a pre-existing heart disease. So definitely working with your clients and patients to make sure that their visits to the veterinary practise are as stress.
Free as possible, whether that's adapting where they're seen, whether you need to see them outside or in a garden space if you have it, or provide a home visit checks and all these kinds of things, maybe reducing the frequency of checks to make sure that we're only checking them when we really need to, then this can all be beneficial to the patient. OK, let's move on to our next disease process we're gonna talk about dilated cardiomyopathy. So this is when our ventricular walls thin and the chambers dilate, and they can dilate quite hugely.
We often end up with left and right sided apical murmurs, because what happens here, if you come across to my pictures, is that you have the tricuspid and the mitral valve annulus. And what this provides is a base for those valve leaflets to adhere to. And as these chambers dilate and get wider, the annulus is stretched apart so that our leaflets don't close, and they can't adhere and oppose as they should normally.
This then lets a lot of blood backflow from the ventricles into the atrium. On both sides of the heart and increase the vicious cycle of chamber enlargement. So we get murmurs on both sides of the heart, with dilated cardiomyopathy with that mitral and tricuspid regurgitation.
And that volume overload. Again, much like the advanced mitral valve disease, we end up with blood sloshing back and forth between atria and ventricles as the the walls thin, the chambers dilate, the contractility becomes poorer, and the movement of blood slows. We also get atrial enlargement and a predisposition to atrial fibrillation because those atrias are so large in size.
And it's a huge systolic dysfunction with dilated cardioopathy along hand in hand with that reduced contractility. So we end with a bi-ventricular failure. We get left and right congestive heart failure signs.
So canine patients will typically present with respiratory distress and pulmonary edoema, but often with a pot-bellied appearance and a sci. Burden as well. They can also then obviously have other effusions like plural and pericardial effusion as well.
So doing TA and AAS in these patients is really, really helpful to evidence bee lines and the presence of ascites. So I thought I'd pop back to my normal echo picture just for a second here, just to refresh again for you and play this video here. So this is what a normal heart will look like under Echo, and we're expecting to see quite that nice little size left atrium, the bullet shape left ventricle, and the right side on the top there quite nicely.
As we move to a DCM. And this is a stage CD patient. You can appreciate the the largeness of the size of the left atrium and also of the left ventricle before we even start.
And you can really appreciate the wall thinning as well before I even play the video. You can really appreciate that the difference between this picture and the previous picture and that right side is real squished at the top there because of the size of the of the left side. So let me play the video for you.
And then, yeah, it's really apparent, isn't it? The lack of contractility, the lack of blood being able to move back and forth. This patient also has atrial fibrillation, which the keno of you will spot on the little small ACG loop there.
But you can also see that the mitral valve is really flickering, the atria aren't doing their proper contractile phase either. So yeah, atrial fibrillation along with the DCM in this patient. So treatment aims here, we want to try and maintain a heart rate, maintain or even improve blood pressure if we possibly can.
O cardiac output is severely compromised in DCM so it's all about improving that blood pressure for the patient. We want to increase contractility with our medications and hopefully get that cardiac output increased there. And that will help our patient improve its exercise tolerance.
And it's very often patients with DCM that present in the syncopal state that they're having real trouble exercising at all because of that lack of cardiac output. Arrhythmia management is a massive part of DCM, particularly as we get down those stages and into that stage C and D, and those arrhythmias become apparent. Atrial fibrillation is the sort of poster child for DCM, but we can also have ventricular arrhythmias as well.
Nursing considerations, it's, it's that the age and comorbidities again, we often find it's our older patients that present with DCM. There are certain breeds that present with a younger age like Dobermans, but there are a large breed again. So again, life span for these patients are not going much beyond into double figures, are they?
Temperament for medication. Again, there's gonna be a lot of medications with DCM. So again, canine patients really need to be on board with with giving those medications daily.
The timing does kind of matter a bit as well, so they do need to be regular. We can't just sort of miss a dose because They didn't happen to finish their food that day. So it's really important to get, as I said before, to work with clients to get a good regime and good tips and tricks for medication giving.
Stage of disease, again, really important to know what stage we're dealing with with DCM, although unfortunately, we do tend to see them present in later stages when it actually becomes impactful. Nutrition very much again, still the omega 3 fatty acids and the alcarnitine taurine is a really pertinent one for dilated cardiomyopathy. There is cocker spaniels often have a taurine deficiency.
Which can give rise to DCM phenotypes when we echocardiograph them, and there is a tenuous link in the evidence with grain-free diets and DCM. I'm sure you, you have heard of it. It's it's quite widely known.
The evidence isn't concrete or, you know, anywhere near concrete actually, but we do find when we're in clinic that with the spaniel breeds, when we do have them in and they do show a DCM phenotype on echo that very often they are actually grain free fed and we will advise that they do move to a grain inclusive diet. And as I said before, the, the evidence is tenuous, but it isn't something that we want to leave to chance when we're recommending, . Things that can help for the, for clients.
Again, avoiding tachycardia and stressful situations is really, really important with these patients because their cardiac output is so compromised and their heart is so unable to increase contractility because those chamber dilations, etc. Then, dealing with a stressful situation and trying to raise heart rate to to cope with that sympathetic drive is really challenging and can give rise to syncopal episodes and even sudden death. So, as the disease progresses down the stages, it's really important to balance any stressful situations.
OK, let's move on then to aortic stenosis. Now this is when we have a fixed left ventricular outflow tract obstruction. We can have subvalvular stenosis, valvular and post valvular stenosis, but by far the most common presentation is a sub valvular aortic stenosis, and that's what's shown in the picture on the right hand side of my slide here.
So where we have the stenosis pictured here and the valve on the top there, this is the subvalvular aortic stenosis. And we have a left sided basila murmur with this one. So it's a much higher up in that left armpit and it sometimes you can even hear it best when you bring your stethoscope more towards the sternum of the patient, particularly in smaller breeds.
So you do want to make sure when you're auscultating that you definitely move your stethoscope around left side, right side, and right up in those armpit areas to get those basila murmurs. So we have a mild to severe affectation, it's mild, moderate or severe, those are the three options. So we don't really grade aortic stenosis like we do with the valvular disease from A to D.
We have a mild, moderate and severe. And with this disease process, because it's a fixed obstruction. And it's a congenital process.
Whatever the patient has, that's what they have. It, it won't degenerate into a worsening stenosis. If they are a mild aortic stenosis, there'll always be a mild aortic stenosis.
Now they might go on to develop degenerative valvular disease and have that to deal with on top, but their aortic stenosis shouldn't change in its affectation. It's either gonna be mild, forever, moderate forever, or severe forever. We also see on echo a post valvular dilation.
Now this is where the the force of blood coming through this narrowing here. It's, it's like, it's like getting that flow through a straw. You know, if you suddenly breathe through a straw, it's really, really hard, isn't it, to take a big lung fall in and out.
So imagine that's the blood flowing through that left ventricular outflow tract. So what happens is, is it speeds up as it goes through this stenosis because it's going through a narrower channel. And we end up with that blood flow jetting really quickly out into the aorta and it hits the wall of the aorta and actually creates a post stenotic dilation of the aorta there before the blood flow then carries on round that loop of aorta and out to the rest of the body.
We get an increased workload for the left side. So, as I said, it's like blowing through a straw. So you end up having to, the left ventricle has to really hypercontractile to get that force of blood.
It's trying to maintain its cardiac output and its blood pressure. It's trying to get all that blood out through this little narrow stenosis, depending on how severe the affectation is. And that increases the workload for the left side, so we end up with a hypertrophy, a thickening of the left ventricular wall muscle.
This can then give rise to ventricular arrhythmias. So when the . Muscle walls increase in size, with cardiac muscle, the blood supply to supply that muscle, the The blood vessels there, they don't also increase in size.
So when you work out any other muscle in your body and you increase that muscle size, the vasculature increases as well to supply that muscle with blood flow. Unfortunately, with the cardiac muscle that doesn't happen. The the vasculature is there and it's fixed.
So as the ventricular muscle increases in size, the, the blood vessels don't. Therefore we get a hyper perfusion and an ischemia and a and a hypoxic heart muscle and that then gives rise to those ventricular arrhythmias. So you'll see ventricular beats on an ECG strip, you'll hear an irregularity on your auscultation as these ventricular beats start to become apparent more and more.
And then if we have a severe affectation of aortic stenosis and something that's impactful . Going down the lines, then we end up then with a left congestive heart failure. And those associated signs with.
So here's my echo loops for you of aortic stenosis. So just go through the plane structure spur. This is the left ventricle here and this is the aorta as it leaves the body there.
And in this one you can see this ridge here, and this is the stenosis. This is the fixed outflow tract obstruction, which is subvalvular, there's the valve there, doing a little heart shaped bit there and this is our stenosis . Action here, let me put my laser on so I actually ever see this, this is the stenosis there, this structure here.
And the valve, there the aortic valve here. So we've got the left ventricle and the aorta as it leaves the body through here, as it leaves the heart, sorry, it doesn't leave the body, that would be fun. As the aorta leaves the heart there, here's the valve and there's the stenosis.
So I'll play the video for you. And you'll see it all moving there and then you'll appreciate the fixed obstruction here in the way of that outflow tract. Excuse me.
And then if I put the colour flow on for you, you can see. There's a lot of green and yellow turbulent blood flow as that blood flow is leaving and going through the aorta, signifying the speed of that blood flow coming through the stenosis, and it's all incredibly turbulent and that gives rise to your heart murmur sound. So treatment aims for aortic stenosis, we actually want to reduce our heart rate.
Now by inducing our heart rate, we then help that lamina blood flow through the stenosis and making sure that as much blood is actually getting out of the heart and leaving the heart and maintaining that cardiac output and that blood pressure, which is also one of our treatment aims. Improving exercise tolerance is also one, so if your patient is a moderate severe affectation of aortic stenosis, they very often will present with syncopal episodes because they're struggling to maintain that output when they exercise. So if we can balance that and get that blood pressure up and reduce the heart rate a little bit, so we've got some more laminar blood flow through there, we'll improve their exercise intolerance as well and manage any arrhythmias that may be showing from that chunky heart muscle.
For nursing considerations, again, ageing comorbidities is also always gonna play a part there, as is the temperament for medication if we're going to reduce the heart rate. This very often involves beta blockade medication, so our patients, we need to be able to take that and knowing the severity of the stenosis. So it's going for that further workup, it's making sure that we have graded them either mild, moderate or severe, and, being able to have that information going forward.
It's really important. OK, so then let's move on then to pulmonic stenosis. So this is stenosis instead of on the left side of the heart, we're on the right side of the heart.
And our stenosis is shown here. And again, it's very, very similar to the left side, but we're again, we're dealing with the right side. So we end up here with pulmonic stenosis.
It's most commonly a valvular stenosis. So it's the actual pulmonic valve itself that has been malformed and is creating a stenosis. So instead of having its valve leaflets, Opening and closing lovely.
Very often these valve leaflets are fused, and they're malformed and they don't open and close properly and blood kind of sneaks through it rather than being sort of directed through it and, and backflow being prevented by the valve. And again, we grade it mild, moderate, severe. It's a fixed obstruction again, and we'll end up with a basal a right-sided murmur.
So again it's listening with your stethoscope right up in the right axilla to try and catch those murmur sounds there. We then have the volume overload to the right ventricular outflow tracked and then through down in backwards through the heart to the right ventricle. And again, it's that increasing of work flow.
Through to the right ventricle, so we're getting a hypertrophy of the right ventricular muscle. And then again, ultimately right congestive heart failure, those effusions we associate as well, and then arrhythmias as well as as the left side, hypertrophy of heart muscle very often leads to cardiac arrhythmias. So here is my pulmonic stosis echo.
Now this is a different echo picture to the ones I've shown you before. So this one we've got the the heart in cross section. So I'm showing the aorta as a circular structure here.
And we've got the the tricuspid valve is this structure here, and then we've got the right ventricle and right ventricular outflow tract coming along the top of the picture. We've then got our pulmonic valve is this structure here and then flowing through out the pulmonary artery. So if I play the video, you will see the turbulence of the blood flow there as a green colour and it's at the level of the valve.
So here is the problem here and it's actually within the valve structure of the. Monic valve there. So that's causing the problem and we've got all this green, yellow, turbulent blood flow.
It should be a beautiful blue column of blood. When we put colour flow on the pulmonary artery with every contraction, we should see a nice blue column shooting down that pulmonary artery. And here we can appreciate the massive amount of turbulence there.
So treatment aims for this condition, it's to maintain that right ventricular pre preload, which is linked to our blood pressure, and we want to maintain that stroke volume, because obviously the blood leaving the pulmonary artery goes off to the lungs and then comes back to the left side of the heart. So by maintaining our right sided preload, we actually then assist. The left side and what's going out to the rest of the body.
We want to maintain our contractility and avoid drastic changes in heart rate. We also want to avoid increased pulmonary pressures, and this comes into ties into our comorbidities with our nursing considerations and the age of our patient as well, because with the increased pulmonary pressures, we're talking potentially pre-existing pulmonary disease and respiratory disease processes, that crispy lung thing that older dogs get. We love those Westies and chihuahuas, that come in with cardiac issues, but they've also got crispy lung.
So increased pulmonary pressures are basically going to backtrack through to the right side of the heart and showing pulmonary hypertension and right sided changes as well. So it's increasing that workload on that right side even more if they've got those increased pulmonary pressures. So assessing a patient with pulmonic stenosis for respiratory issues is going to be really important.
And also getting that history of the patient, of the patient, of the client, if only the patients could talk, but, getting the history from the client as to whether there's any, cough. And how long that cough has been there and if they cough exercise or if it's allergy related or anything like that. So respiratory disease and and the consideration for that with a patient with potential pulmonic stenosis is is really important.
The great thing is we can treat pulmonic stenosis, yay, everyone, yay. It's treated with balloon valvulloplasty in the moderate to severe affectated cases. So what we do is, if you pop down your, your look to my picture on this, on the slide there, what we do is we pass a catheter down through.
Heart through the right side of the heart, which is a balloon catheter, and then we inflate the balloon once it's across the valve. And you can see the slight indent here next to my laser pointer in the balloon. That is the level of the pulmonic valve and the stenosis there.
And we inflate that balloon within the heart, normally sort of 23 times to actually Bust open that pulmonic valve and and break those fused pieces. We completely destroy the valve when we do it, but we also get rid of any stenosis so that there is no issue then with outflow of that right ventricular outflow tract into the pulmonary artery. So it completely gets rid of the issue.
And we, we, we usually have a very successful. Rate of, of treatment with balloon valvularplasty, and we're looking for a 50% reduction in the pressure gradient from start but before ballooning to after ballooning. But it's a very successful procedure and so if your clients are keen, then it's really worth referring pulmonic stenosis cases for potential surgery.
So again, thinking about with our nursing considerations, it's our temperament of our patients, not just for medications, but also for intervention. So is this a patient that will cope well with the surgical intervention? Are our clients in the situation that they could go for that surgical intervention?
Or are we thinking that we're going to need to do medical management options for this patient? Now medical management is quite successful in mild cases, maybe mild to moderate cases, but when we get into the moderate severes, then it really is a question of, of really seeing if, if the balloon valvulplasty can be put into place. With the severity of stenosis, we end up with the issues of capability to exercise.
So again, our severe affectated patients often really struggle to exercise and medical management can help, but as I said, the balloon valbuloplasty is, is, is really successful, so very much worth looking into. OK, moving on to hypertrophic obstructive cardiomyopathy. Now this is the primarily felines who suffer from this disease.
It's a cat disease. We do find dogs that, look on echo as if they do have a a a a hocu phenotype, but it's not incredibly common. It's usually our feline patients.
And this is a diastolic dysfunction. So where the other disease processes I've talked about have a systolic dysfunction where contractility is a problem. With hypertrophic cardiomyopathy and hypertrophic obstructive cardiomyopathy, it's a diastolic dysfunction.
So it's relaxation of that left ventricular muscle is the problem. It's not the contractility. They're often very hypercontractile.
It's the relaxation and the filling of the heart that is the problem. We have a left apical murmur with this condition because it's the left side that is primarily affected. And we get that because of the the increase in muscle wall and the we very, we have a a backflow of blood through the left side.
So we have left ventricular hypertrophy with or without a septal bulge, as shown in the er the Houm picture here as opposed to the HCM picture. But you can see even in the HCM picture the septum itself becomes very thickened. So when we have a septal bulge, particularly, we can get systolic anterior motion of the mitral valve leaflet.
Now I'll come onto a slide and explain that a little bit more as we go on. And we can have a dynamic obstruction only, so this is when the murmur that we hear. And the back flow of blood and the systolic anterior motion of the mitral valve leaflet can happen only at higher heart rates.
So this is when we have a cat in the clinic and its heart rate may be 140, and we're listening to it and we can't really hear a murmur. It's really important to try and raise the heart rate of your cat and then listen again with them at a higher heart rate, maybe of 180 or 200 beats per minute. Now this can be achieved quite simply and nicely by lifting the cap from the table up into the air and popping them down again.
And very often that's enough to increase the heart rate. Another way of doing it is to present a cat liquid treats or maybe a little biscuit treats, etc. And get them excited about what they're doing if they do present you with a lower end heart rate.
So we end up with a left atrial dilation. Because of the backflow of blood and the compromised cardiac output. And this also gives rise to ventricular arrhythmias as the heart muscle increases in size as we've spoken about before, and also atrial fibrillation paired with those that left atrial dilation.
We can also be at risk of developing thrombus in the in the left atrium, in the left orricular appendage. We get some slow movement of blood within that left atrium, and we can see spontaneous echo contrast in the left atrium, which is also called smoke, where we can actually see the blood swirling around because it's moving so slowly, and that's when it's at risk of clotting and creating a thrombus. And we end then in left congestive heart failure and effusions.
Now we do have feline patients presenting with pulmonary edoema, but cats really, really love to have pleural effusion and often pericardial effusion as well. So again, TFAST can be really helpful here to ascertain whether or not there's any pleural effusion present. So here let's talk a little bit more about the systolic anterior motion, the sound of the mitral valve.
So. What we get is we get a thickened septum with a septal bulge. And then as the blood comes through the mitral valve, through the left ventricle, and then goes out the left ventricular outflow tract, we get a a quickening of the blood flow through this.
It's a bit like the aortic stenosis, it's a bit like a lower down aortic stenosis. So because we've got really fast blood flow going out past the septal bulge of our thickened septum. The speed of that flow drags with it the anterior leaflet of the mitral valve, and that gets sucked into the blood flow and opens the mitral valve slightly.
Now this then allows backflow of blood through the mitral valve, going back into the left atrium and mitral valve regurgitation back into there. And we actually see it as a posterior jet that really hits the outside wall of the left atrium, can even curl round in a swirl. And it's quite a a specific presentation you can see it on Colflow Doppler very often where it really it's quite unique to the to the condition of systolic anterior motion.
So this then adds to the backflow of blood into left atrium and the dilation of the left atrium, as the mitral valve basically we end up with that being open rather than shut as that that anterior leaflet gets dragged into the outflow. Now you can evidence this on echo by doing an M mode at the level of the mitral valve, and we end up here. What we've got here is the double open and closing of the mitral valve, and then at this point the mitral valve should be closed completely.
But we can see the flicker here upwards of the leaflet that's being opened. So we should have passive filling, active filling, and then this leaflet bit gets dragged into the outflow tract, and that is the sam of the mitral valve. OK, here's my echo for you of a houm case.
And just to go through the structure here, put my laser on. Here's the left atrium and you can see it's quite large and dilated. Here is the left ventricular free wall and again you can appreciate the size of this muscle mass compared to the other pictures of the echo pictures I've shown you.
And then we've also got a lovely septal bulge here, which is showing there. And then this is the mitral valve. So as I play the echo for you, you'll be able to appreciate the turbulent blood flow.
As it goes out of the left ventricular outflow tract here into the aorta, is the left ventricular outflow tract, and we've got all that green and yellow turbulent flow as the blood is whooshing around this septal bulge. And you can also appreciate a bit of mitral regurgitation here coming back into in Sicily when the contraction of the left ventricle happens and we've got that black back flow of blood there. OK, so treatment aims for hokum.
Oh, I just have to talk about the picture here. So a little video I've got playing here. This is the smoke.
This is the spontaneous echo contrast of the blood swirling in the left atrium. This is a very end stage hocu case. Contractility is is reduced to almost nothing in this case, and we can really appreciate this blood swirling around, and this patient did have a thrombus as well and was on antithrombotic treatment.
But anyway, back to the treatment names. We want to reduce heart rate. Now, again, as in aortic stenosis, reducing that heart rate actually helps that lamina blood flow out of the left ventricular outflow tract past that fixed obstruction of the septal bulge if they have it, but also the dynamic obstruction of the sam.
So we will reduce that heart rate down, our SA is reduced and the flow of blood around the septum is not as quick. So our SA is reduced, so the obstruction is reduced, so everything improves. We also want to try and improve that diastolic function, that relaxation of the heart muscle, and again with a slower heart rate that we've got more time for the heart to relax, and to fill with blood and to improve that whole ejection fraction and cardiac output.
We want to avoid that thrombus formation, so again by reducing our sam and our dynamic obstruction, we're going to prevent the backflow of blood through the mitral valve, and that left atrial enlargement and the presence of smoke and thrombus. We can also obviously start our feline patients on antithrombotic medication. And we want to avoid tachycardia and stressful situations as we do anyway for our feline patients.
That's not a new thing, is it? So nursing considerations as well as our ageing comorbidities, it's really understanding the severity of the obstruction or dynamic component that that patient is suffering under. As I said before, sometimes that dynamic component is only apparent at higher heart rates, so obviously reducing stress for that particular patient is going to really improve their situation.
Massive emphasis on temperament for medications and rechecks, and as I said before, if we're timing our rechecks most appropriately for that patient, if they really struggle with the journey, maybe we can think about anxiolytic medication at home before they're travelling to kind of improve that, working with our clients to do things like Carrier acclimatizations, and all this kind of thing. It's all available on the ICA care website as well. They've got some really great ideas there that you can have a look at for working with your feline patient owners, and also chatting with them about respiratory distress treatment and monitoring plans.
So making that. So particularly when you have a feline patient coming into your clinic. Making sure that we understand at what state they're arriving in, or are they even stable enough to travel if you are working in a referral practise accepting these kinds of referrals, making sure that suitability to travel is also discussed either with owners or with referring vets, and having a a treatment and monitoring plan, that can be discussed for that patient as it arrives or before it arrives.
So I'd like to just go through very quickly some more considerations for our feline patients, particularly, feline patients with heart disease. Obviously it's a really challenging nursing, considerations going on here. So imagine you have this feline patient coming in, they've arrived in this kind of situation.
What are the first things you're gonna be thinking about to do? What's gonna be the process of care for this particular feline patient? Or maybe they're not actually open mouth breathing, maybe it's subtle, maybe you've got a feline patient, and this is more like the respiratory pattern they're presenting as they come in.
Again, what's going through your head? How are you going to get this feline patient processed so that you understand what you're dealing with, and you can treat them appropriately. So oxygen therapy is gonna be one of the first things that we're going to try and get for our patients, for our feline patients, and typically that means using an incubator or an oxygen kennel or a carrier that you can insulate for oxygen and fill that full of oxygen and actually get them in there and just let them breathe.
Just let them breathe. They've just travelled. To you in a carrier that they probably aren't used to, that they're gonna be really stressed, they're gonna be really tachycardic, and they're breathless.
So oxygen therapy first time, but give them that acclimatisation time, keep the hands off and observe unless there is something that really must be intervened on immediately. But the best thing you can do is leave them be in oxygen. Now we often think about utilising buterphenol at this kind of stage, particularly if they are incredibly stressed and they are open mouth breathing.
A little bit of butterphenol intramuscularly can really help to chill them out, and help them actually improve their ventilation and actually get that oxygen in there so they can actually calm and breathe more efficiently. If we do have a heart failure diagnosis already and we're expecting this patient, and we know it's got heart disease and it's just advancing and it's now gone into a heart failure state, it's now a stage C, then obviously we can put into play those medications to treat the heart failure. So we're talking about furozamide intravenously, if possible, intramuscularly, if not, and we're doing that, we're gonna repeat that every hour until those respiration rates come down.
We can then go forward and perform TAT or basic echo and confirm if there's any effusions present, and then we can prepare for drainage of those effusions. If we don't have a heart failure diagnosis at the start, then again, it's employing those TFAST ultrasound capabilities to make sure that we, if we can see any heart chamber enlargement, if you're receiving a feline patient in with those respiratory distress signs, then you are kind of erring on the fact that they either have a chamber enlargement and cardiac output compromise, and that's resulted in a pulmonary edoema state, or they've got a pleural effusion. And they've actually got that weight of fluid that's impacting on them.
So again, it's thinking about the patient that's actually arriving, what those pre-existing conditions that have diagnosis are, what stage of heart of heart disease you're, you're dealing with, and then being able to titrate your treatment appropriate to that patient and utilise that acclimatisation time and anlytic medication would be tophenols, to actually make a deep an impact for those that patient. OK, so here's my summary slide. It's a bit busy, apologise for that, but yeah, the staging of the disease really helpful in knowing when to start medications for mitral valve disease with the EPIC study, knowing that moment where they go into that B2 stage, really, really important, but knowing the stage of disease for any patient with a heart disease process is really, really helpful.
Sleeping respiratory rates monitored by the owners using that Caralis app if they like to, and you're gonna be able to know at home when that progression may have occurred and it's that something that owners can monitor that really does make a difference. Because of the location of your murmur, at the point of maximum intensity of where you can hear that murmur, the loudest to guide your differential diagnosis if you've got a basalt, an apical murmur, a left sided murmur, a right sided murmur. The carddimopathy can result in biventricular failure, so we're looking at those left congestive signs and those right congestive signs.
And the left congestive can cause those effusions of pulmonary edoema, but also the pericardial effusion and the pleural effusion, particularly in cats. Right congestive heart failure can cause ascites, but also watch those coexisting respiratory diseases as well. That impacts on the right side of the heart.
Hypertrophic obstructive cardiomyopathy has that obstructive component on top of HCM either by the septal bulge and or SA, the systolic anterior motion, but it can be dynamic obstruction, so only at those higher heart rates. And those feline friendly. Techniques are so, so, so important to minimise stress and you can utilise buorphenol or antics at home before they travel and to help get rid of that stress and improve the ventilation for your feline patients.
And that's the end. Thank you very much for listening. I hope you've found it helpful.