Hello, it's Anthony Chadwick from the webinar Vets. So pleased to see you at one of our evening webinars. We're very fortunate today to have Dave Dixon, who is a RCVS recognised specialist in cardiology, who's going to be talking about every last drop, squeezing the most from your diuretics.
Dave qualified from the Royal Veterinary College and joined Heart Vett's team in 2011. His research into feline dyspnea won prestigious best research communication at ECVIM's conference, and he is an expert in this area of obviously, cardiac disease. I'm really looking forward to some of the new ideas around diuretics as well, so, Dave, it's over to you.
Thank you very much, welcome everyone this evening. . So then to say, we're gonna talk about diuretics.
Quick conflicts of interest, I'm being paid tonight by Vokinol. The opinions in this presentation are mine. No one has, approved them or reviewed them, so it's all my work.
So we're gonna run through some key questions this evening. First and foremost, what is congestive heart failure? Then we're gonna talk about what diuretics do, specifically what's the difference between rosemide and terrasemide.
We run alongside we're talking we run an advice service for people trying to. Navigate the minefield of diuretics and heart failure. And we get asked a few questions all the time.
So we're gonna run through those questions as well. One, can I give too much diuretic? 2, how do I monitor the response to diuretics?
How do I change a patient from one to? So how do I transition a patient from rosemide totterrasemide? And what do you do er when the drugs aren't working?
So let's start right at the beginning. Congestive heart failure is a syndrome, it's a clinical syndrome where the heart is unable to suck fluid in from the venous system. This causes the pressures to rise within the venous circulation.
And flu then leaks out into the surrounding tissues. We sometimes call it backwards failure because a problem within the heart, such as weak heart muscle or a leaking valve causes signs to appear behind the heart. This is in contrast to forward failure, forward failure is where the heart is unable to push blood forward, out, out of the heart.
And this leads to signs of exercise intolerance, weakness and fainting or hypoxia. So to summarise, congestive heart failure is fluid congestion caused by inadequate fluid clearance. As cardiologists, we divide it up into left-sided and right sided disease.
So left sided heart failure is the result of disease on the left heart such as mitral valve regurgitation. Leading to elevated pressures in the pulmonary veins and then fluid buildup in the lungs, which we call pulmonary edoema. Right sided heart failure is unsurprisingly is as a result of disease of the right heart such as tricuspid regurge.
This leads to elevated pressures in the systemic veins and then fluid buildup in the the organ that these veins drain. So the abdominal viscera, causing ascites, the jugular veins leading to jugular distention. And in extreme cases, the skin causing subcoedema.
So the clinical signs of left heart failure relate to fluid congestion in the lungs, that's increased respiratory rate, increased respiratory effort, and sometimes coughing with exercise intolerance intolerance resulting from reduced oxygen transport in the alveoli. Right heart failure typically presents with ascites and jugular distention. Now hopefully that is all stuff you already know and this is just a quick bit of revision.
So let's look at what's going on inside the heart from a plumbing point of view. Now the pressure in the left ventricle insistle is somewhere around 120 millimetres of mercury, i.e., it's a high pressure chamber.
It has to be a high pressure chamber because it pumps blood out into the aorta, which is a high pressure vessel. Now the pressure in the left atrium is much lower, about 10 millimetres of mercury at the most. And the only thing that protects the left atrium from that left ventricular pressure is the mitral valve.
The left atrium is plumbed directly into the pulmonary veins and thence to the venues and alveolar capillaries. So these blood vessels communicate directly with the left atrium, meaning the increases in pressure in the left atrium are gonna be transmitted directly backstream into the alveoli. Now Let's take this dog and give it mitral valve disease.
So the mitral valve leaks and blood goes from the high pressure left ventricle into the low pressure left atrium. This increased blood volume stretches the left atrium. But it can only stretch so much and so pressure increases.
This pressure increase is transmitted straight along the pulmonary veins. Until it reaches the alveoli, which then flood. Now, clearly this doesn't happen straight away.
Pressures tend to rise gradually. And so in heart failure, we start with pulmonary vascular congestion, followed by interstitial congestion. And finally, we see alveolar congestion.
So in all but the acute cases, left heart disease, whether it's DCM or mitral valve disease will cause left atrial and ventricular enlargement as the left heart starts to compensate for the reduction in cardiac output. Now, As these patients develop heart disease, we see a gradual progression, a gradual change from a normal cardiac silhouette to significant cardiogaly. So here we've got 3 dogs with different stages of mitral valve disease.
On the left we've got a dog with a probably has a small mitral regurg leak and a normal sized heart. In the middle, we've got a decent leak, a significant leak across the valve, and the heart's getting quite big. Although the left atrium isn't huge, so I think it's unlikely that patients in heart failure.
But the one on the right, we've got a huge, a huge a huge left atrium and a high risk of going into congestive failure. What about on the right side of the heart, well. A similar thing happens.
The right atrium is, it's plumbed. In, sorry, the right is is. Divided from the right ventricle by the tricuspid valve.
The right ventricle isn't as high pressure as the left ventricle, but it's still a higher pressure chamber, and the only thing protecting the right atrium from the right ventricle is the tricuspid valve in the middle. The right atrium itself is plumbed into the head via the jugular veins and the abdomen here depicted as the liver. So again, we've got no valves separating the right atrium from the veins that drain into it.
Now, if we give this dog a leaking tricuspid valve, the same thing that happens is on the left heart. So right atrial pressure increases, right atrium stretches, we can't stretch too much, so the pressure then gets transmitted up the jugular veins and out to the abdomen. So we get increased jugular, venous pressure which causes jugular distention and jugular pulsation and the pressures increase in the liver which causes ascites.
OK. So, given all that, what do diuretics do and why do they help? Diuretics work on the kidney, specifically the nephron, to prevent the reabsorption of water.
So by preventing reabsorption, they force the body to excrete more water. And this then reduces the central venous pressure by reducing the amount of water circulating in the bloodstream. By reducing venous pressure, you reduce the pressure gradient across cell membranes and you get less fluid leaking out into the tissues.
Now, if you just give a single dose of diuretic, let's say furosemide, what would happen? For instance, let's pretend that one of your colleagues with a slightly awry sense of humour slips a frozen my tablet into your coffee at work without telling you, and just like to say I've never done this ever. The, the body, what happens if you take a dose of frozenmide, the body is made to excrete a bit more fluid than normal.
This dehydrates you, so all you do is drink a little bit more and compensate and within a few hours you're back to normal. So in a patient without elevated venous pressures, all diuretics really serve to do is dehydrate you. If you keep taking them, you stay permanently dehydrated and you keep drinking more to try and compensate.
But if you have elevated venous pressure because one or both sides of the heart aren't working properly and pressures have risen within the system, then what diuretics serve to do is to reduce the volume of blood circulating, reducing the pressure in the system, and that relieves the fluid congestion. Now in clinical practise, there are 4 main groups of diuretics. In order of potency, we have carbonic anhydrase inhibitors.
Loop diuretics, potassium sparing diuretics, and finally the thiazides. You're probably familiar with the last three, because generally we don't use carbonic anhydrase inhibitors except in ophthalmology, where they're used to reduce ocular pressures. The main reason we use diuretics in practise is for the treatment of congestive heart failure.
So that's what we're gonna talk about. Now I'm a huge fan of analogies, so here we go with one of my favourites. We're going to focus on left heart failure, so I don't have to keep specifying which side of the heart I'm talking about.
And I want you to imagine that the lungs are a rowing boat on a lake. Now I've taken away the side of the boat er so that we can see what happens inside. Now the ideal amount of fluid inside a boat is none.
In reality, however, there's always a tiny amount that leaks with the planks, so you get a thin layer of water on the bottom. This is just like the alveoli, a very thin layer of fluid allowing gas exchange. Now with heart failure, pressure outside the alveoli in the pulmonary veins increases and so fluid leaks from them into the institial tissues and then into the alveoli themselves.
This is pulmonary edoema. In our analogy boat The boat develops a leak and fills with water. Now this is bad as it means the the boat may sink and your feet are definitely going to get wet.
So what do you do? Well, ideally we would fix the leak. But in nearly all cases, apart from it it's something like a PDA where we can surgically close the, the problem, we can't actually fix the leak in most heart disease.
We just aren't good enough at mitral valve repair for it to be a viable option for clients. And we we can't surgically treat cardiomyopathy, so we're not able in most cases to fix the problem. All we can do is manage it.
What alternatives do we have? Well, going back to our boat analogy. What we have to do is bail it out, we have to remove the fluid from the boat to keep everything dry.
So now we use a bucket or a diuretic to bail out fluid from the boat. If you could all just take the time to appreciate my beautiful animations here, I, you have no idea how long this all took me. So here's our bucket and we bail out the boat.
Simple. Straightforward, that's, that's basically on a plumbing level what diuretics are doing. They are removing the fluid from the system, allowing the the organ to function normally.
So our bucket has successfully bailed out the boat. We are drier for a bit, but clearly, because we haven't fixed the hole in the boat, it will just fill up again, although it's gonna do it probably fairly slowly. The rate at which it fills up, i.e.
The edoema returns, is dictated by a few factors. And the main ones are the size of the hole, which is the severity of the primary disease, and how much fluid we took out in the first place. Now in practise we can't do much about the severity of the disease because it's out of our control.
Some patients have relatively mild disease, whereas others have it much worse. Compare two dogs with mitral valve disease, one with a severely leaking mitral valve and congestive heart failure. But the other, another dog with, as well as having severe mitral valve disease also has as a as a consequence of that, a huge flail segment.
Now what that means is that a piece of the mitral valve has become detached and we now have a wide open hole between the left atrium and the left ventricle. This means that the left atrial pressures are gonna be sky high. Both of these dogs are in congestive heart failure, but the one on the right is going to be a lot more diuretics to control the heart failure because the pressures in the system are higher.
So how do we control the fluid accumulation? We have to keep bailing out the boat, it's gonna keep filling, each time we bail it out, it's just gonna keep filling, so we've got to keep bailing out the boat. In most patients, that means bailing them out with a a bucket that we call froamide.
And generally we do this twice a day and use a dose of around 2 migs per gig per dose in a dog. But what happens if this isn't enough to control the disease? Well, we have two options with frozamide.
What most people tend to do is to increase the fruits of my dose, so you just get a bigger bucket. Maybe go from 2 migs per kg to 3 or 4 mg per kg per dose. Sometimes this is enough to control signs, however, not always.
If we hang with the analogy for a minute. It's because beyond a certain point, a bigger bucket just doesn't work, it's too heavy to wield. Or in real terms, it's because frozamide has a ceiling effect, meaning that above a certain dose, it just doesn't work anymore.
Typically, we tend to think that the ceiling effect is around 10 to 12 mg per gig in a dog. Although it it does depend on the animal. In cats, I've got no idea what the ceiling dose is, but again, I would rarely go above 10 mg per kg per day.
So if using a bigger bucket doesn't work, what else can we do? Well, we could just bail out more often. So 3 or sometimes 4 times a day would be enough to keep the fluid down.
Remember that frozamide used to be called Lasix because it lasts 6 hours. So we get a duration of effect following a dose of frozamide of about 6 hours. The problem is, for many owners, medicating an animal 3 or 4 times a day just isn't feasible.
I know I wouldn't be able to medicate my dogs 3 or 4 times a day. I'm just not there most of the time, so we have to have a look at other options. Let's go back up to our nephron and look at the diuretic options and see what else we can do.
We can add another diuretic in. We don't use the carbonics, so we're gonna be left with adding in a potassium sparing diuretic or a phaazide. Potassium-spar diuretics, we're mainly talking about spironolactone.
So that's prolactone or Caralis if you use it alongside an ACE inhibitor. Now I bet many of you have tried adding this into a failing patients regime and I suspect that like me, you've found it pretty ineffectual. That's because spironolactone's a very weak diuretic.
In practise we don't use it really, it's diuretic. We use it for its supposed antifibrotic and neurohormonal modulatory properties. The other diuretic we can use is a thiazide and most often.
We use a combination of hydrochlorothiazide and amiloride or moduretic. Now moduretic if used cautiously, can be really good at saving patients with end stage heart failure. But you do have to be very careful.
If you get the dose wrong, you can very quickly cause kidney injury, so it's one to be really quite cautious with. Adding in two or more diuretics like this is called sequential nephron blockade. In theory, what it does is it allows us to diaries the patients more effectively.
In practise, what it means is you have to watch them a lot more closely and to be careful you don't shaft the kidneys. Be very careful changing dose doses of each drug when you've got 2 or 3 different diuretics on board. Do we have any alternatives to ruzamide?
Well, yes we do. For a while now we've been using terrasemide, and I tell owners it's like rosemide's big brother. So terrasemide is a loop diuretic, but it's more potent.
So in our analogy terms, it's a bigger bucket. This means that with each dose you you remove a greater amount of fluid from the system. It's more effective, it just takes out more fluid per dose.
It's more potent, it's probably about 10 to 15 times more potent than frozamide, meaning that you need to give 10 to 15th of the equivalent frozammide dose. However, its main benefit is that it has a much longer duration of action. So different sources quote different things, but typically we're talking the duration of effect from 10 to 12 hours.
Compare that with ruzamides duration of effect of about 6 hours. So if we give ruzamide twice a day, we can probably get away with giving turasemide once daily. And this is the key benefit for me, is its duration of action.
It's licenced for once daily administration in two forms. The one that I've been using for a while now, which is Upcard from Batokinol. There's also a new product available from Siva.
So the question we all want to know is, is terrasemide better than rosemide? I think from a veterinary point of view, the honest answer is right now we don't know. I was having a chat with another cardiologist, Roger Wilkinson from Vet practise Sport, and he flagged up this paper, this meta-analysis from Human medicine it published last year.
And in it, they show that across most measures, terrasemide performs better in people than rosemide, with better outcomes and improved functional status. So compared compared to rosemide, thorasemide reduced the number of hospitalizations due to heart failure. It improved the functional status, that's the class of heart failure.
It reduced all cause and cardiac mortality and produced no more side effects. So in human medicine it's pretty convincing, thorasemide is a better diuretic. What about animals?
Well, There are now two relatively large veterinary trials published looking at terrasemide, terrasemide versus rosemide in dogs with mitral valve disease. Both studies show that terrasemide is non-inferior, i.e.
That terrasemide is as safe as rosamide. This is because they're licencing trials, so the sort of trial that a pharmaceutical company does to get a drug licenced. Before they're allowed to do trials showing that a drug is superior, they first have to show it's not inferior.
So we call these non-inferiority trials. Both studies suggest that terrasemide is better than furosemide. I think we need to be a little bit careful with that because neither study was specifically designed to answer that question.
They were designed to answer the non-inferiority question, and they've suggested that rosemide, er terrasemide may be better. I think we need to be careful with that conclusion, but it still is really encouraging data because it suggests we may, we may have a new standard of care for managing heart failure in dogs with mitral valve disease. And I expect to see a lot more data coming out in the next few years.
For now, my viewpoint is that we have two excellent diuretics for first line treatment of heart failure. Is terrasemide better than furosemide? Honestly, I don't know, but it's certainly no worse and from a compliance point of view, it's definitely, going to be better to give from an owner's perspective.
I'd like to see some prospective studies looking into this. So if you're listening but talking and all, you've got my email, you know where I am. Right, remember what I said at the start about the definition of heart failure?
Well, another another definition to think about is the dose of, of a diuretic. What's the correct dose of diuretic? And I think one way of defining that would be to say that the right dose of diuretic is, it could be defined as the dose needed to maintain a good quality of life free from clinical signs.
Now, the correct dose is the dose required to clear the pulmonary edoema. Clearly radiographs are a nice tool for assessing that, but we can't be radiographing these dogs every few hours to see how they're doing. Fortunately we don't have to.
We can count their respiratory rates. So in clinic, the best way to to do this is to monitor to the best way to monitor sorry treatment success, is to monitor respiratory rate, so. When I've got a patient in heart failure in the clinic, what I do is get people to count the respiratory rate in the kennel every 30 minutes, and we keep a record of that.
We watch these hospitalised heart fail failure patients, and watch them closely over time, and what we want to see what we're looking for is a steady downwards trend. At home, the best way to monitor control of heart failure is with sleeping respiratory rate. If you want a downloadable guide on how to do that, you can give that to owners, and just visit our website, visit the, owners' area, and then the information sheet page, and there's a whole, sleep and respiratory rate guide you can download and give out to owners.
Incidentally, if you have any suggestions for information sheets you'd like to see on there, just send us an email. There are several apps available, I'm sure you use these already that can track sleep and respiratory rates, such as this one from Cardali, which allows you to create a graph of the sleep and respiratory rate counts that owners make at home, make at home, and this can be really useful to track these patients over time. And you give owners guides about when to act, when to do something different, and they can help owners feel that they're in more control of their disease.
Why bother about all this faff about measuring sleep and respiratory rate? Surely we just give them a good big dose of rozamide and send them on their merry way, don't we? Well.
No, is the short answer, we can't do that. It's not safe, and it's not, not something we should be doing. Look at this patient here, so we've successfully cleared the edoema with several doses of intravenous furozamide.
But I, I suspect a lot of you are thinking, what about the azotemia? What are, what are kidney's up to now, we've given it huge doses of furosemide to clear that fluid from his lungs. What happens when you're giving enough diuretics to control signs, but they're AST Mic, what do we do with these patients?
Well, what I do firstly is fixate on the clinical signs the dog has got, which is breathlessness. They're dynic, they're tachypnick, and we need to clear that fluid to, to get them feeling better. So we give them enough diuretic, the correct dose.
I think they need to clear the fluid and control the signs. And then we back off and we ask the owners to reduce the minimal effective dose based on the sleeping respiratory rate. And what we're looking for them is to be stable at under 30 breaths per minute, like this one here.
So this dog came in in heart failure. We aggressively diared it, got the diuretic down, sorry, got the respiratory rate down and then sent that dog home on, on, the same dose of, of diuretic it'd been receiving in the clinic. What we then asked to do, asked Fiona to do is to start to slowly back off on the dose to see how low we can go.
Really, what we're aiming for is the lower the better, although clearly a sleep and respiratory rate of 0 is not ideal. But I think most dogs in heart failure can be stabilised to the low 20s or sometimes mid teens, depending on how they're doing, without life limiting polyurea or polydipsia. Now if you back off to a point where the respiratory rate starts to climb as it is doing in this sleeping respiratory rate graph, we then say to the owners, OK, we've reached the minimum dose, can you just go back up one dose level and we'll stay there for a while.
Now, if you reach this minimal clinical dose and yet they're still a bit aotemic, you probably just have to accept that and keep an eye on it. If they're very aotemic with steadily increasing renal values, then you do probably have some renal injury to contend with. And these patients, to be quite honest, are a nightmare to manage.
In that situation, I'd be thinking of changing my diuretic to see if they tolerate an alternative loop diuretic more easily. And I'd also start the conversation with the owners that we have a failing heart and potentially failing kidneys. And the end might be in sight.
I think it's really important to remember that our job is to maintain their quality of life. And if we can't do that because the diseases are just so bad, then sometimes euthanasia is the best treatment that we've got available. So can you give too much diuretic?
What happens if you give too much diuretic? Well, the answer's obvious you dehydrate them. And if you keep doing that, you can cause renal injury.
So I accept my analogy is starting to get a little bit thin here, but if you keep bailing out an empty boat, there's no fluid there, what's gonna happen is you're gonna scrape the bottom of the boat and start causing damage. The problem is, is figuring out how much damage the diuretics are doing. We all know that kidneys don't give us much warning until things are really, really bad.
And we commonly see mild reversible azotemia in patients on diuretics, that's pre renal aotemia. So how far can you go with these drugs? Now, I don't have actual numbers to guide you.
Each case is different and there is no urea or creatinine value that I have in my head for OK versus not OK. What I do is watch the trend. So many patients I see have a mild azotemia, but provided it's stable and they're well, they're not suffering from the AMS, they're eating, they're keeping the weight on, then I don't mind too much.
So I accept a a small degree of azotemia in patients on high dose of diuretics, like you just have to learn to live with it. The important point is that you need to be able to monitor a trend, you need to have some starting values. So you need to get baseline bloods before you do things, and you need to follow those patients every time you make a big change.
So when you switch them from just being on Pimerenda when they're in stage B2 to adding a diuretic, you need some bloods before you have a diuretic. And you need the, if you're gonna switch them from prosemide to thorasemide, you need to run bloods before you switch them over because there's no good running bloods once you've changed them and then thinking, oh Christ, these kidneys look awful. They might have looked awful before, you don't know that it's the drugs that have done that.
So it's really important to monitor these patients as we go and not just to react when things start going wrong. What else can I monitor apart from sleep and respiratory rate? Well, the two of the signs we look out for are coughing and exercise tolerance.
Now, coughing is a minefield. Lots of dogs with mitral valve disease cough, but just because they cough does not mean that they're in congestive heart failure. In fact, I, in fact, I'd go so far as to say that I think most dogs with murmurs who cough do so due to lung disease, airway disease, not congestive heart failure.
You definitely shouldn't use cough as a sign to confirm heart failure, but nor can you use cough to exclude heart failure. Basically, the owners bring them in because they notice the cough. The cough is the reason that they, they present the animals, so the cough is the owner's concern.
What you need to do is put the cough to one side and figure out what's wrong. And effectively from a diagnostic viewpoint, ignore the cough. So don't trust cough, and certainly what you mustn't do is adjust the diuretic dose on the basis of cough alone.
If you've got a patient who's coughing and breathless. And you change or increase the diuretic and the cough improves, but that's good only if the sleeping respiratory rate also improves. If you have a patient who's breathless and that sleeping respiratory improves, but the cough doesn't get any better, then you need to investigate the cough as a separate issue.
Don't keep upping the diuretic just because the dog is coughing. If the respiratory rate is controlled, you're controlling the edoema and the cough is a different, problem, a different entity that needs different treatment. Conversely, if you find the cough improves the diuretic but the sleeping respiratory rate doesn't, you need to give them more diuretic and check your original diagnosis because something else might be going on.
What about exercise tolerance? Well, I said at the start that exercise tolerance is a sign of forward failure that is reduced cardiac output. But it's also a sign of backwards or congestive heart failure because wet lungs can't gas exchange as effectively.
If you've got wet lungs, you can't run around properly. Now I think exercise tolerance, intolerance is probably the first sign of heart failure. The problem is that most patients aren't like this retriever with a tennis ball.
They're more like these dogs. They're unable to exercise properly or their owners are unable to exercise properly. So we miss the more subtle signs of exercise intolerance in early heart failure.
How do I change my patient over from one drug to another? Now this is something we get asked a lot. I've got a dog on ruzamide, but it stopped working.
How do we change it onto terrasemide? We get asked this probably at least once a week. It's, it's not something we can answer simply straightforward Lee.
We need a bit more detail, we need a bit more context to, to know how to advise in this situation, because really there are a few parts to our answer. Firstly and most importantly, are they in congestive heart failure? You need to make sure the diagnosis is correct.
We're often asked to suggest those changes for diuretics in patients who turn out not to have heart failure. Why? Well, I think it's because people struggle with radiographic interpretation.
Now believe me, I know it can be hard, but you need to give yourself a fighting chance and take decent radiographs. This patient was referred to me, diagnosed in congestive heart failure, but the ruszeide at 10 mg per gig per day wasn't working. Why?
Well, because the dog isn't in heart failure, the dog has bad lung disease. I, it's easy to see why on the left radiograph why why the diagnosis of heart failure was made, but actually what you should do when you look at that radiograph is say that's not diagnostic, I need to think of another test. And that test might be an anaesthetized inflated radiograph.
It might be an echo to have a look at the heart structure and see what's going on. But one of the most common reasons that your diuretics aren't working is because the patient's not in heart failure. I think misinterpretation of radiographs is really common.
We, we're all guilty of seeing what we want to see and not what's actually there. I think if you struggle with radiographs, just be honest with yourself and either send them to someone else for help or take yourself on a CPD course. There's plenty online courses now, helping you to brush up your skills.
One of the things that I, am a big fan of are these little BSAVA guides, and there's a great one on radiographic positioning, just helping to tell you, how to get good chest radiographs. So I would suggest you go and buy this. It's not very much from BSAVA Publishing and have it somewhere in your radiology room, so you've got access to it.
So are they in congestive heart failure? Well, we need to ask why you want to change diuretic. What are you trying to achieve, i.e., what sign are you trying to control?
We get problems because people are chasing the wrong sign. I often get asked, should we increase the dose of diuretic because the dog is coughing? Well, usually I'd say the cough is not cardiac and actually the problem is in the lungs.
Look at this dog. It was sent to me again in congestive heart failure, but actually the dog has mild mitral valve disease and severe airway collapse. The dog is coughing and the diuretics aren't working because the cough is not cardiac.
It has some heart disease, but it doesn't have congestive failure, so a diuretic was the wrong drug. We take some inflated radiographs, we see the heart is clearly a normal size, there's no left atrial enlargement and no evidence of congestive failure on that. And we put a camera down and we can see why the dog is coughing.
On bronchoscopy, this dog has got severe airway collapse with all sorts of horrible stuff going on down there. Yes, this dog is exercise intolerant, yes, it's breathless, but we can see that FHM's not enlarged, so it can't be congestive heart failure. It, it's got to be lung disease or airway disease of some kind causing the problem.
So for a dog who is in congestive heart failure, I'd expect them to be dysnic and titnick and have an elevated sleep and respiratory rate if the owner is counting it and capable of counting. If not, if I haven't got that information, then I need radiographic evidence that they're in congestive heart failure before we commit ourselves to a diuretic. OK, so you're happy that we've got a patient who's in congestive heart failure.
They're showing us signs of congestive heart failure, they're breathless, they're tachy nick. But you, and they're on a diuretic, but you're convinced that the diuretic isn't working. Now here we've got a panel of 4 dogs in congestive heart failure.
The first thing that should strike you is that they've all got huge hearts. It's really important to never diagnose a patient as having congestive heart congestive heart failure on a radiograph without first seeing a big heart. If you're thinking to yourself, mild cardiomegaly, think very, very hard before calling it as congestive heart failure.
These dogs all have tall hearts, they all have big left atria, and they all have varying degrees of interstitial and alveolar congestion. So all of these are comfortably in congestive heart failure. So the drugs aren't working.
Why is that? Well, next question is how much diuretic are they on. If these are on one meg per cake frozen twice a day, it's no surprise that congestive heart failure is not controlled, because that just isn't enough for most dogs.
So in this, if that were the case in any one of these, the first thing I'd do is just double the frozen my dose. And I might give a dose in the middle of the day as well if the owners can cope with it, just to try and clear up that fluid. Now if you've already got this dog on 4 migs per gig 3 times a day, then yes, you're giving a frozamide and no it isn't working.
So what do we do now? Well, you've got 3 options. The first is to increase the dose of rosemide, or if they're on terrasemide, increase the dose of terrasemide.
With rosemide, I'd start by increasing by 1 MB per kg per dose. So, let's say we've got a 10 kg dog on 20 milligrammes of Fruzamide twice a day, I'd push that up to 30 milligrammes twice a day. I'd expect to see some improvement fairly quickly, like within 1224 hours, and the dog would be much better than 2 to 3 days.
If they're no better, I'd increase again to the 40 milligrammes BID. I haven't found a ceiling dose for terrasemide, but I'd probably do the same, so increase by about 50% of the dose and watch for a response. If you feel you've maxed out on the dose, give it more frequently.
So for fruzemide that goes that means going from BID to TID or even 4 times a day if you've got a really dedicated owner. For terrasemide, that means going to twice daily. I've never gone more often than twice daily with terrasemide yet.
Now if you're on something like 12 milligrammes per kilogramme per day of rosemide, then yes, I think you do have to change to terrasemide. This is the way things get a little bit tricky. Because swapping from Fruzammite to terrasemite, there's no one stop shop.
It depends very much on the case, the individual particulars of what's going on in that animal to decide how to change it over. The rule of thumb that I use is to go somewhere between 1/10 and 1/15 of the current frozen my dose. But the higher the current fruzamide dose, the lower equivalent terrasemide dose I use.
I'll, I'll give you some examples to explain how I do it. So here we've got a 10 kg cay with congestive heart failure. Let's say he's on rozamide at 3 mg per gig, twice a day.
Now that's 6 milligrammes per kilogramme per day. If we're gonna put him onto terrasemide. I'd go for somewhere between 10th and 1/130th of the daily fruits of my dose.
So in this dog, that's gonna be 0.46 to 0.6 mg per kg per day, or about 4.5 to 6 milligrammes once a day.
In this case, I'd probably only give it once a day because the frus of my dose is relatively low and I'm quite comfortable that we can get away with this dog once daily dosing. For a dog who's on 3 milligrammes per kilogramme 3 times a day, we're already at a 9 mg per gig per day dose, which is quite a big dose. So I'd go for a slightly lower equivalent dose of terrasemide, 12 to a 14th.
So about 0.65 to 0.75 mg per gig per day, which works out to about 3 to 3.5 milligrammes BID.
For me, once a dog is receiving frozenide TID I'm gonna keep them onto terrasemide BID. I'm not gonna use it once a day in that case, I'd be too worried about it decompensating. And finally we've got a dog who's maxed out on ruzemide 12 mg per gig per day, so I'm gonna be dosing the terrasemide somewhere between 1/13th and 1/15 of the dose of rosemide, which is somewhere between 4 and 4.5 milligrammes of Upcard twice a day for that dog.
Why does my dose change? Well. Experience of using the drug.
And listening to people talking about the way that the drug works, I think terrasemide, well we know it's more potent, but I think it has a higher ceiling effect, meaning that higher doses do give a more profound diuretic effect. So if you've got a dog on 12 milligrammes per kilogramme per day of rosemide, that dose actually probably isn't having much more of an effect than a 9 or 10 milligrammes per kilogramme per day dose of roamide would. I.e., the rosemide doesn't give you more diuresis despite that higher dose.
However, I'd be pretty worried about changing a 10 kg dog onto 12 milligrammes of frozen wine a day, so I'd go in a little bit lower and see how they respond. Then once we've made the change, we titrate them into effect. I'm gonna warn the owner the dog could become breathless.
So watch them like a hawk and be ready to put the dose up. If the dog's signs start to ease and everything's looking good, I'd start slowly reducing the thora ofide dose until we could reach the minimal effective dose. Usually that's by waiting for a spiritual rate to start creeping back up again, or to if if they're showing signs of exercise intolerance.
But then we, once we've found it, we keep them at their minimal dose. So to switch over, I give them a good dose of terrasemide and then I back off slowly to see what we can get away with. Often you can get them down quite a bit on your starting terrasemide dose, but I think it's better to go in a bit heavier, dry them out, keep them dry than risk them going back into overt fulminent failure.
But it is very different for every dog and it's hard to give a recipe, so instead, go with your best guess, your best educated guess, and then just be ready to adjust based on how the dog's doing. Once you've reached the steady state, get some bloods and check on how you're doing compared to your, your pre-changeover bloods. If you've got high kidney values, do see if you can lower the dose of thorasemide.
You may be able to get away with a bit less. But if you can't, you just have to accept you're gonna see some azotemia as a side effect of this, this level of diuresis. I've been using Tresemide for quite a while now and I find I get far fewer problems with azotemia than I was worried I was gonna get in the early days, so I don't, I think it happens, but it's not something that I er worry about overly much.
I'm much more concerned with keeping the lungs dry. OK. What about a CITES?
Where are we with the right heart? Well, with the CITES you need to think a little bit beyond just diuretics. Remember, a patient with ascites has right heart failure, backwards failure from something going on within the right side of the heart, causing fluid congestion in the abdomen.
If you've got a dog presenting with a SITES, the first thing you need to do is check the jugulars. If the jugulars are distended or obviously pulsating, then it's almost certain the patient has got elevated by atrial pressures. And in practise, the three most common reasons for this are a pericardial effusion, pulmonary hypertension, and in a young dog, congenital disease such as tricuspid dysplasia or pulmonic stenosis.
We do sometimes see DCN causing ascites, but usually these patients also have profound left sided signs such as dyspnea, cough, exercise intolerance, arrhythmias. So if you're seeing isolated ascites, isolated right heart failure, you need to be thinking about these diseases on the right here first, because they're the, they're the big ones, they're the ones that you mustn't miss. Specifically in pericardial fusion, why does pericardial fusion cause right heart failure?
Well, if you think in pericardial fusion, what we've, what we've done is we've got the heart inside a bag, the pericardium. The pericardium is full of fluid and the fluid within the pericardium is at a higher pressure than the fluid within the right atrium, the blood in the right atrium. So what happens is, pressure from the pericardial space pushes down on the right atrium, collapsing that right atrium.
The pressure can't go anywhere within the atrium, so it's transmitted back up the jugular vein and the jugular veins fill. And it's transmitted backwards into the abdomen through the liver, so we get ascites. So same mechanism as for er disease with inside the right heart.
This time it's external pressure on the heart. And the problem is that you can't give these patients diuretic. If you try and reduce the venous pressure, all you do is dehydrate them.
So giving a dog with a pericardial effusion and tampona causing right-sided heart failure, diuretics are the the last thing you want to be doing. You're gonna dehydrate them. You actually need to do the opposite.
You need to drain them and you need to put them on a drip to restore their circulating fluid volume. So the patient who presents to you with ascites but no obvious left heart changes, don't just whack them on a diuretic and forget about them. You need to get to the bottom of the problem.
Equally, if you put them on ruzamide and you get no response, don't just instantly reach for terrasemide or modurate because you're gonna cause more problems. The first thing that these patients need is an echo because it usually gives you the diagnosis. If it's a pericardial fusion, as I said.
You need to stick a catheter in, drain that pericardial effusion, and probably get them onto some fluids to restore their circulating volume. If it's got pulmonary hypertension, then it needs more case workup to work out why. And then specific treatments such as if it's got lung worm, you need to give them a decent worming, programme.
You may want to treat them with something like sildenafil, but it's unusual, uncommon for me to use a diuretic in a patient with pulmonary hypertension unless we've got a profound right-sided heart failure. Normally what we want to do is fix the problem in the heart and let the circulation sort itself out. Congenital cases like pulmonic stenosis need referring to a cardiologist like us at heart vets because you've gotta make the diagnosis and then advise on specific treatments such as ballooning or a catheter-based procedure.
So the bottom line is that you need to be careful with diuretics in cases of right heart failure because they nearly always need more case work up and just sticking them on a diuretic is often not a good idea. Here's a little example. This is Max.
Max is an eight year old shih-tzu with a history of a murder. He's a huge fan of biting my fingers. But I'm a big fan of my fingers staying on my hands, so we make him wear this lovely mask.
We diagnosed him with stage B2 mitral valve disease about 2 years ago. 6 months ago he went from stage B2 to stage C. He went into congestive heart failure.
So we started him on UCA. He was already on vet meine for his stage B2 mitral valve disease. He's been doing well until recently, he's only noticed that he's got a swollen belly.
His referring vet decided quite wisely that her fingers were valuable as well, so she referred him straight back to me to have a look at. Now, on examination which was understandably limited, he did have abdominal distention, and he's got a fluid wave on percussion. We had a look at his jugulars and his jugulars are distended, which starts to increase my index of suspicion.
He has a thrilling murmur, but he has done for over 2 years, so that tells us nothing useful. What is interesting, however, is that his heart rate was over 200 beats a minute with a chaotic rhythm. We did a quick echo but it's hard to make out much at this heart rate.
Clearly his heart is unhappy. I didn't see any evidence of primary pul pulmonary hypertension, although I, I, I wouldn't say I'd be confident of that at this heart rate, but I didn't see obvious pulmonary hypertension, something else is causing this dog to go into right heart failure. So we did an ECG.
Here we've got a narrow complex tachycardia with a chaotic rhythm and absence of P waves. There's a little zoom in on the baseline. This is the hallmark finding of atrial fibrillation.
So I think that poor little Max has developed tachycardia induced heart failure, i.e., his heart rate is simply too fast to allow proper function.
And in most cases of tachycardia induced heart failure, it's the right heart that goes first, hence why he's now presented with ascites. So what do we do? We slow his heart down, we give him some digoxindtize him.
These nicely slow his heart rate, and we check his heart rates at home by fitting a halter. And what we see is that even when he's in the clinic, his heart rate's still 160, 170 beats a minute, but once he goes home, he calms down and his heart rate, his resting heart rate at home is in between 90 to 100 beats a minute, which is much better con considering the disease that he's got, and allows us to control his heart disease. So.
This patient was in right heart failure, but we didn't er control it with diuretics, we controlled it with heart rate control, allowing us to er to keep him out of right heart failure. OK. So the key points of all of this.
First and most obvious, diuretics are used to treat heart failure. I know that's an obvious point, but you've got to make sure that they are in heart failure in the first place. The most common reason that diuretics don't work is because you're using them inappropriately, use them in the wrong patient population.
It's important I think to run bloods for renal values and electrolytes before you start diuretics and before and after you make a big change to to how you're treating them. Make sure you use the minimal effective dose based on the the clinical signs, which is nearly always gonna be the sleeping respiratory rate. Use the lowest dose needed to relieve congestion, regardless of azotemia.
So you may have to accept a small amount of azotemia in in in exchange for keeping the lungs dry and the patient breathing adequately. It's really important that you never use cough on its own to rule in or rule out heart failure. Cough is a tricky customer, and it's best to put it to one side and focus on the respiratory rate and effort.
And be careful with the CITES, don't just chuck diuretics at them. They need a bit more investigation and they needed a little bit more careful handling. And finally, I think terrasemide as a first line diuretic is safe and it appears to be at least as good as rosemide, plus it's easier to give, so we now have once daily treatment for congestive heart failure patients.
Well, that's it. Don't forget you can visit our website where you can find out more about us and the services that we offer, including Halter Rental, and we've got a new digital ECG rental service. Russell's gonna have a little mention now from theok and all, but I'm gonna hang around and if anyone's got any specific questions they want to ask me, I'll be here for a bit, so please do fire away.
Thank you so much, Dave, that was fantastic. I, I'd love your . Your model of the boat with the water coming in and out, what a great analogy, and I, I'm, I'm glad you were prepared to spend so many hours preparing it was well worthwhile.
Good. Looking forward to Russell now coming on. Thank you so much, obviously, Dave, for, for the webinar and thanks for sticking around for questions.
Obviously, thank you also for Beuinal to make this possible as a, as a piece of free CPD. Obviously times are difficult and hard and it's been interesting, you know, looking at the various, for as well, that people are struggling to do their CPD. Because they are overwhelmed after practise, so the fact that you've come tonight and spent an hour with us, I think just shows the commitment that you've got.
So, you know, congratulations also for showing up, but Russell, over to you, do come and share your screen so that we can . I see some of the things that Vettaquinal are doing at the moment. Russell is the senior tech services manager at Betaquinal.
While Russell is getting his screen up, do let us know where you're listening in from. It's always fascinating to see all the different countries. I noticed somebody in Malaysia is listening.
Russell, that's probably very early o'clock in the morning. Do let us know what time that is in Malaysia, but again, huge commitment, so thanks so much, and Russell, over to you. Yeah.
Thanks, Anthony. Thanks, Dave. I'm fortunate enough to, to get to hear Dave speak quite frequently, and every single time I learn something, it's, it's great to be able to work with people such as himself.
And at Vetinal, as Dave mentioned, we do work with heart vets for cases that get a bit tricky. And, we are in regular contact, as, as Dave said, sort of. Weekly calls or weekly cases definitely coming through.
So we've had Up card for a few years now, Dave says a key factor to the addition of Up card to your armoury is once the administration. Great for any compliance. I think one of the things that I maybe didn't appreciate quite As much in practise is this compliance is very important, but also when you're looking at diuretics, every time you give a diuretic, there's a consequence.
So it's not just one tablet once a day, it's one tablet followed a few hours later by urination. So the more frequently you're giving diuretics, more frequently that has to be considered. But we don't just sell the up card.
We do things to try and support you as our customers in the management of cases, putting on CPD alongside companies like Webinar Vett is one of the things we're doing. But we've also got a few tools to try and help you, as Dave mentions. Sleeping respiratory rate is so key to help you and your clients monitor these cases.
And there's an app that you can download from our website, which is called UpLife, just to highlight, there's no spelling error on this page. It is just Uplife.uk.
There is no code in there. But if you go onto Up Life to download the app, you'll also find a number of other things that will hopefully help. There's diagnostic tools, information to help you manage your congestive heart failure cases.
There's a few case challenges, hypothetical situations, what would you do next type of situations, but also a number of webinars and the most recent one that we've put up there is is one given by Dave himself on the golden rules of congestive heart failure, which is One of those 40 minutes that I wish I'd had before I left practise because it would have made a big difference to me managing some of my cases. So pop on, have a look, register on there and see what information is there. But that's us, don't want to take up too much of your time, so Dave's talk was absolutely fabulous, really pleased to be able to hear it again.
And obviously if you want any information on Up card or have any case questions, just give us a call up at the office or send us an email. Thank you so much, Russell. I'm sure both of you will you will stay on as well just to answer any questions.
I think it's really useful as well this is obviously a presentation that we will put up on the site. I certainly would like to go over it again and I'm sure, particularly if you're in practise, it's always useful to be able to just re-refer to it. So give us 24, 48 hours, it should certainly be up by Friday at the very latest, for you to look at.
Often, dawn is so efficient, it might even be up by tomorrow, so do look out for it. I. Dave, the difficulty with webinars, as you know, is you don't hear the tumultuous applause at the end, because there's, there's never any tumultuous applause when I speak live, so I'm used to, I'm used to silence at the end of, you're doing better here because Benedict is listening in from Malaysia and it's 5 o'clock in the morning there, so this is commitment, he said a thrilling presentation.
So, there you go. Thank you. Yelena is listening in from Croatia.
We've got Thea Thea from Norway, Adele from the Lebanon. So I bet your weather is a bit better than ours, Adele, so I hope you're enjoying it. Also quite late, so again, amazing that you're staying up.
Queen Arvon from Louise from the Netherlands, so thank you Louise for listening in, . Now WA state, so I don't know if that's Washington State, Alicia, listening in from America, which is brilliant. And then The is listening in, he says it's almost 5 a.m.
Here in the Philippines. So, a lovely international audience that you've brought together. We have got a few questions, so I'm really pleased you can stay on to, to answer those.
And Alison is saying thanks for a great talk, as always, so there you go. Alison. It is, she's she's waxing lyrical about you here.
Hi Alison, I used to work with Alison, so she's paid to say nice things. Oh good, well, the, the fiver is in the post, Alison, at the end of the talk. When you reduce the diuretics to lowest dose by monitoring SRR, how do you do it?
Do you reduce by 25% and then monitor for a week or reduce daily? And that's. Oh, I, I'd somewhere between probably a week, depending on the owner, but I wouldn't go daily.
I'd probably give them 3 or 4 days to acclimatise and depending on the owner, yeah, step back every 5 to 7 days, something like that. Brilliant, and. Aansha is saying, are there any studies on the ceiling effect of terrazamide?
If not, have you seen it in practise? Now, I went to a presentation about the pharmacokinetics of terrasemide and and I guess like most people, I struggle, struggle with pharmacokinetics. I think there are data that exist saying there is a ceiling effect, but I think the ceiling of terrasemide is way above what we would consider using, in clinical practise.
So I've never seen it, and I've had some animals on eye-watering doses of terrasemide to control their heart failure. So I, I haven't found it yet. I think it's always, it's a difficult one to know, and I guess we'll get, we'll get more of that through experience and practise.
So potential, but it's a potential problem rather than an actual one in your experience, exactly, yeah. Now Benedict, listening in again from Malaysia, so well done, 5 o'clock in the morning, but he says, please, how do we differentiate between ascites caused by heart failure and that caused by liver failure? Well, I'd start by looking at that, looking at the jugulars, because if you've got elevated atrial pressure, then you'll should see big jugulars and, as well as ascites, so that's the first thing I would do.
I, I, I had a slide in my talk which I got rid of, a little neat little test, but there's another thing you can do called a hepatojugular reflux test. And basically what that is, is, is you get someone to look at the jugular, or you look at the jugular while someone squeezes the abdomen, cranial abdomen, fairly firmly. So you stand sort of legs over the.
Top of the dog and you push each side of the abdomen firmly and slowly but push in. And what that does is it elevates the pressure in the abdomen. And because you've got a, a, a column of blood direct directly communicating between the abdomen and the jugular through the right atrium.
In a normal dog, you squeeze the liver, you push blood back in, and what happens is the right atrium stretches. To accommodate that and nothing happens. But in a dog with elevated atrial pressures, the the atrium can't stretch.
So what happens is the blood is then pushed up the jugular. So it's a pretty cool old school test from human medicine. It's called hepatojugular reflux test, and if you Google it, you'll, you'll see some information about it, and that's one of the tests that I would do.
So I do that and say, and if I've got big jugulars, pulsating jugulars or positive hepatojugular reflux, I'd have a high index of suspicion for. Heart failure, whereas I wouldn't for liver failure. Then obviously the obvious things to do are run some bloods and scan the heart directly, but don't forget the old school, tools, the clinical examination will usually get you most of the way there.
Well, there you go. I always say with webinars, if you can, you know, and, and webinar that was set up for people like myself as a GP, if you can learn one thing from a webinar that you can take away into practise, then it's been worth going for that hour of, CPD. So that's certainly one for, for people to try out in practise in the next few weeks and let us know how you get on with it.
I've not heard about that before, so thanks so much for that, Dave. We've got, thank you for the nice and useful presentation from Mikey. Elizabeth, thank you for the great presentation from Slovakia.
We've also got, Joe listening in from Lisbon, Anna from Texas. I've got to say this name, Sna Fri Fride from Iceland. Suyo from Romania, Croatia.
Bit saying thank you very much for the very practical webinar. Demetrios, listening in from Greece, it's 11 o'clock in the night there. Not so sunny, Dev and Emma.
Never mind. Thank you very much for listening from Poland. Let's see if there's any more questions.
There's a few more over here actually, so let me ask about that. Is there any evidence for the use of terrazamide in cats? Oh, good question.
Not really. There's, I think there's one retrospective paper that just reported using it inA saying yes you can use it. That's the only one I'm aware of.
This is something I am very keen to do and I've spent a few years now twisting people's arms to let me do this study. I need we need some funding to do it properly. I've spent a long time in the bar with with Russell, trying to convince him to give me, give me money to er to study this because I think.
I, I used, I'm, I'm allowed to say it cos you've asked me. It's off licence use, but I, I use terrasemide in cats probably more than I use furizamide now, simply because it's once a day. And for an owner with with a cat, it's a massive advantage.
Yeah. So I think there's a huge, well, if you're a drugs company, there's a huge market for terrasemide in cats, as clinicians, there's a massive indication there to use it in cats. So I do use it.
I use about 0.75 milligrammes per cat. So that's roughly equivalent to maybe 7.5 milligrammes of rozammide.
So that's, that's about the right dose really for a cat. And I find most cats can be controlled on, on that once a day. Some need higher, some need lower, but that's, I do use it, and I, I know lots of other colleagues of mine use terrasemide in cats as well, so I'm a huge fan of it in cats.
Brilliant. I'm not gonna bring Russell in because he's always difficult on webinars to ask people to talk off licence because you know, you can't do it. So we know we have the cascade system in the UK, obviously there'll be different systems all across the world, so it's, it's one for you to use clinical judgement on, .
Claire has said what a fantastic CPD thank you so much, so informative and so well explained. Do you take bloods for troponin to assist in making diagnosis of CHF versus lung disease? Occasionally, so, maybe I use troponin in practise looking for evidence of occult arrhythmias or evidence of things like myocarditis, endocarditis.
So troponin is a marker of heart muscle damage. So if I've got a disease that I think is causing heart muscle damage, I might run a troponin. If once I know the animal has heart disease, troponin usually doesn't help differentiate congestive heart failure from non-congestive.
So I tend not to, with the odd exception of a case where maybe they've got. A combination of respiratory disease and heart disease. And I'm really struggling to make my mind up about the difference between the two, which, which is causing the clinical signs.
I might then run both troponin and pro BMP to see and if I've got elevations in both, then I might be more tempted towards heart failure, but it's not something I routinely do. Probably is it one of those tests that we're more likely to use in general practise because we're thinking, we just want to get into the right area. Whereas a, whereas a cardiologist will kind of know where they're at, they need to.
I, I just, you know, I'm lucky I just go straight to the echo, and the echo usually tells me the things I need to know, so. You know, pro BNP and troponin are mainly used, certainly from my perspective as screening tools, you know, does this animal have heart disease? Let's do the screening tools.
There may be a role in monitoring patients in heart disease with the biomarkers, but we still haven't got there yet, so I don't run them very often, and, but troponin is mainly for me. You know if I've got a, let's say I've got a, a Doberman and the owners are worried about arrhythmia, we haven't documented anything. Someone's heard something, but we haven't found anything.
Before we do a halter, I might run a troponin to see because if it's high, I've got more indication that it's gonna be cardiac. It's not proof, but it's just, it, it's it's another. Another piece in the jig in the jigsaw.
Now, this is where we are all giving away age cos unfortunately Arthur has said to me, to think we only had miloin in my early days. And digoxin as well, Arthur, come on digoxin came from the plants, so don't, you, you're not, don't be forgetting that one, but I do remember Millaughlin, any sort of use, is that a drug that you still use or has that been thrown out now? Pretty much thrown out I'm afraid.
Yeah, yeah, yeah, I thought so, but I'm a dermatologist, so I thought I'd better check. I I can only do the skin stuff. When my boss, Mark Patson, he qualified, they used to use the HTS pill, which is the heart tonic stimulant pill.
He's really old. The little red pills. Yeah, they've long gone.
Carlotta is saying, hi, she's in Denmark, but she's Italian. I have a Jack Russell, 16 years old, on rozamide and Pimmendin for moderate, mitral valve disease. She started to cough at night, excluded CHF.
She developed dry cough, which disappeared only with Medrol. I presume that's Medrol steroids is, Medrol contraindicated with furosemide. Thank you, great presentation.
I'm just doing a quick Google for Medrol. So, I wonder if it's . Yeah, I guess so.
So, well. The problem is, I think you probably, your dog's probably got some airway collapse, airway disease, airway collapse. Yeah.
What steroids will do in the short term is, is help with the cough, but in the long term, especially if you're using high doses, they're likely to start making things worse, so they're gonna start causing Pickwick syndrome and you're gonna get a lot more airway collapse simply because of that. So I think if you can use low doses intermittently, it's probably acceptable, especially at that age. You've got to keep the dog comfortable and you know.
Leading a good quality of life without too much intervention, but what you don't want to fall down the trap of is keeping giving higher and higher doses of steroids. So I'd reach for cough suppression, if you've got radiographs, you've excluded congestive heart failure, if you've exclude the other bad stuff going on, then I'd be using cough suppression in that dog, codeine, or if you can get it lofenoxo to try and alleviate the cough. Is is Tobutrol, it's not around, is it?
It's stop being available. Is that a drug that you might use? Yeah, yeah, we used to use it when we could get it.
I find codeine linked was always a bit more effective and to be quite honest, cheaper, so it made it a lot easier for owners. For a while we had, lofenoxo, which is, diphenoxylate, which is a, it's an anti-spasmodic drug, I think they use it for diarrhoea in people, but it also has antiussive properties. That's a fantastic antiussive drug.
The problem is getting hold of it. So if you can get hold of that, buy, buy boxes and boxes of it because it's great for those collapsing airways and Yorkies and Chihuahuas, those horrible coughs that you can't fix with anything else. Fantastic.
Russell, do you want to come in? I, I, I made, I made sure that I swerved you from the difficult question that you might, I might have pulled you in on, but any, any comments you want to make? Generally about the questions or any other comments you want to make at this point.
No, I think, I mean, certainly some of the questions are way above my head, so very glad Dave is, is here to, to sort them out, but, no, nothing really to add at the moment. That's great. Well, listen, thank you so much, Russell, for making this possible, you know, well over 300 people on and, and many more will see it as recordings as well over the next weeks and months.
So, so thank you so much for making it possible for the, for the sponsorship of the webinar. But Dave, you know, you, you were very hard, we're very, . What's the word, polite, aren't we in Britain, we don't sing our own praises enough, like, like the Americans might do, but I think it's been a splendid webinar.
Lots of really com you know, good comments coming through as well. I've really enjoyed it. It's certainly available to watch again in the next couple of days and and do tell your friends about it if you've found it useful, but I really appreciate it, Dave, and hopefully it won't be too long before we see you on another one.
Absolutely. Thank you, thanks Russell, thanks Dave, thanks everyone for listening in and we will see you all soon. Take care, bye bye.
Thanks, Anthony, thanks Dave. Cheers, bye bye.
