Good evening and welcome to tonight's platinum webinar on the topic of cardiovascular emergencies approach to the dyspneic cat. Before I introduce our tonight's speaker, a little bit of housekeeping for you. I'm sure many of you joined us previously on one of these webinars, but if a a newcomer or just need refreshing, then just a little couple of little bits to make sure that you get the most out of tonight.

We have a Q&A box which you will find at the bottom of the, screen. That Q&A box enables you to pop questions in there throughout the presentation. What we do is we keep all the questions till the end and then and ask the speaker at once the presentation's finished, just to make sure that we don't interrupt the flow of the presentation and we can also keep the time as well.

But please do put any questions you have in there. It's great to as a way to engage with the speaker and also add a bit of interactivity to it. We don't have any poll questions tonight, so no need to worry about that.

You can just sit back and relax for the duration. If you do have any technical issues, we're joined tonight by my colleague Lewis. Lewis is on hand to answer any of your queries and deal with any issues you may have.

So, all you need to do if you've got any issues is either go to the chat box, which is at the bottom of the screen, click on that and type in your message, or alternatively send an email to office at the webinarett.com, and Lewis will be on hand to respond to you immediately. So, on to tonight's speaker.

I'm delighted that we're joined by James this evening. James graduated from the University of Bristol in 2008 and took up a position in a busy out of hours and referral practise the same year. He gained a certificate in Small Animal Medicine in 2012 and has just finished his second certificate in veterinary Cardiology.

James currently works at Bets Arrowfields in Manchester, dealing with the referral, internal medicine, oncology and cardiology cases. His particular areas of interest are cardiorespiratory diseases and gastroenterology. So without further ado, I'm pleased to introduce you to tonight's speaker James, over to you.

Hello to everyone, from myself James, thank you for all signing on to this session tonight about the approach to the Disney cat. So we've got quite a lot to get through, so I'll crack straight on. So we're gonna break down the aims of this lecture, so hopefully we're all gonna walk away having understood the following things.

Firstly, to be able to define dyspnea and understand why it can be so challenging in our feline friends. Secondly, to understand the many different causes of dyspnea and how they may present in our felines. To get a good understanding about how we can effectively triage the dysna cat, and this can be really quite tricky, as I'm sure you all know, in some of those most dystonic cats that that rock up in the wee small hours of the morning.

How are we going to rapidly achieve a working diagnosis so that we can start to implement effective therapy, and how we stabilise the dyspneic cat so that we can get them from the point of being dyspneic, to stable enough to either go home on oral therapy or to be able to undergo further diagnostic evaluation. So defining dyspnea. It's pretty straightforward really, it's simply the difficulty in breathing, OK?

So this may range from relatively subtle clinical signs in some cats which may go unnoticed by the owners to really quite fulminant presentation of open mouth breathing, which is posing an immediate threat to life. Now, most people think of dyspnea and think of the most extreme situation with that open mouth breathing cat, but certainly from my experience working in general practise and referral practise, I've seen a fair few of dyspneic cats that the owners were completely unaware of, so I've been. For general health checks and vaccinations on some geriatric cats and had to flag up to the owners that your cat's breathing with quite considerable effort.

Have you noticed that before? No, do you mind me doing a quick ultrasound? And lo and behold, that cat had a pleural effusion.

So it's not always, straightforward to even diagnose, in, in some, instances in small animal practise. But tachypnea is defined as the increase in the rate of breathing, and we'll go through some specific numbers a little bit later on in the talk. Hyperea is the increased depth of breathing with or without an increase in the rate of breathing.

We'll talk about that again a little bit later on. And orthopy is a term I'm gonna use quite a bit, which is that adoption of a standing or sternal position. Of the cats to aid respiration, so they're on the consulting room table with their elbows generally abducted in an external recumbency, enabling them to move their chest wall as much as possible to maximise their ventilation and often with an outstretched neck so that they're also able to straighten their airway as much as possible to maximise their oxygenation.

So why are we here to to talk about it, mainly because it, it can be really quite challenging and, and quite scary, to deal with these guys in first opinion practise. . Some of the reasons for that is that they genuinely are true emergencies and can present at any time of day or night, sometimes without prior warning.

So I talk later on about the preparation of these patients landing at the clinic. That's not always the case, you know, it's not uncommon for you to get a knock on the consulting room door as you're wrapping up your last consult of the day thinking you're on your way home, and the receptionist comes in with a cap that's open mouth breathing. .

This also means that you might be quite rushed to deal with some of these patients. You might not have as many staff members as you would like if it's the early hours of the morning. So, you know, all of those things can can sort of compound the problems of dealing with these guys.

Felines as well are, as I like to call them, sneaky gits, they're very good at hiding the signs of illness, and as a result of that, a lot of these patients present as acute emergencies with really advanced disease because they're so good at being able to hide their clinical signs. I often joke that the presenting signs for almost all feline diseases is lethargy and anorexia, for quite a long period of time until really the final stages of the disease ensue and perhaps in a cat that's had congestive heart failure, it finally starts to open mouth breathe, at which point the clients notice that and present them to the clinic. So they often present much further on down the line with their dyspnea than than dogs do.

We know that cats can be very fractious at the best of times, but certainly dyspy at cats is even more so, and even minimal physical restraint in these guys can further compromise their respiratory reserve, meaning that sometimes just handling the patient and performing even a basic physical examination can be quite challenging. Patients are often too unstable as well for extensive diagnostic testing, and I'm putting brackets here, even radiography as extensive testing for these guys and I'll just highlight at this point that I'm probably not going to talk about X-rays much more throughout the rest of this talk, because we're really not able to perform radiography very effectively in, in cats. So essentially we have to formulate the working diagnosis as quickly as we can and treat that and monitor our treatment response, .

To be able to stabilise stabilise these guys before we can do any extensive testing. There are also multiple causes of dyspne in cats and, and often with very similar clinical history and or physical examination findings. So just to move on to some of the causes of dyspnea.

I'm gonna talk through a couple of studies, looking at dyspne in cats, and, the first one is the rapid cat study, which is pretty recent from 2017. And this was a prospective analysis of 92 cases of feline dyspnemia, which initial initially, sorry, presented in first opinion practise and then were referred on to tertiary referral level for a definitive diagnosis. And within this group of patients, they found that cardiac, respiratory and neoplastic causes, were by far the most common.

And out of those, cardiac made up the vast majority, being 65% of all cases, and respiratory cases being about 16%. This is certainly very representative of, of what I find, in, in general, practise and also in referral practise as well. And I, I imagine you guys are pretty much seeing the same types of cases as well.

The University of Liverpool, did a retrospective analysis of 90 cases that were referred through, the cardio respiratory service, and this was published in 2009, and they looked at the causes, and again, cardiac respiratory and neoplastic were the three top causes, and again, cardiac was the most common, although not quite as, as, frequent as in the more recent rapid CAT study. So already, before our dyspneic cats even turned up at the clinic, we're starting to think about what causes dyspnea they may be based on their frequency, OK? So just going through some of the approaches to the, the different types of, of dyspnea, the different areas that that dyspnea can be originating from.

So I like to break it down into these sections. Firstly, primary respiratory tract disease. So if we break it down into the anatomical regions, we'll start thinking about causes of upper respiratory tract disease.

And we're talking about disease that affects anything from the naries back through the nasal chamber into the nasopharynx, the pharynx, the larynx, and then down into the trachea. We then think about the lower respiratory tract diseases, so the diseases of the bronchial tree which are particularly common in cats. Onto the pulmonary parentchimal diseases, so, interstitial pneumonias, pulmonary fibrosis, haemorrhage, non-cardiogenic pulmonary edoema.

Then onto the plural space diseases and and mediastinal diseases as causes. And then finally, thoracic wall diseases as well, including the ribs, intercostal muscles, and diaphragm. Generally, the diseases of the thoracic wall, are secondary to some sort of trauma, so those patients present generally with quite clear signs of trauma, scuffed nails.

And and a mandibular synthesis fracture from an RTA or a bite wound to the thorax from a dog, so I'm not really going to talk about trauma cases too much in this presentation, but primarily concentrate on the ones that are listed above. So within the primary cardiac causes of dyspnea, we're gonna be mainly looking at patients with acquired cardiomyopathies. So we do see congenital disease in cats, of course, but I think the vast majority of dyspneic cats that present have acquired disease.

Even if they are as young as 1112 months of age, you know, it's really quite common for unfortunately cats to develop acquired heart disease at quite a young age. So the primary cardiomyopathies we're thinking of are hypertrophic cardiomyopathy, with the subset of that being hypertrophic obstructive cardiomyopathy. They make up about 70% of all feline heart disease and therefore most common.

Then the second most common form is restrictive cardiomyopathy, which depending on your classification system can be mixed in with feline unclassified cardiomyopathy, so they make up about 20% of all feline heart disease. We then have arrhythmogenic right ventricular cardiomyopathy, which is quite an unusual, form of heart disease in cats. And then we can get things like DCM.

DCM traditionally was, because of a nutritional disorder, taurine deficiency, whereas these days we actually see DCM more frequently as an end stage of some of the other primary cardiomyopathies. So a HCM over a period of years can change quite dramatically in its appearance and it's phenotype and end up looking much more like a, a DCM in its final stages, and we sometimes class that end stage or burnt out cardiomyopathy. We've got to remember that cats also get a lot of secondary cardiomyopathies, so hyperthyroidism, hypertension, nutritional, neoplastic, secondary to acromegaly, and even secondary to corticosteroid use.

So. Corticosteroid use is something that that has been shown in the literature to with chronic prednisolone therapy, and some cats seem to induce congestive heart failure, so it's something that I often ask in the history. Is a cat been on prednisolone for, you know, chronic skin problems and things like that.

We may also see our patient with dyspnea being presented with, evidence of an aortic thromboembolism. So if we do see that, it makes, obviously, congestive heart failure as the cause of this at the top of the list and sort of sends it down a very specific diagnostic pathway, so we should always be checking for that in our patients. What other causes of dyspnea do we have?

Well, I've sort of listed them as other causes of tachypnea, plus or minus open mouth breathing really that can really look like dyspnea but perhaps aren't dyspneia because of primary, you know, cardio respiratory problems. So one of these would be anaemia, certainly it will cause tachypneia in our patients and potentially open mouth breathing. But it's amazing to see how low cancer PCVs can go before it actually affects the breathing.

In the last 4 weeks I've had 3 cats, present with PCVs in the range of 5 to 10%, and they were tachyneic, but none of them were dyspneic, they were much more profoundly weak, than anything else. Pain will obviously cause tachypnea, fear, also very commonly, and, and even panting as well, which can easily be mistaken by the untrained eye, as open mouth breathing. So that has to be differentiated based on clinical suspicions and physical exam.

Hyperthyroidism will induce tachypneia and causes quite fractious stressy cats who like to open mouth breathe. Metabolic acidosis will also cause tachypnea as we blow off CO2 to correct our acidosis. Abdominal distention and and pressure on the diaphragm will induce tachypnea, and neurological disease as well.

So these are the things that we just bear in mind when we've got a patient in front of us that that may be dyspneic. So moving on to triage of these patients. The first part being the initial call.

So this is the first point of contact with the client, and at this point, we want to really log as much information as possible. The more we know at this point, the more prepared we can be when this patient arrives. But also, we can start to gather information and form a list of differentials, which is the bread and butter of, of being an internal medic.

And even start to refine those differentials and have a sort of top 3 or top 5 potential problems before this cat even arrives. So we're going to ask to make sure we've got up to date case notes available if it's coming to us for practise. If it is one of our clients, we're going to be double checking to see if this cat has any history consistent with cardiac or respiratory, disease.

Is the patient's already, on any medication, anything like that, OK? We're then going to have to advise the owners on safe transport to the clinic. And we need to then prepare our clinical staff for the arrival of the patient.

So, continuing to think about the important features of history and signalment in these guys, this is what's really going to help us unravel the mystery of of what's causing this knee and help us answer that golden question that we're often stuck with, has this cat got cardiac or respiratory tract disease? OK. And the first thing that we need to be thinking about is the age of the patient, so.

Younger cats are more likely to get infectious disease and to suffer from a lower airway disease. But as I said before, they don't read the textbooks and they can also have congestive heart failure at pretty much any age. OK, so it's a bit of a generalisation, but something that it can bear in mind.

Older cats conversely, are obviously more likely to present with neoplasia than younger cats, and also more likely to present with cardiac disease. Than younger cats as well. So, coughing in cats, this is something that I will always ask a client, .

About has your cat been coughing at all in the last few days or the last few weeks? And I think this is because certainly in my experience and in quite a lot of the literature, I think it's well known now that coughing is not very well associated with congestive heart failure in cats. Even in dogs, coughing is more likely to be associated with respiratory tract disease than it is congestive heart failure, but certainly if I've got a cat that's been coughing and then presents dyspneic at some point further down the line.

I'm much, much more suspicious that they've got bronchopulmonary disease, versus cardiac disease. Now Going back to the study that I mentioned briefly earlier, the Rapid Ca study, they conversely found that actually about 25% of cats in that study that that were diagnosed with congestive heart failure did present with a cough. So.

It just sort of shows how difficult it can be to to sometimes draw conclusions in these cats just for a bit of history and signalment but other things to consider are certainly the breed, so we know that Siamese and Burmese, are prone to bronchopulmonary disease. I mean Siamese, you know, it's almost like bronchopulmonary disease is going out of fashion you just can't get enough of it, . And if I therefore have a, a Siamese cat that presents me just the very first thing I'm thinking of is bronchopulmonary disease, and I'm already reaching probably for the tebutyle.

Maine Coons, Norwegian forest cats and rag dolls, as we know, are prone to cardiomyopathy, so that's something to bear in mind. So we've had a little bit of a scratch of our heads with regards to the patient's signalment and the history. The patient's still not arrived and we're gonna do everything that we can to prepare for the arrival of that patient.

So it's sensible to select an area of the hospital with adequate space, oxygen available, a crash kit to hand, and other facilities as well to be able to perform cardiopulmonary resuscitation. And certainly to make sure that appropriately trained staff are available where possible. So with respect to some of the sort of specific things that I'm going to reach for, these are things that I would furiously scramble around and grab, grab, sorry, before that cat arrives at the clinic, or if you're lucky enough to have a special triage area as we do at our clinic, we have all these things already set up, ready to go in the event of an emergency.

So the certain things that we're going to need are a range of appropriately sized intravenous catheters. Because we talk a little bit later on, intravenous catheterization of these guys is gonna be really, really important for the delivery of intravenous medications and also to be able to perform effective CPR, should that patient rest. We need to get a laryngoscope with appropriately sized blades and a working bulb, which is sometimes not always the case.

And that's obviously to aid, endotracheal intubation if needed in patients who generally have upper respiratory tract diseases, OK? We always have a suction device available. We use a simple surgical suction unit and just have it attached to a sterile, suction nozzle.

And we use that quite commonly for clearing secretions from the pharynx of patients, who maybe have upper respiratory tract dyspnea, or patients who have, expectorated up pulmonary edoema in the sort of, you know, most forminent form of, of congestive heart failure. We need to make sure we've got a range of appropriate sized ET tubes for our patients. Again, should they arrest, we need to intubate to be able to perform IPPV.

And also, if our patient has got upper respiratory tract dyspnea, it may become severe enough for us need to intubate and ventilate those patients to see them through. I also like to have a urinary catheter available to aid intubation of the airway, should we need to intubate it and it's too small for, an ET tube to be passed. So we'll simply pass a urinary catheter through the larynx and connect that up to, the oxygen and be able to provide 100% oxygen that way directly into the trachea.

A tracheostomy kit is always sensible. We have, kits that are, that are made up and that are sterile and available at all times. But fortunately we don't have to perform tracheostomy, particularly common in cats.

It's much more common to have to do it in dogs, but it's certainly worth having that kit available. Local anaesthetic spray for obvious reasons, and an appropriate size, circuit, so a tea piece or even an ambu bag, if not for performing, IPPV in these patients if needed. We then always have a thoracocentesis kit available and a couple of sizes of thoracic drains.

We go on to a tiny bit about thoracic drains later on in the presentation. We also want to be sure that we have the following drugs to hand. These are my sort of go to drugs for the dyspine cat ruzamide, tebutyle, dexamethasone and borphenol.

It's all very commonly available drugs. And also be sure to have the following drugs drawn up and immediately available should they be needed for CPR. So atropine plus plus or minus, glycopyrelate and adrenaline as well.

We should then also have a reasonable amount of monitoring equipment for these patients, and what I tend to go to, as my sort of four, main things that I want to be monitoring in these CATs is firstly an ECG and really I'm only worried about lead 2 at this stage, I'm not worried about 6 leads or anything like that. And, we also want to be able to monitor blood pressure, OK, because we may have a cat that's got lower congestive heart failure, or we may have a cat that's, you know, also hyperthyroid or hypertensive, and we want to, just make sure that we know, if that's going on as well, . We tend to use Doppler estimation for systolic blood pressure, or we will use an oscillometric cer cuff as well to be able to do systolic, diastolic and mean.

Pulse oximetry, everyone should have that available at the practises, and, capography as well is is really, really useful. Now all of these are available on the commonly used, in practise multi-parameter monitoring devices that that we commonly use, in theatre for for anaesthetic monitoring. And it's exactly what we use in our clinic, we have one of these devices on the side that's multi-parameter just for use triage patients and never moves.

Now, most first opinion practises obviously don't have that luxury, so at this stage, you know, if you have this monitoring device and it is in theatre, you can kindly ask your, nurse in there just to borrow this machine for a short period of time to be able to, do a bit of monitoring on your dis cap when it arrives. But otherwise if you don't have a multi-parameter, device, you can obviously use a standard, you know, paper trace recording ECG, . Doppler estimation, blood pressure and separate, you know, pulse oximetry devices as well.

So this is a photo that I took of our triage area at our hospital. And as I say, it's always set up and ready to go. And over on the right hand side here we have our crash trolley which has all our crash drugs all made up.

It has all of our thoracostomy tubes, our . Equipment to drain pleural effusions, oh, sorry, masks, ambu bags, all that sort of stuff to hand. We've got the defib here, we've got some paperwork for, being able to, to sort of perform, a triage assessment immediately and, and record, any events that may occur, during CPR.

We then have a nice, laminated chart with emergency drug dosages for different weights of patients, which can be invaluable in the emergency, and I recommend you getting one of these, even if it's not on the wall, just stick it inside, of your crash kit with your drugs. We've then got stuff available for volume resuscitation should they need it, or appropriate circuits for delivery of oxygen. We then have our multi-parameter machine, which is always sat here, ready to go for monitoring on these patients.

All the disposables like catheters and things and bandages, that we have sort of stored here. But we also have individual trays, that we make up for catheter placement. So they have a couple of sizes of catheter in each one, some tape, .

A bone or you know, a connector, everything that you would need to place an IV in a patient and, and sometimes that can really make the difference between getting an IV quickly into a patient that really needs it rather than having to scrabble around the hospital area trying to find a catheter here and a bone there. So it's quite a good idea to have one or two of those set up. And then we have our point of care ultrasound machine.

Which you can see here, which is just for use of triaging patients, it's on a little wheeled base, and we talk a little bit more about point of care ultrasound in these guys towards the end of the talk. So obviously If you can, you know, be able to create an area like this, that's fantastic, but otherwise these are some of the things that you can think about grabbing prior to that patient arriving at the clinic. So we move on now to the immediate steps that we're gonna perform once that patient has arrived.

Well, the first thing to do is obviously remain calm. The second thing we want to do is initiate oxygen supplementation. We talk about that in just a few slides.

So straight away, it's the responsibility generally of one of our nurses, to start providing oxygen supplementation whilst I start to, perform an initial triage of the patient. So I work my way through the triage in the ABCD sort of manner that's that's very commonly known. Looking at the airway and the breathing, and circulation and demeanour.

And if at any point during, this set of examinations, I detect any problems with these vital organ systems, I sort of stop, immediately and institute treatment at that point. So there's no point assessing the airway and saying, yes, it's obstructed. I'm going to now start listening to its lungs.

OK, now I'm gonna move on to listening to its heart. We need to establish an airway before we do anything else, OK? So we'll go on to that in a few more slides.

If at all possible as well, we want to get this intravenous catheter in place as well. Now it's often easier said than done in these fractious dyspneic cats and sometimes a hands-off approach is much more appropriate, OK? So in the most dyne cats, it may be most sensible to simply put them straight into an oxygen rich environment and just observe them.

OK, you can tell a lot from a cat's respiratory rate and from observing the type of respiratory pattern that it has without even putting your hands on that patient cos sometimes they're too unstable to even auscultate as as I'm sure many of you will know. It may also be sensible in some of these cases to mildly sedate them at this point as well. Now, that will, reduce anxiety in these patients, and that can often, therefore reduce oxygen consumption by peripheral tissues, but also it can sometimes improve ventilation as well.

So I tend to reach for butorphenol in these patients at sort of 0.2 to 0.3, migs per kg and that can generally be given IM or obviously IV if we, if we place that, OK?

Hernia trauma patients should be analges and my go to drug would would be methadone in the vast majority of these patients at 0.2 to 0.3 mg per kg.

IM or IV and repeat that 4 hourly. So then, oxygen supplementation, what are our different options? Well, we start off by thinking about room air being 21% oxygen, how can we improve on that?

The different, methods, of oxygen supplementation will also depend on various factors such as the patient size, the patient temperament, oh God, it's a cat, not good generally. The duration. The available equipment that we have and also your familiarity as well with that equipment, OK?

You've got to be confident, when you are looking at oxygen supplementation and, and what are some of the sort of suggestions that I'm gonna make are food for thought, but I'm not saying tomorrow go out and change what you're doing, you know, for something that you're perhaps not totally comfortable with. So the main techniques we're talking about is flow by oxygenation, which includes the use of the mask as well, nasal prongs, oxygen cages, oxygen incubators, and then a couple of other methods as well. So oxygen supplementation by flow by or mask, well, we tend to use this most commonly, I would say in the triage of our dyspin cats, and we tend to use flow rates of about 2 to 3 litres per minute.

We will select a T piece and an appropriate sized mask with diaphragm. So. We need to make sure that our mask is a decent size and not too small, because a mask that is too small will cause our patients to rebreathe CO2 and it won't do them any good.

We also ideally want a diaphragm on there as well, so that we don't have oxygen, leaking around. The outside of the mask in the patient's head. So what are the pros and cons of flow by, for oxygen supplementation?

Well, the positives are that minimal equipment is needed. Pretty much every first opinion practise is gonna to be able to provide flow by with a mask. It's rapid to set up.

We generally need minimal restraint of the patient. And it is also suitable for patients on immediate arrival. What are the negatives?

Well, some cats just will not tolerate it, as you will know. Some cats won't tolerate the masks, some cats won't even tolerate, just float by from the end of the tea piece because of the sound, just because they're so distressed they won't keep their heads still. It is also only applicable really for short term use, and generally we only use this for during our triage, procedure or sometimes, .

You know, post, CPR once the patient has been extubated, for instance. There is, as I say, the risk of CO2 accumulation in little masks, and also the, inhaled oxygen concentration or the FIO2 can also be quite variable from as low as 30, up to 60%. So I found this picture on, on Google of a cat on a mask, and I thought it was quite interesting because you know, I like the size of this mask that's been selected.

It doesn't have a diaphragm, which means that oxygen might be leaking around the outside of that. There is a bit of tape, attaching that mask to a bit of suspicious bit of tubing, so there could be some leakage of oxygen there. And also, as you can see, the cat's been scroffed, which generally, you know, I wouldn't advise in cats at all.

OK. Moving on to oxygen tents and cages, so, a reasonable number of first opinion practises will have access to these, and if you don't, you can sort of cobble them together yourselves. Generally these use quite high oxygen flow rates of 3 to 10 litres per minute.

And the various options for for different tents and cages are paediatric incubators, which we think are great. You can get these secondhand from hospital auctions and sometimes they are heated, sometimes you're able to measure the FIO2 that's in there with them, just really, really useful bits of kit, . Sometimes if we don't have specifically made incubators, we can create something similar by covering the front of a kennel with clear plastic.

Note it does have to be clear plastic so that we can observe our patient at all times. We may be able to buy a purpose-built, Perspex cage door to convert a regular kennel into an oxygen cage, or we may buy a purpose-built tent such as this cruise one here, and we have a couple of those in our practise to find them really useful, plus they can collapse down to the they're good for storage and easy to move around. It's one of the positives of using this method, well, we obviously don't need any restraint.

It's suitable for patients on immediate arrival, and, it's also suitable over several days. For patients on immediate arrival, I do recommend pre-oxygenation of these incubators. So as you get the call, just turn the oxygen on to that incubator prior to the arrival.

What are the downsides though, well, there's obviously potentially a delay in reaching oxygen concentration if there's no warning. Of the arrival of the patient, disruption of oxygen supplementation also occurs every time that we open the cage door to go in for an intervention or an examination, so, I don't think this is such a big problem because once I've done my initial triage, the vast majority of my monitoring on a dyspneic cap is respiratory efforts, respiratory rates, which we can do totally hands off. So that's not a big, big problem for me.

High flow rates of oxygen do mean it can be expensive and obviously there is the risk of hyperthermia in inside these cans they get really, really warm and sweaty. Buster colour and clingfilm, I'm not really going to talk about it because I don't find it works particularly well. It does achieve high concentrations of oxygen, but it is very rarely tolerated by cats, especially when dyne, and they love to just stick their heads through the cling film or shred it to pieces on the, front of the kennel.

So I very rarely, if ever use these, OK. Nasal catheters, again, they are something that we do use, flow rates of 500 to 100 mL per kilogramme per minute. And if you're going to use them, we tend to start at a low flow rate and then titrate it up so that the patients don't get a real shock and they're more likely to tolerate the oxygen flow.

It's good because you can use them in both nostrils and can achieve high oxygen concentrations, but sometimes they can be as low as 40%, . But they can be used for several days and they do stay in place if a patient is moving around. They do, however, cause drying and irritation of the nasal mucosa.

If the animal is panting, they basically are not breathing through the nose at all. they may not be tolerated, once they've been placed or even placing them. And I think in any dyspneic cat really these are far too dangerous to use.

So maybe in the tachypne cat that has improved but you need some oxygenation over perhaps a few more days, it may be appropriate. But it's also contraindicated in nasal disease, such as chronic rhinitis or in a patient that's had trauma of the face, or in any patients that have coagulopathies or raised in cranial pressures. So finally, just a quick one to mention, should you ever have a cat with upper respiratory tract obstruction, which, as I say, is not that common, but it does occur, and we're perhaps unable to intubate that patient's airway because they are so obstructed.

This is a technique that I've used a few times where you can pass, a catheter between some of the tracheal rings. And then advances over the stylet, attach, a 3 millimetre ET tube connector to the catheter and attach that to an oxygen supply and be able to effectively oxygenate this patient, with upper respiratory tract, obstruction rather than wafting oxygen in their face, which is obviously not, not going to be of any, effect. So how do we determine that our oxygen supplementation has been effective?

Well, we're gonna monitor for improvements in respiratory rate and effort primarily, but also in the patient's mucous membrane colour, heart rate, demeanour and level of anxiety. We can also use pulse oximetry, and we're measuring there for improvements in the haemoglobin oxygen saturation. So hypoxia recurs at an SPO2 of 95% and below, which equates to a PAO2 of 180 millimetres of mercury if if you're able to run arterial blood gases.

We want to try and maintain our SPO2 above 95%, therefore, at all points. Scarily enough, if we've got a cat that's presented in its cyanotic, that cat probably has an SPO2 in the order of 75%. So it just shows you how severely hypoxemic, a lot of cats with cyanosis are.

Be aware though that hyperpigmentation of the skin, shock, and anaemia will interfere with our readings on pulse ox, OK? So we've talked about oxygenation and that's going to be hopefully underway, with the aid of a nurse using flow buy mask, whatever we've decided. And at this stage we need to now quantify the severity of the dyspnea.

Identify if we can, whether the patient has signs comparable with primary cardiac disease, primary respiratory tract disease or metabolic disease, for instance. And also to get some baseline vital parameters so that we've got a base, to be able to work from and monitor our patient on treatment to make sure that our therapy is being effective. So moving through my ABC examination, these are just some of my tips and also some things that I picked up from the literature as well.

So you want to listen for breathing sounds consistent with upper respiratory tract obstruction, when you're assessing the airway. So that typically is a really, really prolonged inspiratory phase, OK, with a quite short, rapid expiratory phase to respiration. If we hear that we instantly need to assess that airway and make sure that it's fully patent before we continue the physical exam.

Listen out for. The signs associated with the upper respiratory tract, so stor is that sort of sound that our brachycephalic dogs make, which generally, is associated with disease in the nasopharynx. OK, so a dyspneic cat with stor, may have a whacking rate, polyp in its nasopharynx, OK, for instance, if we hear strider in our cats, which is really not that common when compared to dogs, but that's that sort of.

High pitched inspiratory sound, when breathing in. That really does commonly pertain to laryngeal disease, so we can start to think about laryngeal neoplasia, laryngeal collapse, or laryngeal paralysis. As I said earlier, if the airway's not, patent, we need to perform immediate endotracheal intubation, under anaesthesia and provide ventilation and or tracheostomy in those patients until we can, definitively treat their upper airway obstruction.

Sometimes in patients with upper airway obstruction, a little bit of mild sedation, as I say with butorphenol can be really, really useful to improve their, their ventilation. So moving on to breathing, I tend to think about it with OAP, not old age pensioner, but observation, auscultation, and palpation. So we're going to observe them for their posture.

Is this cat happy looking around, but a little bit dysmic? Is it orthopneic, or is it in lateral recumbency gasping for its last breath, OK? We're going to look at the respiratory rate.

Now, tachypnea in hospital generally is defined as a respiratory rate over 30 breaths per minute. And certainly for a patient to have congestive heart failure, it's generally been shown in studies that they generally have heart rates over 30 breaths per minute. It's really dysmic with a res rate below 30, it's probably more likely that they've actually got primary respiratory tract disease.

If their sorry, respiratory rate is very high and over 80, that was shown recently in again the Rapid CAT study, that that was more consistent with congestive heart failure again as a cause of dyspnea rather than primary respiratory tract disease. We want to get a good baseline of our respiratory rates so that we can use that to monitor our treatment. How much effort is there, as I said, inspiratory effort is indicative of upper airway obstruction and expiratory effort is quite indicative of lower airway disease such as feline asthma bronchitis.

Is there any abdominal movement, which is quite often seen in patients with lower airway disease, OK. And have we also got evidence of paradoxical breathing movement. So that's where the chest wall moves out as the cat breath breathes in.

But the abdominal wall, paradoxically moves inwards instead of outwards, during inspiration. And that tends to happen in cats that have got restrictive breathing pathology, and have, you know, real fatigue of their, respiratory muscles, and that's most commonly seen in patients with quite large pleural effusions. So if you see that paradoxical respiratory movement, it's not a good sign, and they probably have, pleural effusion.

So onto auscultation. We're going to listen to our patient's lungs and heart dorsally and ventrally and the left and the right. And specific things that we're going to listen for, well, muffled lung sounds might be consistent with consolidation of a lung globe or plural space disease.

We may percuss the lungs for evidence of pneumothorax, and we may have displacement of the apex beats with severe pulmonary parentchimal disease, OK? We're then going to listen for a couple of these classics such as Wheezes and Crackles. Now when you open any textbook, it it says, you know, feline lower airway disease, you will hear crackle, er sorry, wheezes.

And cats with congestive heart failure, you will hear crackles because of pulmonary edoema. I don't know about you guys, but I very infrequently hear these classic sounds in cats. The vast majority of cats, with lower airway disease, dystonia, I don't have wheezes.

If they do have a wheeze, great, it makes it highly likely that they've got lower airway disease, you know, and probably asthma, but if you don't hear it, it certainly does not exclude those diseases. The crackles as well with pulmonary edoema, I find that cats have to be, You're almost drowning in pulmonary edoema before you will start to hear crackles, you know, bear in mind that in the early stages of pulmonary edoema, the fluid is actually within the interstition and not in the alveoli, and therefore you really aren't gonna hear any crackling in certainly in the very early stages. So if you do hear crackles, yes, it certainly could be congestive heart failure, but the absence of those doesn't work out.

So at this point we're starting to think, are we dealing with primary respiratory tract disease and if we are, are we looking at upper or lower respiratory causes? We then Going to move on to palpation. So we are going to, sorry about this guys, we're going to check a cranial rib spring, so we slide our hands along the front of the patient's thorax and give the ribs a bit of a squeeze just in front of the heart, and you should have a nice springy release from the front of the cat's thorax.

If you lose that springiness, then it might be that cat has a large meaty style mass as the cause of its dyspnear. We're also going to check our patients by palpation for crepitus, or emphysema, asymmetry of flail segments of the chest, which generally are all things that we're going to associate, with trauma. So again, we're not gonna talk about those guys too much more, during the rest of this webinar.

So we're on to assessing the circulatory system, we're going to look at mucous membrane colour. So pallor is often associated with congestive heart failure because of reduced peripheral perfusion, and we may see cyanosis as well, although I find more commonly cyanosis is associated with primary respiratory tract disease versus congestive heart failure, but. Again, it's just not hard fast real.

Prolongation of the capillary refill time is also often consistent with congestive heart failure. And we're also going to feel pulses for pulse quality, whether that's the femoral, the central pulse, or the dorsal pedal pulse, the peripheral one. And we're also going to check for pulse deficits we hear in a regular heart rhythm.

We're then going to have a look at the heart rate, OK? So, cats, again, don't read the textbooks, OK? We know that dogs generally when they're in heart failure have normal to high heart rates, and when they've got primary respiratory tract dyspnea, they have normal respiratory, sorry, heart rates.

With cats, not always the case. So cats can present with normal heart rates, they can present with high heart rates in congestive heart failure, or they can quite commonly present with bradycardia as well in congestive heart failure. Now what are we classing as normal heart rates?

Well, perhaps 140 to 220 beats per minute would be normal, but certainly if we're over 240, that's definitely what we class as an actual tachycardia. Bear in mind with bradycardias as well that in cats we can see that with primary respiratory tract disease, and generally those are the diseases that stimulate the vagal nerve. So any mediastinal space occupying diseases such as the mediastinal mass or any upper airway obstructive diseases such as nasopharyngeal polyps will stimulate the vagal nerve and will lower the heart rate in a can.

Again, going back to the rapid CAT study, they looked at heart rates and found that generally if your heart rate was over 200 beats per minute, it was more consistent with congestive heart failure and primary respiratory tract disease. That's the cause of dyspnea. Rhythm wise, we're gonna listen to see whether it's regular or irregular, and cats that have irregular heart rhythms are much more likely to have congestive heart failure than respiratory tract disease for obvious reasons.

On auscultation, we talk about murmurs, on the next slide, but also do listen out for your gallop sounds as well. Let me mention that in a sec. Temperature, something that's quite often overlooked in the dyspneic cat, but again the rapid cat study looked at this and found that a lot of cats that presented with congestive heart failure had heart rates below 37.5 degrees C.

So that could be used as a pretty handy cut off for trying to determine the cause of that dyspnea. And they also found that patients with temperatures over 40.5 degrees C were more likely to have respiratory tract causes of their dyspnea.

I also finally pop on here, be aware of cardiogenic shock in felines. So that's a form of heart failure that essentially causes low output forward failure from the heart, and it typically presents with a triad of clinical signs, hypothermia, hypotension, and bradycardia. So if you ever see that in a dyspneic cat, it could well have cardiogenic shock, which is unfortunately quite a difficult thing to treat in felines.

Moving on to the murmurs then, cats with murmurs, are more likely to, sorry, murmurs are more likely to be significant, with age, OK, in cats, so younger cats with heart murmurs, there's a higher chance of there being physiological innocent murmurs than than in older cats. Feline murmurs are often loudest sternally, so when I'm auscultating these guys, I'll run my stethoscope up and down the sternum and rock it slowly from left to right, to localise the murmur. And beware that murmur grade does not correlate well with disease severity in cats, and in fact a lot of cats with heart failure don't have any murmur at all.

And that's because cats don't get primary valvular disease, but primary cardiomyopathies. Generally as well, murmurs in cats don't go any louder than a 4 out of 6, so they're not often that easy to, to, to auscultate sometimes in a dissonate cat that's got quite loud lung sounds as well. So just very briefly about gallop sounds, they're a third heart sound, an S3 or a summated S3 and an S4 that generally are representative of diastolic dysfunction, and these are really almost always associated with heart disease.

Definitely if you hear about this account, it's likely to be cardiac. So this is just a little flow diagram that I pulled off the rapidAT study that can be quite useful just to work your way through if you've got a cat in front of you based on your physical examination findings to help determine whether or not that's likely to be, cardiac or, or non-cardiac in origin. So on a point of care ultrasound, I can't overemphasise how useful this is, at our clinic, and I think really it should be used more frequently in general practise because you don't need a particularly high tech machine to be able to do this.

You don't need a lot of experience, OK? So we call it a point of care ultrasound or a pocus. It's otherwise known as a TFAST, so a thoracic focused assessment with sonography for trauma, a bit of a tongue twister, .

But we basically use this to help differentiate different causes of dyneing cats, and it's great because you can perform this on a cat that is sat in sternal recumbency on flow by oxygen without any physical or chemical restraint by simply spraying spirit onto the side of the thorax and applying the probe directly to that. We don't need to clip the fur, we don't need any gel, and you can get a really nice image just from doing that in this sternal cap. And the four things that I tend to look for are, firstly, the size of the left atrium on the right parasternal long axis type of view.

And I'll show you an image of that in a second. And basically, if you can measure a cat's left atrium and it is over 16 millimetres in diameter, that cat is disne because of heart failure, OK? So really, really easy diagnosis to make heart failure, and at that point we can then initiate treatment and look at potentially referring to a cardiologist for full laco later down the line.

We're going to look for fluid within the pleural space, whether that's anechoic or hypoechoic. We're going to look for things called bee lines which can indicate pulmonary edoema, so we don't need chest X-rays in our cats to diagnose pulmonary edoema or pleural effusion. Brilliant, OK, we don't need to sedate and pin cats down with sandbags to be able to diagnose these problems.

And we can also use ultrasound to diagnose pneumothorax because of the loss of a thing called glide sign. So just to quickly go through some images. This is a picture of a patient who's got bee lines, OK, so you can see these vertical striations of white and black lines, they are caused by fluid accumulation within the lungs.

So this is a patient who's got wet lung or pulmonary edoema, as we may call it. And this is your plural line here, and in pneumothorax, what you don't get is the normal to and froing, of this membrane, against the side of the chest wall, OK? So, a glide sign is something you can really demonstrate on a, on a video rather than a still image.

But this is, the simple long axis view of a cat's heart, taken from a FAST scan of the chest, and this is, a frame that we pause at the maximum. Diameter of the left atrium and we simply draw a line across the left atrium, parallel to the mitral annulus, we measure that distance. It's over 16 millimetres, that cat's got heart failure.

You can also quickly have a look at its, left ventricular wall as well, and from this cat it quite clearly looks like it's got HCM because it's a form of cardiomyopathy. So this is an image of a patient with a pleural effusion, and what we can see is nice anechoic fluid here. And these are little basically connections between the pericardium, the lungs and the chest wall that you often see floating about.

So I hope even though it's quite a rapid run through a point of care ultrasound, that sort of highlights how useful it can be with that cat that's in front of you and you're still unsure from your physical exam and your history about whether it's cardiac or not. Pop that probe on the chest, measure the left atrium, check for bee lines, pleural effusion, avoid x-rays if possible. So a little bit about NT Pro BMP because I had a feeling people might want to ask about it.

So this is basically measured in the blood and it is increased in patients that have cardiac disease because of stretch of the cardiac myocytes, OK? And we can either measure this externally at a laboratory with the IDEX Cardio PET Pro BNP that gives us a quantitative number, which is really, really nice, but really, really not so useful in a designate cat. We need our answers there and there.

So the much more frequently used option is the IDEX Snap feline Pro BMPLlyzer, which is a qualitative, you know, positive or negative, snap-based test. So just a few points to remember about this test to take home. Firstly, it's been well studied in feline cardiomyopathies, the usefulness of this snap, but it's actually not been well studied in patients with feline respiratory tract disease, so it's hard to draw consumption at too many .

Conclusions, sorry, about what, what, what it might do in patients with primary respiratory tract disease. But essentially, a normal snap test can rule out, cardiac disease as the cause of dyspnea, in a dyspneic patient with reasonable accuracy. OK, so a normal test in a dyspneic cat makes it pretty damn unlikely that it's cardiac in origin.

And that's basically because a positive snap test correlates with an NTropion P concentration of over about 100 to 120 pecamoles per litre. So cats that have . An NT Pro BMP over 100 peaks per litre generally have moderate to marked cardiac disease and therefore it's more compatible.

As the cause of the dyspne than if our level is below. 100 peak moles per litre. So a positive snap indicates that congestive heart failure is probable in a dyspneic cat with consistent clinical signs of heart failure, OK?

But an echocardiogram is warranted for definitive diagnosis and to classify the underlying type of, cardiomyopathy. So a couple of things to be aware of are that elevations in anti-probMP will be caused by systemic hypertension, hyperthyroidism, azotemia, and even anaemia. So that's a bit of a problem given that a lot of our dyspinic cats that are presenting are geriatric, and a lot of those cats can have comorbidities, OK?

And actually, a lot of those cats may have congestive heart failure, but it's because of systemic hypertension or hyperthyroidism. So just bear that in mind. Ideally, I suppose it means that before running an NT Pro B&B snap, we should rule out systemic hypertension, run a total T4, check the renal values and things, .

And it's really for these reasons, and the fact that we're so used to doing, point of care ultrasound at our practise that we very, very rarely use these SNA tests. You know, a snap test only has certain sensitivity and specificity, but a really good cardiac ultrasound, you know, in, in, in the hands of a good operator, has about 100% sensitivity and specificity and really negates the need, you know, for an antiprobMP in some of these patients, OK? So at this point we should have reached a provisional diagnosis based on signalment history and physical exam.

And we're gonna start at some empirical therapy at this point based on our suspicions to stabilise the patient. You have to bear in mind that empirical therapy must be used cautiously as it can have detrimental effects if we are incorrect. So we need to monitor our patients closely to be sure that our therapy is having, and causing an improvement.

In their vital signs. So just to go through some of my choices, for upper airway dyspnea, of which the common causes have already been through, I tend to use low dose sedation to reduce the oxygen demand and improve ventilation in these guys, and I typically go for something like butorphenol. We have to consider active cooling because these patients are gonna struggle to thermoregulate.

And We will often consider the use as well of a glucocorticoid if we think there's quite considerable soft tissue, swelling obstructing the airway. So I tend to reach for dexamethasone, 0.1 to 02, mig, IV or IM.

If the dyspnea is non-responsive to the above, then I will generally have to start to think about anaesthetizing that patient and intubating them to provide, appropriate ventilation, OK? So our lower airway dyspnea cats, of which by far the most common cause is gonna be asthma and chronic bronchitis, we're going to reach for, a good old bronchodilator. So my go to, bronchodilator choice is tebutyle.

And we administer that IV or IM if we're unable to to place an IV in these guys. And if we don't have tebutyle which is available as a brick injectable form, we can opt to use a salbutamol inhaler via a spacer, sorry, an aerocat spacer chamber, pretty damn effective and we can repeat that salbutamol as frequently as needed, generally every sort of 10 to 30 minutes, it's fine. I'll often also administer a short acting glucocorticoid in these patients to reduce inflammation, so dexamethasone at the dosages previously discussed.

But do bear in mind that we have the option of inhaled glucocorticoids, so fluticasone, which is an af flixotide inhalers. The problem with the use of that in the dyspneic patient is, well, two things. Firstly, the cat may well be too dyspinic to tolerate, having a mask being applied to the face.

But also it generally takes anything from 1 to 3 weeks for a steroid inhaler to have its maximum effect. So I tend to reserve the steroid inhalers for chronic therapy as an outpatient and use injectable glucocorticoids on my dyspin cats. We may also consider the use of antibiotics in these guys, but I always bear in mind that most of these patients that our clinic are going to end up having further investigations, including bronchoscopy and bowel, and the use of antibiotics may affect those results, and that generally bacterial infections are often secondary in these patients, such as mycoplasma, and that really, you know, they're going to respond to more chronic therapy as an outpatient rather than an immediate, you know, intravenous antibiotic therapy.

Cardiogenic pulmonary edoema, I think everybody will have a pretty good idea about how to treat this. I tend to start off with a ruzamide bolus of 2 to 4 migs per kick. IV is best ifO, because it does also cause vasodilation which can help reduce preload and therefore, pulmonary edoema.

But if we're unable to get an IV, I would probably go IM or then subcut. We can repeat the boluss at 1 mg per kick every 30 to 60 minutes as needed. And if that's not working our diss cats, we can consider the use of additional vasodilation, such as a topical ointment like glycerol trinitrate, which we can apply to the cat's pinner, put a little dressing over it and, and change every sort of, 8 to 12 hours.

If not, we can use, nitropruside in combination with dobutyine. Now both of these things obviously can reduce pre-load, by causing vasodilation, but also with some arterial dilation, they will lower blood pressure, so we definitely need to check that our cats are not hypotensive, prior to the use of these drugs by checking their, blood pressure. With therapy of congestive heart failure in cats, it's very poorly studied.

And you know, as a result of that, the guidelines are really anecdotal, but we tend to use an ACE inhibitor in combination ruzamide for chronic therapy. With my dyspneic cats, I don't tend to use an ACE inhibitor, and the reason for that is you can very rarely tablet them when they're tachic dyspneic, but also these medications can also reduce your blood pressure. So we need to be sure that they're normotensive before we medicate them with an ACE inhibitor.

We also know that ACE inhibitors work really, on the RAS system in more of a chronic fashion to down regulate it, so that really very little use in the acute scenario. So I tend to just prescribe the ACE inhibitor upon discharge of the patient, not prior to that. And even though it seems very obvious, I do have to state it, we do want to make sure that we always avoid intravenous fluid therapy in our heart failure cats, OK?

Because, the problem is venous congestion and any fluid we add to that pool is really gonna negate the effects of our rosemide. Unfortunately, we do make a significant proportion of our cats with dyspnea dehydrated, and often azotemic and sometimes that azotemia azotemia, sorry, unfortunately, persists, but it's the lesser of two evils really in a very acute scenario, controlling the congestive heart failure and dyspnea, in spite of reducing renal perfusion. I'm not really gonna touch on bronchopneumonia other than just say be aware of which drugs have what type of spectrum of activity and how well they penetrate into the lungs.

Be aware that generally we want to cover for gramme positives, gramme negs, anaerobes and consider mycoplasma. So again, I don't tend to use these very commonly, . Sort of intravenously, unless they've got a well established bronchopneumonia, but are very commonly discharge patients, you know, with, with a diagnosis or suspicion of, of, Bacterial infection of the lower airway on a course of doxycycline cause it penetrates well and it's also effective against mycoplasma species, OK?

So finally, a couple of slides on plural space disease. We can rapidly confirm this using our point of care ultrasound. We can also perform, thoracocentesis, not only as a therapeutic option to drain our effusions, but also as a diagnostic procedure.

So if you've not got access to, an ultrasound and your cat's 2 dyspic to X-ray. You can actually pop a needle into that patient's chest if you're suspicious of pleural space disease and draw back and see what you get, and that's called a diagnostic tap and you're very, very unlikely to do any harm in a patient that doesn't have pleural space disease, but if you have pleural space disease, you can rapidly diagnose that they've got it and and have a sample available to know what type of plural space disease that they've got. When we're doing, thoracocentesis, we want to retain our samples for external laboratory analysis, and I tend to use an EDTA tube, for cytology, sterile plane tubes for culture, and if it's a pyotthorax, I'll quite often inoculate that into culture medium type of blood culture bottles to try and improve my cultures, these very fastidious organisms.

We can almost always perform, thoracentesis without sedation, OK? And often we can achieve that with the use of local anaesthetic techniques such as the intercostal nerve block. So that's something we, we readily, use in our practise, and I can't remember the last time I've had to use sedation to, to do thorachocentesis or to even place, one of these sound like your chest drains.

So. Chest strains, will need to be placed in our patients who've got tension pneumothorax, it's rapidly refilling and often patients as well, with pyothorax for effective treatment, using, regular drainage and sort of twice daily flushing of the plural space. So it's just to sort of finally say really that we tend to use Seldinger chest strains in our conscious patients, and as I say we need minimal chemical restraint, a little bit of physical restraint.

And it's using, an over the wire technique, with one of these really nice kits, that you can see a photo of just to the right hand side here. So these are really, really, easy and rapid to place into the plural space of cats, and generally really, really well tolerated for plural space disease. So thank you for listening.

I know it's been a bit of a whistle stop tour of dysphonia, but there's a lot of things to talk about. So I hope I've, explained things clearly enough and, I'm open to any questions you may have. Fantastic, thank you very much for that, James.

I understand we overran a little bit, but I thought the, you know, what it was important that we let you get to the end because some really, really useful stuff in there. So, fantastic. Thank you very much for that.

As James says he's happy to take any questions. I can see we have got a couple of questions already, but, please do. We'll allow for a few more minutes, because Love Island's finished and no one's got anything to run off to these days and the World Cup's over.

So what else is on TV? So stay with us and we'll, answer a few of your questions. Just a little reminder while you are thinking about any questions.

As you navigate away from tonight's webinar, there will be a, a little short survey in your, browser. Please do take the time to complete that, because it does really help us, understand, from yourselves what you're enjoying, what you'd like to see more of, and also it gives great feedback to the presenters as well. So please do, take time to complete.

It'll only take you a couple of minutes. So, on to the questions. What do we have here?

So we've got a question from Paulette. She says, do you agree that the recent consensus is that Doppler readings and cats are closer to the mean rather than the systolic BP? We, we normally use Doppler estimation to measure the systolic BP, and, and certainly I think that is more accurate than using oscillometric, techniques, you know, with the, the cuff, that will give us the diastolic, systolic, and means.

So yeah, we tend to use, Doppler, you know, most frequently. And really, when we're looking at our patients with cardiorespiratory disease, it's the systolic blood pressure that we're most interested in anyway. Because we're either looking for has this patient got hypotension because of low output heart failure, and if their systolic blood pressure drops below 75 millimetres of mercury, they're at risk of AKI development.

But also, in the chronic, . Treatment of patients with cardiopulmonary disease, you know, if you're very hypertensive, and your systolic blood pressure, you know, is over 180 millimetres of mercury, it significantly increases the afterload and therefore the work on the heart. So we often want to treat hypertension in patients, to maximise the effectiveness of our therapy.

So yeah, we tend to use Doppler most commonly and with most other about systolic depression. Fantastic, thank you. We've got a question here from Greg.

Greg's one of our regular attendees. He says in humans with certain lung disease, e.g.

COPD, you can get oxygen retention, which means highO2 levels given intranasally or otherwise can dangerously increase blood CO2. Does this also occur in animals and does this affect the acid-based balance? Good question.

Not, not really in animals, to be honest, we don't tend to achieve high enough, levels of oxygen delivery, or FIO to, to really experience that problem. So in my experience, no, it's not really an issue, you know. Fantastic.

Thank you. And, I think, you know, it's always good to see this sort of crossover with, I know BVA doing more around one health and sort of those crossovers between the two disciplines. So, good to see the use there.

A couple of nice, comments coming in also, from Sue. Brilliant. Thank you so much.

And, Hilda also says thanks, very useful webinar. I have noticed I've just got a question in the chat box over here as well. It says, excuse me if I pronounce this, wrongly, as I haven't got a veterinary background, but, do you use a Pimo Bendon in the management of CHF?

And if so, what are the criteria you use to decide and under what circumstances would you use it? I knew this question was coming. Well done for asking it.

So Pima Bendan in cats, it has been studied, but in the literature, a lot of them are retrospective studies, and it's very debatable as to the conclusions we can draw from those. Some of them have shown spectacularly improved, outcomes in HCMAs on chronic emoendan therapy. But I think at the moment we don't have enough evidence to really know how much it changes the, the outcome in our chronic patients now.

The criteria for using it, well firstly you you really need to have done a detailed echocardiogram because we need to rule out hypertrophic obstructive cardiogramopathy because you will make that worse with a positive. Iotrope, but I tend to find that patients who have systolic dysfunction, which is quite common in, patients with sort of end stage cardiomyopathies, whether it's global systolic dysfunction or actually more commonly segmental dysfunction, for instance, of the left ventricular free wall. If I have reduced systolic function there, I will probably consider the use of a pinma bend down in those cats.

The other option is, To look at the patient and say, well, if I'm treating them and I've maximised my chronic therapy with ACE inhibitors and furosemide or whatever diuretics, and they're still not getting better, as long as I've not got hokum, why not try Pimoendin in those patients, but we really don't know what dose range is best and also how long it's duration is because it seems to last longer we think in cats than it does in dogs. . In the patients who are dyspneic and have low output heart failure, you know, I don't think Pendan is suitable for those guys, but you'd probably use dobutamine instead as a positive ionotrope for the emergency treatment and low output failure.

It's a really good question, I think, unfortunately, as with almost everything in feline cardiology with regards to therapeutics, we don't really know. No problem. So, so it's watch this space and they're keep an eye out for any studies that are taking place to.

Hopefully give some more information and guidance when they have a clearer idea of the impact it can have, yeah, yeah, exactly. OK, and we've got one time for one more last, one last question, which is from Paulette again, and she says, when using ex-hospital incubators for oxygen rich environments, are you able to gradually reduce the oxygen percentage using valves as we do in the oxygen tents, . We see a lot of patients at our hospital and already have the specifically designed oxygen tents.

Do you think an incubator would be a useful addition for other benefits or not required? Probably not required really, . No, I don't think that there's any advantage over what you've already got there, I'm honest.

Fantastic. No worries. And, Cathy's just, texting saying, thanks.

I learned a lot. So, some really good comments there. Thank you, James.

I think, people have got a lot to take away, which is, you know, part and parcel of what these webinars are about. It's been able to, give updates, but also provide some useful hints and tips that you can take into everyday practise as well. So I'm glad that people are getting a lot of, use and information out of the webinar tonight.

So thank you for that. If you are, if you have enjoyed James's webinar, James has also done a previous webinar with us on, feline primary hyperalersterinism. Is that common disease, is it?

Syndrome, yeah. So that is also available on our website, for you to access as well. So, please do check that out if you haven't had a chance to look at that, already.

The web, this webinar will be on our website within the next 48 hours. So once again, if there's anything you'd like to refer back to, then please do check in in 48 hours' time and it'll be available for you to watch again. So, all that leaves me to do is to say thank you to Lewis, er, for helping out this evening on the technical side.

I know he's been helping a few of you along the day along this evening. Thank you to yourselves for all attending. We've had a fantastic turnout today.

And, obviously, not all of you are on holiday as I thought it might be the case. And, finally, thank you to James for another fantastic, webinar, and we look forward to welcoming you, James back hopefully in the near future and also yourselves. So have a good night and I look forward to seeing you soon.

Thanks a lot.