Hello, it's Anthony Chadwick from the webinarest, welcoming everyone to the final evening of BC 2023. Thanks everyone for coming on today. I know it's the end of the week, you've had a big long week and I hope you're relaxing a bit now with a cup of tea, maybe something a bit stronger, and sit back and enjoy these last two sessions, which for various reasons are recorded today.
We were. Hoping to have David on, but unfortunately he's got a sickness in the family that he'll probably explain to you later on in the video. So both of them are recorded.
We therefore suggest that if you're listening on the website at the moment, sometimes the sound is not great when it's being . When it's being streamed, so you may want to go on to Zoom. It's always best to watch these webinars on a tablet or a laptop or or a, a PC.
So if you're on your phone again, if you can get onto another device, do, but hopefully the phone will be fine. I would like to thank everybody who made this possible to make it a free conference for everyone. I'm thinking particularly.
Of our sponsors and our partners and I will just read them through because I know I will forget one if I don't. So that's simply that's, Mars Veterinary Health, Royal Canon, nationwide, HT ett and obviously Wiki Vett as well, the veterinary student encyclopaedia. We've had all sorts of sessions this week, but we're going to finish off with something that may send you to sleep.
It's anaesthesia. Sorry, it's a, it's a poor joke, but it's a Friday, it's a Friday evening after all. And we're very fortunate to have Stacey Parker, who's giving.
Webinar for us. Stacey is a RVN, a registered veterinary nurse, what you in America, if you are listening from America, called veterinary technicians. She's since gained an extra certificate in anaesthesia and dentistry.
She has, a BVNA oral care nurse certificate as well, BSAVA merit in anaesthesia and Emergency critical care, and, international, . Society for feline Medicine certificates in feline nursing and Advanced feline dentistry. Staceyer currently works with Rachel Perry, who's a very famous veterinary dentist at Perry Referrals.
She's passionate about animals' teeth and veterinary anaesthesia and analgesia, and she provides training in that er for vets and nurses. She also regularly lectures to local, national and international audiences and has had several articles published, and she's going to be talking about local anaesthesia and support of drugs including Vasopressors and anticholinergics, and using the drugs that we may need to use for hypertension under general anaesthetic, so lots of things to be covered, just to move on quickly so I introduce both and let the videos play out and then we'll spend some time at the end. Dave Dickinson is an RCVS recognised specialist in cardiology, he's a director of Heartbets.
He lives and works in South Wales, where he offers cardiology referral clinics and helps lead a 20 strong team at Heartbets. Dave regularly lectures to local and international and national levels, and he's published award winning research, strives to balance expertise in his field alongside a sensible, practical approach to his cases and. Tetralogy of fallow is probably one of the best named disease conditions.
The cardiologists do seem to have the best names for their conditions, don't they? But he's gonna be talking about that today and saying it's not as common as you'd think a practical approach to small animal congenital cardiology. So, really looking forward to these two sessions, do feel free to ask questions, we will pass those over to the speakers and then probably create a blog at the end, so that you can all listen to it, you know, next week or the week after.
Just finally, if you've missed sessions and you do want to see them, the recordings will be available next week that we are charging for the recordings and for the notes. Of course you get your certificates next week as well. But yeah, if you want to buy a ticket, Dawn can put that URL into the chat box and feel free to buy now.
We'll obviously get the recordings to you next week. Anyway, without further ado, I know I've gone on a bit, but thank you so much for for coming to these sessions. It's been a real thrill to see so many of you here.
It's looking forward to hearing what Stacey and Dave have to say. Take care and we'll see you at the end. Hi everyone, thank you so much for joining me on managing hypertension under general anaesthesia.
What a topic to talk about. It's a huge subject that we could easily talk all day about, but what I'm aiming for today is for you to understand, it doesn't have to be too stressful and breaking down why we make some of the choices that we do, or perhaps choices that we should be looking at making. We cannot treat hypertension with just one rule, everyone wants to know how do you treat hypertension, what do I do?
There's many, many ways of treating it. So we're gonna break it down together on this webinar today. What we're not going to do is be horrifically over scientific because I think there's a lot of CPD out there, and the books that you read, they can be really scientific, which is absolutely fabulous.
The more information we have, the better we can be. But I wanted this to be more of a hands-on, practical, what can you take away? And I've broken it down into a way that makes sense for me.
So we'll get started and hopefully this makes sense for you as well. As always, any questions, you can email me, and we can go through things together. So thank you very much for the webinar vet for having me.
I'm Stacey Parker. I qualified in the UK as a veterinary nurse in 2014. I've got my N in anaesthesia and dentistry, and I'm currently halfway through completing my advanced anaesthesia certificate as well.
I've also got the ISFM feline nursing certificate and my official job title is referral anaesthesia and Dental nurse. At Perry Referrals the specialist veterinary dentistry and oral surgery. I also provide in-house and external CPD learning aids and patient warming packs, and please do get in contact if you would like to go through anything that I've covered today.
There's my email. You can also keep an eye on what we get up to and get some tips and pointers and see some interesting cases on our Facebook and Instagram. And if you're interested in any learning guides or patient warming packs, then have a little look at Bertie's boutique on Etsy.
That's Bertie there on the right, he was my absolutely gorgeous boy who we lost recently, and his legacy lives on through all of our lecturing and. Learning aids and things that we can do from there, so let's get started. Today's objectives are together, you will leave understanding how to obtain an accurate non-invasive blood pressure.
Reading, also known as MIBP from now onwards. Know the limitations of our measuring devices. You will understand the component components that make up blood pressure.
You'll learn how to recognise hypotension and acknowledge why we really must avoid hypotension. You also be confident in how to avoid hypotension, and that's what we're really gonna focus on for the first sort of 50% of this lecture is how to avoid hypotension, because if we can avoid something, surely that's a lot less stressful and better for our patient and us, to avoid something rather than need to treat it in the first place. However, no matter how well we look at trying to avoid something, it may well happen, so we need to understand different treatment choices for treating hypotension.
It is a big subject and sometimes it feels like you want to pull your hair out when you keep having hypertensive patients. But as I said, together we're gonna break it down into bite-sized pieces so that it's much more manageable and less stressful for you. So the first question I have for you is which patients should I be monitoring blood pressure for?
And hopefully the outcrying answer is absolutely everybody for every procedure, but I'm aware that sometimes you may not have enough monitoring devices in practise, but hopefully the more you learn about blood pressure, the more we can encourage our practises to be fully equipped so that every patient for every surgery can have their blood pressure monitored. Particularly if you have the machine, whether it's the topler. Or maybe it's an oscillometric and we're gonna focus more on the oscillometric today.
Maybe you don't use it as much because you don't know what to do if your patient's hypertensive or you just don't know how to use it. Get used to using it on absolutely everybody rabbits, cats, dogs, kittens, puppies, long dogs, short dogs, all of them. And then if you're used to seeing using it on a healthier patient, for example, hopefully your pas and castrate the more sort of routine procedures, then you'll be more comfortable using it for your more poorly patients.
Cats can historically be left out from having their blood pressure read. They're more likely, I think, to have more erroneous readings, the more difficult perhaps to get a blood pressure from because they're smaller. Perhaps the Doppler isn't picking up a smaller pulse, but we mustn't leave them out just because it's a little bit more trickier.
The American College of Veterinary and theologists recommends blood pressure monitoring as a minimum standard for managing the anaesthesia care of moderately to severely ill patients. So therefore we really should be trying to meet these minimum standards. So what is blood pressure?
We're gonna talk about it for the next hour. So what is it? Blood pressure is the pressure exerted by blood on the wall of a blood vessel, and this is made up of a systolic and diastolic component.
The systolic is created at the end of the cardiac cycle when the ventricles are contracting, and this is when the pressure in the arteries are at its highest. And then the diastolic is created at the beginning of the cardiac cycle, when the ventricles are relaxing, this is when the pressure in the arteries are at its lowest. So what makes up our blood pressure?
And we're gonna be looking at this calculation the entire way through our lecture today to really pinpoint why we make some of the decisions we do, because as I said at the beginning, there isn't a one-stop recipe for how to treat blood pressure, we need to know what element of it we're dealing with. So your main arterial pressure is your cardiac output, also known as CO, by your systemic vascular resistance, also known as SVR. So that's great, but what does that mean?
So let's start with the cardiac outputs. That's made up of your heart rate by your stroke volume, and the heart rate is how many heartbeats occur per minute, and your stroke volume is the amount of blood pumped by the left ventricle of the heart in one contraction. So therefore, if the heart rate or stroke volume increases, the cardiac output and therefore your blood pressure increases.
Conversely, if the heart rate or stroke volume decreases, as does the cardiac output and blood pressure. So let's break that stroke volume down a little bit further within that cardiac output. This is made of 3 parts, cardiac preload, this is estimated to be the volume of blood in the ventricle at the end of the diastole, representing the amount of blood remaining in the heart after it contracts.
It's also made of cardiac contractivity, the ability of the heart to contract. And that's a big one when we're thinking about some of our heart diseases such as DCM. Cardiac afterload to the resistance that the left ventricle must overcome for blood to leave the heart during contraction.
If any of these 3 parts are suffering from any defects, there will be a decrease in blood pressure and potential hypoxia. Second part of our regional equation, systemic vascular resistance. This is the resistance to the blood flow as it travels around the body.
Systemic vascular resistance assesses the degree of vasodilation or vasoconstriction of the blood vessels. So that's broken that equation down for you, and you'll be seeing that again as we go through the lecture. So don't worry who didn't sink in, we're gonna break it down and show how it all fits into this puzzle.
Let's start by how you can get an accurate blood pressure reading in the first place, because if you're getting something that's. Not reading correctly, this is something that we've done, and you may be trying to treat something that you don't need to treat or ignoring a concern because you're not aware of it because you haven't set your equipment up properly. First of all, ensure the cuff is 40% of the circumference of the limb or tail that you're using.
Most of them are more modern cuffs will have measurement guides on them, so use them. It's a lot easier than trying to measure everything with a tape measure. Have the cuff placed as level to the heart as possible, and please do not use tape on the cuffs.
Order new ones, they're not too expensive. And whilst you're waiting for them to come in, if you do have to use the last cuff that doesn't have any good belt growth, use a tiny bit of tape just to close it, not tape going around the whole circumference of the cuff. So this is what I'm saying with some of the more modern ones.
This is a PET map, cuff, we use those with the PET map machine only, and these have got a good optimum zone, so the video will show you where you can place the cuff so that it's going to read accurately. And that's where we want it at the end there. So do you have a preference?
Do you like using the Doppler? It can be quite comforting and satisfying hearing the whoosh whoosh whoosh of the pulse. Do you have something like a handheld pet map, this is what we rely on primarily, or do you have more use of the multi-parameter?
There's no wrong or right answer here, it's just interesting for what people do or don't have or to show you what else is available if you're only used to seeing one place. Today we'll be focusing on non-invasive blood pressure. We're not gonna go into invasive blood pressure monitoring, that would be another couple of hours, another day maybe.
And I think majority in GP practises, we are tend to be using the non-invasive blood pressure along one of these measuring devices here. But how accurate is the oscillometric, and this is what we're calling our PET maps and our multiparametters. They tend to be most accurate in medium sized dogs and normotensive patients.
Now we know that not all our patients are medium sized dogs and that a lot of our patients aren't normal intensive. And this is why we work on trends and we don't get absolutely fascinated with single figures. And that's why we record on our anaesthetic charts at least every 5 minutes so we can look at trends and what they're doing.
The cineometric will be less accurate if your patient is tachycardic, bradycardic, on smaller patients, if your patient is hypotensive, if your patient is struggling with hypercapnia, if your patient is hypothermic, and if your patient is undergoing any ventricular arrhythmias, this can all throw off the blood pressure reading on the sciometric device. So now we know how to get as fast as possible and accurate blood pressure reading or certainly know the limitations of our monitoring devices. We need to discuss what hypertension actually is, we've already ascertained what blood pressure is, but what does it mean, hypertension?
So the hypertension is classed as a mean blood pressure below 60 or 70 millimetres of mercury. When using a Doppler, a systolic. Below 90 would be classed as hypertension.
And some studies over the years they've shown that cats, when you're using the Doppler, it can actually be closer to the mean blood pressure. So we may tolerate lower thor such as 80 millimetres of mercury. And this is because the body can auto-regulate blood flow to internal organs for the blood pressure of a mean between 60 and 120.
Anything below or above that, and they can no longer auto-regulate and we're looking at damaging the internal organs. Which leads us nicely on to why should we be so concerned about maintaining blood pressure. Well, if we allow that blood pressure of remain below 60 or systolic below 90 for more than 15 minutes, then we're risking our patient of having reduced tissue perfusion.
An accumulation of lactic acids, which is acidosis, which is not good for our patients. We could damage their kidneys, which might not be seen immediately, they may come back just off colour a few months later and you run a blood test and we've given them kidney disease, kidney injury. If they're already struggling with chronic renal disease, then we can actually make that worse if we allow them to become, to become hypertensive under anaesthesia.
Severe hypertension will provide reduced coronary blood flow, and this will cause arrhythmias and potentially cardiac arrest. And being hypertensive can cause a really prolonged recovery, which unfortunately can lead to death, and these are all outcomes that none of us want to be witnessing. So therefore prevention is always best, and you may think, well why on earth have you got pictures of ad the curtain.
Boosters and things, we're talking about hypertension, for goodness sake. It's because I try and simplify things to make them work in my mind, and I think, you know, we don't want our patients to get all these horrible diseases or flea and worm infestations, so we recommend, and it's well known, we, we push and we recommend flea and worm treatment and boosters, and I think the uptake isn't too bad. But if we can also try and prevent anything bad happening to our patients, including hypertension under anaesthesia, then this is best.
So the fact that you're listening to this webinar is amazing. I'd recommend reading around the subject if you're new to it, particularly as well afterwards, because as I've said before, and I will say again in this lecture, prevention is always best from any element of veterinary medicine and science. We can prevent something happening and don't need to treat it.
That is always going to be in our patient's best interest. It's also going to be a lot less stressful for you. So let's look at some prevention of hypotension under anaesthesia together.
I'd recommend a clinical assessment on the day of surgery, ideally by the person performing the anaesthesia. Is your patient dehydrated? Have they had recent losses of any vomiting or diarrhoea?
Are they still having these fluid losses? What's their heart rate? Is it already slightly low?
Are they already a bit tachycardic? And what's their blood pressure? I know we can't get this on every single patient, but you would be surprised at how many you can get them on.
Are they on any medications which may change their heart rate, how their heart works, or how their blood pressure is being regulated? We need to know what's normal for our patients, so by obtaining that preoperative heart rate, we can at the same time, we should be listening for murmurs or any arrhythmias. If any are noted, we should be recommending a workup.
Therefore, the client can make an informed choice. I think it's very easy for us to say, oh, we struggle to get them in for this procedure because of the costs, so I don't think they'll go for it, so we just go for it. That isn't really a decision that should be in our hands.
It's not our patient, it's not our, we're not the owner. They are the property of the owner, and you'd be surprised at how many people would perhaps want a workup. Obviously in some emergency situations, this may not be applicable.
But in our day to day work, although it may be a pain to reschedule or the patient may have waited some time, they may well wish to wait and have that workup if it means things can be safer. They also may decline having a further workup, even if you've noticed something different with their heart. But now the owner has made an informed, educated decision, which is what consent is all about.
As I said, where feasible, obtain a preoperative blood pressure. And when you do, note down what device you used, what limb you used, and what cuff was used, so that you've got a fair comparison once the animal is under the anaesthesia. And ideally you should take 3 readings and note down the average of the 3.
Reading the patient's history is super super important. Have they had a hypertensive episode under general anaesthesia before? And for us, we get so many patients referred to us purely for the anaesthesia side of things.
And yes, we, we, I do mainly perform, oh excuse me, anaesthesia for dentistry and oral surgery patients. But I do also work in other areas at times as well. And I'm not looking just at the history of their dentistry, I'm looking at any anaesthesia episodes they've had, and often our clients are referred to us because they had a hypotensive episode that primary care vets weren't able to stabilise, and that's why they're coming to us, so the anaesthesia team can manage any potential further hypertensive episodes.
However, this could be dealt with in-house. They may not be referring, they may have already had a hypertensive episode with you or with somebody else. And so it's so important that you read their history because then you know what drugs were given at that time.
Did they use any rescue drugs? Were they effective? How did that patient recover after that episode?
Also, we need to be looking at any comorbidities that may make them more likely to struggle with hypertension under anaesthesia. So getting a real picture put together, getting that jigsaw puzzle put together before we start, because if we've seen that they've had a high dose of perhaps ACP and they had a hypertensive episode, we know to try and avoid that drug, or at least hopefully use a much lower dose. So we're on the fore foot opposed to the back foot there.
So planning, as you've probably ascertained, is key. So here's an example of a patient. He is a 16 year old feline patient who has reduced appetite, and I feel that's down to oral pain.
She has chronic kidney disease and she requires dental extractions for painful resorptive lesions and also a fractured canine. Because he's been feeling quite sore, he's also likely quite arthritic, he hasn't been going into the water bowl too much, he hasn't wanted to put cold things in her sore mouth. He's 5% dehydrated.
She's not an aggressive lady, but he's also not overly relaxed in the hospital. So the aim for this little one is to get some analgesia on board as soon as possible. A painful mouth means a painful cat, painful cat will eat if they have to, but not as keenly and not as well.
They often just throw the food to the back and they're more likely to throw that back up. We're also a bit dehydrated, so if I can get them to get some oral fluids and food on board, that's going to be a good thing. If I get this mealgesia, this arthritic cat is also more likely to move around and be more inclined to drink and eat.
I'm therefore going to tempt them with warm, soft, smelly food, and I'm going to admit this lovely lady to the hospital the night before surgery is due. With 5 to 10 mg per kg of gabapentin orally to reduce her anxiety, to reduce my pre-medication anaesthesia requirements, to have a smoother recovery, and also as another form of analgesia. Due to her chronic kidney disease and the fact that she's slightly dehydrated, I am going to avoid the use of non-steroidals at this point.
I will obtain a preoperative blood pressure and we start fluid therapy intravenously, 3 mL per kg per hour. Once she's admitted until the surgery, however, we will be measuring and ensuring that that is an appropriate dose for her by doing regular dehydration checks and regular chest auscultations to ensure we aren't affecting the heart or lungs. I will place this lady first on the surgery list, easier for me because we purely do dentistry.
But as soon as possible in the day to reduce her stress levels, because if I've got a stress, I'm going to need higher doses of pre-medication and anaesthesia, and the higher doses we use, the more likely I am to have negative cardiovascular side effects such as hypertension. Also, I'm more likely to be able to get her to go home that day where the owner can continue the oral medication. She's gonna be much more comfortable, she's gonna be less hydrated, and she can spend the afternoon in the hospital having post-op fluid therapy to support her chronic kidney disease before she goes home.
Be aware with these kitties that they're likely running hypertensive. So the threshold for hypertension has shifted upwards. So we would like to maintain this patient with a mean closer to 80 rather than 60.
As I mentioned, we must think about ongoing losses and replace these with crystalloids. So 4 mL per kg per episode of vomiting or diarrhoea, or other studies have suggested 50 mL per vomit or 100 mL per diarrhoea for a dog, and that would need to be adjusted for cats. As we've spoken about our lovely lady before, we should be checking our dehydration status of our patients and correcting this pre-operatively where possible.
There's lots of different charts out there which will tell you how you're going to notice your patient is dehydrated and how that can be corrected. And remember, particularly if it's an elective surgery, even if the patient has waited a little while to get into the booking system, we can stop. If you're worried that our patient isn't in the best place for surgery, then we can look at stopping, and I know that's not appropriate for all cases, particularly emergencies and such.
However, it's better for us to stop and get our patient into a better, healthier place. And we're less likely to experience issues under anaesthesia, including hypertension, rather than us to just plough on through and try and deal with something that we could have prevented from happening in the first place. And I think an owner will always appreciate an honest discussion regarding that because it really proves we are putting in the health and the welfare and concern of their patient first.
So, let's move on to common causes of hypotension. I think the main one is excessive anaesthesia debt. Inhalants will cause reduced cardiac contractility and vasodilation, and that's isoflurane and sevoflurane, are the two mainly used in veterinary now.
Inherents are often run at too high a percentage, and I wanted to sit down and think why that could be, and I think some of that can be habits. Have you been told how it should be, or are you, is your pre-medication perhaps inappropriate and so your patient is just not stable or settled under the anaesthesia, so you're having to use a higher percentage? Are you worried, particularly if you're new to anaesthesia, or if you're a student, I used to be terrified that my patient was going to get too light under anaesthesia and potentially wake up, when actually we should be terrified that our patients won't wake up.
I'm not saying I want the patient to be coming off the table or having movement at full, of course not, but sometimes maybe we need to educate ourselves more to try and remove the fear. Of our patient becoming too light and look around what we can do to be truly multi-modal with their anaesthesia to allow us to reduce the percentage that we're using on our on our inhalants. I think there can be a lack of understanding about how our drugs work.
We're not taught about every drug and how they work and all the side effects in college or university. So it's all about having a deeper understanding and education, which is obviously what you're getting, which is great by joining us at the congress this week. Another cause of hypertension is hypovolemia, and that can be down to dehydration as we've discussed, or bleeding preoperatively or during the surgery, and we'll discuss blood loss a little bit later on.
It's a huge subject, but we will dedicate a couple of slides to it a little bit later. Hypothermia can also cause hypotension, as can hypoxia. A decrease in surgical stimulation if you've had your percentage of your inhalant for a little while and it's been something a bit more painful, but now we've moved to something a little bit less painful, you may not have realised and looked at adapting your, inhalant levels accordingly.
If your patient is hypoglycemic, they can also become hypotensive, and many, many drugs, ACP being one of the biggest culprits, can cause hypotension. Also, positioning and surgical sites could be thought about. Pressure on the vena cava will reduce the return of blood to the heart, resulting in less blood leaving the heart, causing a drop in blood pressure.
So your patients having C-sections or diaphragmatic hernias, thoracic surgery, large abdominal surgery, look at angling the table to take the pressure off and also communicate with the surgeon if they may be packing something that may have actually put a little bit of pressure there. We're gonna move on to finding this perfect balance that we keep talking about of your patient being lovely pre-medicated, sedated, they've had a good level of analgesia, they're ready for their induction, and then you haven't given them so much that they're gonna become really hypertensive, but you've given them just the right amount, so you don't need much of your induction agent or inhalant, and that's a really fine balance to find. So if we look at this video of this cat, and I think we should be looking at all of our patients before we induce them in deciding whether we feel they're appropriately premedicated or not, and see what you think.
So for me this cat is far too alert and aware and awake and mobile to be appropriately premedicated. So he would be receiving some more preoperative medication. Now it's never wrong to stop and say this cat isn't ready for surgery because if you anaesthetize them when they're quite wired and not relaxed, you're gonna have a stormy anaesthesia and a really stormy recovery, so it's, it may feel like it's quicker to just plough on and crack on regardless, but actually in the long term that's just not going to be the case.
So conversely we look at this gorgeous boy. And I would say that he's having quite a nice time. He is appropriately premedicated and we're comfortable to start pre-oxygenating and go ahead and induce him for anaesthesia.
As I said, it is a real balance, and it takes a little bit of practise and lots of education and communicating with one another to find that. One of the biggest things that can cause hypertension is too much induction agent, whether it's propofol or faxolone, and given it too quick a speed is a big issue. It can cause apnea, it can cause bradycardia, it cause hypertension.
So this video is one to give me a little break to have a drink, but mainly to Show you guys how slowly we actually administer our propofol to our patients. This cat is in for dental extractions, and it has had 0.15 mg of methadone IV and 3 mcg, so 0.003, meg kg of meatomidine IV.
And he's warm in his nice fleecy jacket and he's being pre-oxygenated as he's having his induction. And the induction area is dimly lit, it's quiet, no one keeps walking past, and that will allow you to use far less induction agent and your premedications to be far more effective as well. OK, so you can see that we really do go very slowly with our propofol, and that little fella really needed 1.5 meg per gig IV.
So let's look at how we're maintaining our anaesthesia. Did you know that the Mac of Sifluorine is only 2.5%, and that's the percentage needed to keep over just around 50% of patients asleep under surgical stimulus, the mean alveolar concentration, we'll call it MAC.
The Mac of isoflurane is just 1.2 to 1.7.
If you're thinking that you're regularly having to run these at higher numbers, then we need to look at how we can reduce their use. So a nice calm environment for induction, appropriate premedication, a calm, smooth, slow induction as we've just shown you, and appropriate analgesia and sedation on board and facilitating local nerve blocks as well. And that's for all surgeries and there's many local nerve blocks.
We're not gonna be able to talk about them all throughout this presentation. Hopefully there'll be another one coming soon where you can look at all different local nerve blocks to be used within practise, but they will make a huge, huge difference to you being able to reduce the percentage you're using on your inhalants. There's different ones available, including bivvicaine and lidocaine.
Lidocaine has a quicker onset, but a shorter duration, and buppivicaine has a longer onset, but also a longer duration. So my patient's becoming too light. We need to think outside of just turning up the inhalant for the sake of our blood pressure.
We haven't lost track. We're still talking about avoiding hypertension here. Is your patient due more analgesia?
That could be better for them than just turning up the inhalant. Has your sedation worn off? Do you need to look at topping up that sedation or analgesia?
Can we place a nerve block so I can reduce my inhalant? Do I need a different type of analgesia? If you've given your patient a good dose of methadone?
And you've tried topping it up a little bit and your patient is still reacting. There's no point just topping them up with the same medication. It's clearly not doing anything.
So do you need a little bit of ketamine? Do you need to go upwards and look for some fentanyl? Can we place a local nerve block?
Also, thinking outside of the surgical site, is your patient arthritic? Are they therefore uncomfortable in their positioning? Are they quite long limbed like our greyhounds?
Are you cushioning between their knees or are they touching and becoming uncomfortable? And does your patient quite simply have a full bladder, or are they trying to go for a wee or are they trying to pass faeces, because that can all look like your patient's becoming a little bit too light with an increased heart rate, but actually they're OK. So look at your analgesia protocols.
Are you using and utilising pure opioids such as methadone or are you just using togezic? A local nerve blocks being placed, can you use a bolus or a CRI such as fentanyl or ketamine? And do you ever top up your patient's analgesia?
Did they have their analgesia hours before but now it's worn off? Or did you just not give enough in the first place perhaps? So we keep an eye on when you've given it and at what dose so we can anticipate when we might need to top that up so that we don't then become so reliant on her inhalants, which, yes, you've guessed it, will then cause hypotension.
And these are some of the amazing drugs that we can use. That will help us. So we're gonna look at a few case managements and then we're gonna look at treatments and then we're gonna look at examples for you to think how you may treat cases.
So the first one, obviously I've chosen a dental procedure, but we have got others that are not dental procedures. This is our feline patient who's 18 months old. He has gingivo dermatitis, so he's therefore having full mouth extractions behind his canine teeth.
He's a worried boy, but he's very friendly. We'd seen him at a concert previously, and I knew he was worried, so he'd been dispensed 13 mg per kg gabapentin orally at home. The owner didn't want the liquid, so we used a tablet, and that's why it's a little bit of a strange amount perhaps, but the 13 megbaki equated to one tablet.
He's already on non-steroidals at home, so I'm happy that he's got good analgesia on board. We are going to give him, as you can see on the right, methadone 0.2 mg per gig.
Meatomidine 4 mcg, so a very small dose per kilo. He's also having some potent because I find our gingerous dermatitis cases, the inflammation can actually go down into their oesophagus they've seen in some studies, which can be quite uncomfortable and painful. And I feel like when you're doing quite a big drug cocktail, it might potentially make them feel a bit nauseous as well.
We've induced our patient with propofol and ketamine. It's really good for pain, particularly skin pain and oral pain, so we've given him one big perig IV and that's also allowed us to use less propofol. As soon as possible, once we've cleaned the area, we'll get 4 quadrant local nerve blocks with your pivocaine going in, and because it could be quite a lengthy surgery and we're using a nice low dose of meatomidine so that we don't have huge cardiovascular side effects, I'm gonna be prepared that that might need topping up perhaps by 1 mcg per kilo later on in the procedure.
We got through this procedure with absolutely no GA concerns, a real multimodal approach, and he remained normotensive and comfortable throughout, including into recovery. This is a case management for a brachycephalic patient who's come in for boas surgery, a 4 year old pug, healthy except for the boass concerns and slightly overweight, a little bit wiggly but has allowed us to place an IV catheter, is prone to regurgitation, so is having omeprazole, and the anaesthetist on this case also wanted him to have some Rappitin as well. Because he is brachycephalic, if he gets very stressed in recovery, we're really going to struggle with the swelling in that airway even after the barra surgery particularly.
So we're looking at some premedication of ACP, but a very low dose of 5 mcg per kilo. It's not something we reach for very often at all, but in these cases, we really want to know that they're gonna have a nice smooth recovery. However, we are going to be prepared that we are now looking at vasodilating our patients with the ACP.
So we're gonna look at treatment options for that preemptively, so we have that ready. We're gonna give methadone 0.2 megbag, it's a really good pain relief, and we're gonna add in some meatomidine as well, a very, very low dose, so that we've got that nice muscle relaxant and that we shouldn't be struggling as much with our vasodilation because of the vasoconstriction from the alpha 2.
I know some people aren't comfortable using ACP with meotomidine. We find using them in conjunction together in a very low dose, we don't tend to have any issues. We also then introduced our patient with propofol and we haven't used any non-steroidals in case we are going to be using steroids in case there's any swelling of the airway.
As predicted because we have used ACP, our blood pressure is trending down, our mean blood pressure is the line going straight across. Our heart rate didn't come down enough for me to be concerned that the heart rate was causing a hypertensive episode, and we'll talk more about that later. That as we knew we'd vasodilated our patient, we knew we may need to support that and help with some vasoconstriction for our blood pressure, so against our systemic vascular resistance.
So we had ephedrine 0.1mgbag IV which was given, and you can see the line that had got down to just below 60, has then gone up to 70 and nearly at 80. We chose Ephedrine because it's short acting and we knew we were towards the end of this procedure.
So we have 2 more case managements. This one is for a stay. This is a stressed shih Tzu who's 10 years old, but she does have mitral valve disease stage B1.
A recent echo, we like to have an echo within the last couple of months of anaesthesia, it's stable. No clinical signs at home, which is great, and she has allowed us to place an IV catheter. So this lady had methadone 0.2 mg per kg and then a very small dose of ACP smaller than our previous patients, so just 3 mcg per kilo.
We don't like to use alpha 2 with our patients of mitral valve disease, but actually a small amount of ACP can be quite helpful. We then did a co-induction of propofol and diazepam, so that's nice and sparing our induction agent and adds in a little bit of that muscle relaxant without upsetting the cardiovascular system. We used a local nerve block for the stay as well.
And no assistance was required during this GA for this patient. Had we used now for 2, I thought we would have been in a different situation. And our last example is a pre-medication for a laminectomy.
Our patient is a canine, 8 years old and 11 months. This is likely quite a long procedure of a C5 to C6 dorsal laminectomy, and we've looked at giving just 1 mcg per kilo dexamedatomidine IV for this patient alongside 0.3 mg per g methadone.
We know it's gonna be a long procedure and we really want to look at reducing our inhalant percentage that we're using. So we're looking at a ketamine CRI, so a constant rate infusion during the surgery, so that we can really bring down the inhalant levels. We're also going to use paracetamol, this is only for dogs that's not appropriate for cats at 10 mg per kg intravenously.
Because we have used quite a low dose of the dexametomidine that is going to wear off, so I feel like it's appropriate to prepare another rap for two, same amount again, in case we do need it during the surgery or afterwards, instead of keeping on increasing the inhalant should we need to. And our final one is this gorgeous boy here. He's a male in Thai, he's therefore not had any previous anaesthetics, and I've read his history.
He's 18 months old, he's a Maine Coon. His heart auscultation at Admet was clear, however, he was quite anxious with an elevated heart rate on his preoperative check. His blood pressure was also elevated, but as he was quite stressed, that was dictated down to that.
He had methadone 0.2 mgBig IV and meatomidine 4 mcg per kilo IV. His coinduction was propofol and ketamine so that we could reduce the amount of propofol and inhalant needed, and as we've mentioned, ketamine is really good for skin, and he was having multiple mass removals.
Straight away from inducting this patient became hypertensive with a map of 52. His heart rate was normal, so I'm not going to put the heart rate to blame or try and increase that, but they do need to help how well the heart is working and increase the systemic vascular resistance. We gave him ephedrine 0.1 mic IV, which he was completely non-responsive to.
We then trialled a 5 mil per kilo Hartman's bolus over 15 minutes, which we then noted a new heart murmur which turned into a gallop rhythm and a continued hypertension of a map of 54. At this point, we felt as an elective surgery for mass removals, we were stood only clipping and cleaning. We aborted the surgery and we recommended a follow up echo.
Unfortunately for this patient, it showed that he had hypertrophic cardiomyopathy and that he was also entering congestive heart failure, and medication has been started and this patient is being reviewed monthly by the cardiology team. And this is an example of you don't always have to push through if the surgery allows you to not proceed, because had we proceeded with this patient, we may have had a very, very tragic ending, and that's not something we want to do. So we've looked at preventing everything we can with this patient and haven't been able to prevent it.
We also haven't been able to treat it very well and therefore we've decided that we need some further investigations going on. So, moving on to probably why you're here, my patient is hypertensive. Please help me.
So let's get started on this chapter of the lecture. Do I need to give a fluid bolus? Do I need to use a vasopressor such as dopamine, dibutamine, ephedrine?
Do I need to use an anticholinegenic such as atropine or glycopyonium, which from now on we will just call glyco because it's less of a mouthful. So let us look at how to troubleshoot our hypotensive patients. First of all, we need to try and find out what is causing the hypotensive episode.
In order to safely treat the hypertension, we must first understand what is causing it. So this brings us back to our very first slides that we went through together. What makes up our blood pressure?
Let's go through that briefly together again. Our mean blood pressure is a cardiac output times our systemic vascular resistance. And just to break down my cardiac output a little bit further one last time, your cardiac output is made up of your heart rate and stroke volume.
So there's 3, if not more, but we're gonna focus on the 3 highlighted elements to our blood pressure, and this is why there isn't one fix, because there's already at least 3 elements going on that may need some assistance to get our blood pressure normal. Step one, very simple, not scientific at all. Check the cuff.
They move, they break. Maybe someone put it on incorrectly in the first place. Has it come open?
Has it slipped? Has the velcro given up? Have you put a load of tape on it?
Is it even the right size in the first place? Has the limb or the tail moved below or above the heart? And as I said, has it even been placed in the right location in the first place?
This would be a really nice, easy, simple fix, and it happens more than you would know. If you don't check the cuff and you start pumping all these extra drugs or treatments into your patient, you can do much more harm than good. Step 2, is this just one naughty reading.
If nothing else has changed with your patient, this could just be the machine having a wobble. It could of course be your patient having an issue, which is why you'll be checking all your other parameters, but also why we work on trends. So I'd recommend taking another reading in just a few minutes' time if everything else has remained stable and seeing what's going on.
Is your patient bradycardic? For us, we don't like cats to be below 100 beats per minute. Dogs are much more varied, and we must remember to reflect on their preoperative heart rates.
And this would be to do with your cardiac output because remember the calculation for your cardiac output is your heart rate by your stroke volume. If my patient is bradycardic, I'll be looking at reaching for an antichonogenic. These can reverse a vaguely mediated bradycardia.
They do this by removing the effect of the vagal effect on the sinoatrial node first, and then they move on to the atrioventricular node. This will allow impulses to reach the ventricles. The heart rate may 1st decrease when given.
It can also cause unwanted tachycardia, particularly if your patient was hypercapnic, and particularly if your patient wasn't actually bradycardic in the first place. This will soon settle over 15 minutes or so. Remember you're given this drug because you want to increase their heart rate, so please don't confuse this elevation in heart rate with a lighter plane of anaesthesia and then turn up your inhalant because you're then gonna cause the vasodilation, you fix one problem that caused another.
There's a few drugs you can reach for. Me, I'm a fan of glyco, big fan. I see it's more of a cheerleader, it's more gentle on the heart, it lasts a bit longer.
Atropine, I will reserve for my true emergent cases, but it might be that you don't have the joy of having both of these drugs, so I want to educate you on both of them. Now atropine is capable of crossing the blood brain barrier. It also crosses the epicentre.
It has a rapid onset of action, literally seconds. Duration of working is 20 to 40 minutes. And our doses are 0.02 to 0.04 mg per gig, and they must always be given IV and we need to flush that well with 5 to 10 mLs of saline.
As we said, this does cross the blood brain barrier, so therefore their pupils will dilate and be very light sensitive, so recovery must be in a dim room until they can constrict their pupils appropriately. Atropine, unless it really is a true emergency, is actually contraindicated in glaucoma, and like I said, it's best used in an emergency, but it will not be effective in rabbits. Now glyco is one of my most favourite drugs ever.
It produces a more controlled increase in heart rates and it still has a slightly longer onset, but it's still within minutes, and we've got a nice video to show you. It doesn't cross the blood brain barrier. Please don't give it subcu RIM and don't dilute it.
It's such a slow uptake, and these, you're using these drugs because you want them to work quickly, so use it intravenously only. It can dry out the secretions, they may have a dry mouth for 2 to 4 hours, but the effect on the heart rate can last 1 to 2 hours. It may reduce the heart rate at first, you could use the dose that's too low, so you can repeat that.
And also you can repeat it if it's been effective but not got you quite to where you want it. And doses of 5 to 10 mcg per kilo IV, we tend to start between 7 and 10, to be honest with you, and we find that nicely effective. And just to remember what can happen with the eyes, this is Spider-Man.
Before atropinene we can look a little bit like this. And after atroprine we will look like this. So all the lights going in, they're probably gonna get absolute brain aches, so if you have used it, just be aware of that for your patients for post-op care.
So if a patient isn't bradycardic, perhaps that's tachycardic and elevated heart rate and hypertension can be signs of reduced volume, which brings us back to our cardiac output because our stroke volume is now reduced. Intravenous fluid therapy should always be given, as it says in the title, intravenously. It will not absorb subcutaneously appropriately for what we need it to.
Crystalloids such as Hartman's are ideal, and we start with a 5 mL per kg bolus given accurately over a 15 minute period. This can be repeated up to 3 times if it was effective initially, but remember that fluid therapy is a drug with dose dependent effects. A bonus will be much more effective than just increasing your maintenance rates, but remember, if the problem is that your heart's got a low rate, it's going quite slow, your bradycardia, and fluids will not help.
But yes, it's still part of the cardiac output. But it's not to do with the heart rate, this is to do with the stroke volume. So if you're gonna give lots of bonuses to a patient that's bradycardic, it probably won't be as effective because the issue is that your heart needs to pump faster, no that it needs more to pump around.
We do need to be careful with how much fluid therapy we're giving intravenously. The American Animal Hospital Association guidelines for fluid therapy dictate that dogs should have 2 to 6 mL per kg per hour and cats 2 to 3 mL per kg per hour. And we're not talking about animals they deficits here or ongoing losses that would also need to be calculated in, but for your more routine procedures, we really don't need to be doing the historic 5, 1015 mL per kg per hour.
It's not needed and can cause much more harm than good. Just wanted to throw in here about cats and fluid therapy, as we said it shouldn't exceed a maintenance rate of 3 mL per kg per hour, and just to break it down as to why this is so important, because in studies it has shown that, Patients that, you know, could potentially pass away after anaesthesia with cats, overuse and overzealous use of fluid therapy can be a real culprit. So if we think a total blood volume of a cat, it's only 50 to 60 mL per kg, so the total blood volume for a 3 kg cat is only 150 to 180 mLs.
If we've got a long procedure, it can be any procedure, not necessarily a dental procedure. And you've put your fluids at 10 mL per kg per hour, this cat would then receive 30 mLs of intravenous fluid therapy. Now you may feel like that's not a lot, you know, it's only a tiny syringe, but if you look at the percentage of what that is of their blood volume, you've actually increased their blood volume by the total of 20%.
This will overload the heart and you have to question the patient dependent and surgery dependent, is that necessary? Consider your ongoing losses and think of what exactly you are treating, not just because you've always done it. Promise that we touch on blood loss.
We should be measuring suctioned blood and deducting the irrigation fluid used. We should be weighing saturated swabs and I should say drapes, they should be weighed too. Therefore, we can calculate the blood that has been lost and preoperatively, if we feel there's going to be blood loss or the potential for blood loss in our procedure, we should be calculating your approximate blood volume and what amount can be lost before.
Anything becomes a concern. The blood volume of dogs is 90 mL per kg and cats 50 to 60, on average 56 mL per kilo. When we're looking at a blood loss in our anaesthetized patients, if they've lost up to 10% of blood, then we can replace that with crystalloids, but that 3 to 4 times the volume of the blood loss.
It's recommended and it depends what literature you read as to what colloids you use, but at 10 to 15% we can look at replacing that with some colloids, but you do need to be careful when you use them. And above 15% of acute blood loss will require a whole blood transfusion. This is a really, really good book to read a lot more about blood loss.
This is in brief and as I said, we could be talking about blood loss for a whole session or, you know, a good couple of hours. So this book is really, really good. It has a huge amount of information regarding everything veterinary anaesthesia.
I love it. It's my go to book at the moment. I was kindly gifted it by a colleague, and I cannot recommend it highly enough.
And this will give you a lot more information on everything we've covered today. So step 4 of why is my patient hypertensive? Have you vasodilated your patient?
Have we used a hefty dose of ACP? Have we used a hefty dose of an alpha 2 such as methotomidine or dexamedotomidine? Is your vaporised setting far too high, and this is on the other part of the equation that we just keep going back to our friend there, and this is systemic vascular resistance.
In this cases. We will need to be looking at giving them some medication to counteract that, which we will cover shortly. Or maybe you just need to reduce your inhalant in the first place and that should always be your first step.
Step 5 is your heart contracting efficiently. Now, of course we cannot see what exactly was going on with all of our patients' hearts with the naked eye at all. However, if we already know they have an issues such as mitral valve disease or dilated cardiomyopathy or hypertrophic cardiomyopathy, then this could be the case.
This can also occur in geriatric patients just due to the reduced cardiac reserve as they get older, and this brings us back to our cardiac outputs when we broke down our stroke volume earlier. So choices of treatments could be ephedrine. This is ideal for mild hypertension of a map between 45 and 60.
It will increase your map, your heart rate, and your cardiac output, and it does this by increasing your systemic vascular resistance. Bolus for dogs is 0.05 to 0.2 mg per kg IV and bolus for cats slightly less than 0.05 to 0.1 mg kick IV.
The duration is very short, which is why we only showed you us using it earlier for our Briss procedure because we knew we were on the way out of surgery. It only lasts 5 to 15 minutes. You can repeat it a couple of times, but actually you'll be better reaching for something like dopamine instead of keeping on repeating a drug.
We do dinote this so that we can give it slowly prior to administration and be careful in patients with cardiovascular disease, particularly for their own digoxin, because it can cause arrhythmias. Therefore, we ideally should have our patients on an ECG if we're going to use this. If you're pregnant, please wear gloves and do watch for tachycardia or arrhythmias at higher doses.
So for me we'll increase the cardiac output and the systemic vascular resistance, the mean arterial pressure and the heart rates, it's a good all-rounder. It's a CRI you do not give this by a bolus. The dose is 2.5 to 10 mcg per kilo per minute.
It's very potent and short acting, and it will increase your cardiac output. Accurate dosing is absolutely imperative, so you must use a syringe driver, do not just be pushing this in a syringe by your hand. And discontinue the dose or reduce the dose of cardiac arrhythmias or seen.
So, well done, we are nearly there, and we're gonna go through some examples together. Have a little think. Are you happy with this blood pressure reading?
So for those of you not familiar with a PET map, the asystolic is on the top at 134, the diastolic is next at 74, the mean is 91. My heart rate is 86. My SPO2, because that's on this as well.
We've got a nice fancy one, is 98%, which is great, and my heart rate, according to the pulse, matches what it is on my blood pressure reading as well of 86%. Are you happy? How are you feeling if this was on your monitoring device?
I would be happy, relax. It's not a a trick at all. This is a normal reading, particularly as the heart rate matches the machine's reading of the heart rates.
I will still continue to intermittently check the cough position to make sure that it's not reading in thin air, and I think everything's lovely, so we need to get into a good practise of checking our cuff position, even if we're getting nice readings. So for me, I felt very, very pleased, like this smug little cat on the right, and I discontinued as I would with all my patients to continually closely monitor them. How about this one?
So like 103, diastolic 52, the minus 73, and the heart rate is 72. What would you do in the first instance here? If I told you this was trending downwards.
We can check the cuff position, check the depth of the patient, the palpable reflex, and the jaw tone. We can look at reducing the inhalant here as we seem to be trending downwards with our blood pressure. And remember, on the indolent, we don't have to go from 2.5 to 2 to 1.5 to 1 or 2 to 1 or 1 to 2 to 3 to 4, and I hope you're not going to 4.
We can go in between, so 1.2, 1.4, 1.
Check to see if any of the other parameters have changed, such as respirator or ide or CO2. And also remember we're not gonna just worry, instantly unless a lot of other things have changed over just one reading on one vital parameter. So we'll get another reading 3 to 5 minutes later.
So for me, I checked the cuff, I had a look at my tidal CO2 and noticed that the trend had increased slightly with that one. I didn't have a palpreil reflex and I had a nice relaxed jaw tone. So I reduced my inhalant, which at the time was isofluorine, from 1.5% to 1.2%, and my next reading was much more enjoyable with a mean of 86.
So tell me what you think of this reading, or, I know you can't talk to me, but think of amongst yourself. Are you happy with this reading? Systolic of 145 with a diastolic of 79, a mean of 100.
So, as we've gone through, check the cuff, check for a change in any other parameters and see if the surgeon has maybe moved to a new surgical site, because this is actually looking a little bit hypertensive. And I think we get so stuck and worrying about a patient being hypertensive, we kind of forget that they can experience hypertension, and that's not something we want either. Again, check the cuff, check for changing any other parameters and see if the surgeon's moved to a new surgical site.
This is what I did. I also noticed that the heart rate in myrate had increased and my idal CO2 had decreased, and that's all telling me my patient might be a little bit light under the anaesthesia. So I liaised with the surgeon as to whether we had started on a new quadrant of the mouth of which we had.
I increased my inhalant, which is isoflurane from 1.2 to 1.5, and I monitored for any further changes of my patient becoming too light under the anaesthesia.
I took another blood pressure reading in 3 to 5 minutes' time and then my map was 83, which is fabulous. My heart rate reduced slightly, my respirate also settled a little, and my tidal returned to normal. So for that, my patient was just a little bit too light under the anaesthesia.
I started by gently increasing the inhalant, not by huge amounts, but to see where that got me. If that had reduced my, I mean, below 70, then I would be looking at adding in other medication at that point, instead of just increasing the inhalant because otherwise I'd just be pushing my blood pressure downwards. We're nearly there, well done.
So this is tonic of 107 with a diastoic of 31, a mean of 56, and my heart rate is 99. Are you happy? I'm not overly happy, I'm gonna check the cuff position.
I'm gonna check my other vitals, including heart rate and respir rate. I'm gonna look at whether I can reduce my inhalant. And what if I told you this is actually a feline patient?
The heart rate's only just under 100, admittedly, but I do kind of like my patience of cats to be sort of around 110, 120. All my other vitals were within normal limits. However, my heart rate was only 99 beats per minute, my respiratory rate was 12, my Nidal was 37, my temperature was normal, and I'm only on 1% of the isoflurane, and local nerve blocks had been placed.
So for me, I feel like this blood pressure dropping like this is to do with the fact that my heart rate has dropped to just below 100. And yeah, you guessed it, I'm reaching for the glycopyonium. This video shows you the nice onset and sort of the cheerleading effect that we can get from the glyco.
So bear with it and you'll see I've administered it and then started to film and you'll see a difference on the heart rates. And by the time I've reached for my glycoin for my calculation, I've dropped the heart rate already, it's already gone from 99 to sort of 89, so I can see that this really is a hypertensive episode caused by bradycardia. You can see it's starting to kick in now.
But we're not going tachycardic, we don't have a sudden scary increase. Nothing else has changed either, so I don't get this confused with my patient trying to wake up. And this is a much nicer heart rate for my feline patients.
I'm comfortable with this. Nice 1:30. Our last slide is just to discuss paediatric patients because they do run a little bit differently and they can be a little bit more of a tricky anaesthesia, I find.
This is because the paediatric patients will rely primarily on their heart rate to maintain their cardiac output, so you must be careful with using alpha 2 doses and also high opioid doses because both can reduce the heart rate. We must avoid fluid overload with these guys as well, and they're more likely to require an anticholinenogenic such as your glyco or atropine. We mustn't confuse the base increased heart rate with a light plane of anaesthesia that's easy to do and then we keep turning up the inhalant because they've got a higher heart rate, but that's just gonna cause vasodilation and bradycardia, which, yep, you guessed it, will lead to hypertension.
They're also gonna have a high resting respiratory rate, so don't confuse that with being light. And if they're hypothermic and hypoglycemic, and that is more common in our paediatric patients, as we know, that will also predispose them to bradycardia and therefore hypertension. So coming soon to Bertie's Boutique, we will have some posters, pocket guides on managing hypertension.
So email me if you'd like to go on the waiting list for those. And well done, for one, joining us. You've probably had a busy week, a busy day, 2, for choosing a hyperintensive and how to manage it webinar.
If you're feeling like this gorgeous cat on the left, I completely understand. We've covered a lot, in a different way perhaps than you've been taught it before. Don't worry, take one piece of information and see if you can apply that to your patients next week.
And also read around the subject. You won't be able to know and remember and be able to implement everything just from one webinar, but it's a really good step. This might be the 2nd or 3rd step for you.
As I said, I do recommend this book, but there's plenty of others out there. This one's really chunky, but it kind of talks to you like someone's chatting to you. And I really appreciate that with this book, so this can really help you to further learn what we've gone through together.
Thank you so much. Well done for sticking with me, for what I think was exactly an hour. Please feel free to get in touch in any of the ways that are on here or through the webinar vets.
It's been really nice to be asked to lecture for them again. It's always a pleasure, and I hope that you've found something useful, and I would love to hear from you if you have any feedback or any questions. So thank you so much and enjoy what's left of the conference, and I hope you've enjoyed it as the week's gone on.
Thank you for inviting me to speak. My name's Dave Dixon, I'm a cardiologist at Heart Vets. And this evening I'm gonna be talking about terology of fallow.
It's not quite as common as you think. Hopefully this will be a practical approach to small animal congenital cardiology. I have no conflict of interest to declare, and I will be donating my speaker's fee to the Motor Neurone Disease Association.
Oh wait, it's Monday morning. Your favourite client has just walked in with a brand new puppy. Everybody is all smiles and waggy tails.
Your client assures you that the puppy was the pick of the litter from the best breeder around who is also a close family friend. And merrily tells you the whole litter have been checked already and are super healthy, so no problems. But you know what's coming, don't you?
Yeah, you guessed it. This poor little pup's got a heart murmur. Let's have a listen.
So what's your diagnosis? You've had a listen. There's a lots of possibilities, but there's a few common ones, and I want you to think of these possibilities, what, what could be on the list.
It's tricky, isn't it? It's a very tricky thing to do, to listen and know for sure what's going on. And instead we're gonna play a little game.
Here's a quiz, you've probably seen these before, these emoji quizzes. And they are films. So have a look at these and see if you can work out which famous blockbuster films all of these emojis represent.
Hopefully the first one is already come to you. It's Ghostbusters. Number 2, well, that's the Martini, it must be James Bond.
Number 3, I see an alien phoning home. What's number 4? Well, this is a emoji representation of a puppy vaccine consult turning into a heart murmur investigation.
And I think that's a pretty fair representation of the steps involved when you find these cases. And that's because approaching congenital heart disease is not easy. We have a whole list of diseases to learn.
We have, well, pages and pages of them if you get down to the detail, but even in the common ones we've got a whole load of, of things to know and the species' differences. So whilst we can load all the ones for dogs, what about all the ones for cats? And this is a clearly a, a tricky area of medicine.
Then we've got the problems of figuring out which disease it is, so we not only have to know all these diseases, we have to know how to diagnose all these diseases. We've got to talk to the owner about costs of investigation and worse, the costs of treatment. Treatments run for these can run into the thousands or even tens of thousands.
And also we need to be ready to break potentially devastating news to the owners of a, a cute puppy or kitten that nope, we can't do anything and their pets, their their lovely brand new shiny pet is probably going to die, possibly quite soon, of a disease that we can't fix. And you've got to do all of this. In 15 minutes.
You know, if you're lucky, if it's not a double booked appointment slot or 4 puppies in the boot of a car. You guys are absolute legends, to be quite honest, it's no wonder you all look so tired. So what are we going to do?
We can't just bury our heads in the sand, we can't just ignore the problem and hope that someone else will pick it up, although I know that is pretty tempting to do. We've, we've got to have a structured logical approach to these cases, so we know how best to manage them, we know what to do and when, and how to get through the 15 minutes of hell. First, I'm gonna talk about the approach to the clinical examination, making sure that you get all of the available clues to help guide the rest of the consultation and and investigations to follow.
Then we'll have a quick look through the most common congenital diseases, so you know what's most likely. And what to look out for. And then finally we'll we'll discuss the treatment options that are available so that you know which cases to prioritise.
Obviously it, it becomes pretty academic when we're diagnosing these incredibly rare defects that can't be cured. It's brilliant for cardiologists, but not great for anybody else. However, there are some common conditions that we can treat and some that we can even cure if we get to them in time.
So it is not a, a, a totally academic process. There are cases that will really benefit from input and treatment. Here's a ACDO being deployed in a PDA, you can see the little plug being slid into position, and that's a classic one that we can cure, you know, if we get that dog early enough before too much damage is done, as long as the owners can afford surgery, then we can fix and cure it for life.
Let's start right at the beginning then, so what is a murmur? A murmur is flow that we can hear. Now, normally in a healthy system we don't hear flow aside from when it stops, i.e.
When the valves close. So we hear the normal heart sounds, lubbed up, which are the the AV and the outflow valves closing. But otherwise we don't hear normal blood flow most of the time.
That's akin to a river, nice wide river running in its channel with no turbulent flow, so it makes no sound. However, if you stick some rocks in that river and you create rapids, all of a sudden you can hear the flow. It's the same flow, it's just now turbulent, which and it creates noise and therefore we hear it exactly the same thing in the heart.
The reasons that we get, the, the, the reason that we can hear the sound is because it's turbulent, and we're able to pick it up with a stethoscope. Now there are 4 main reasons why you get a murmur. The first is simply hearing normal flow.
That can occur for a variety of reasons, but we call them by lots of names, but typically I, I, I like the term flow murmurs. Just implies that we're hearing normal flow, and it's, it's not primary cardiac disease. The next is the next cause of, of a heart murmur is a leaky valve.
Here we've got the classic example, mitral regurgitation. So valves are meant to seal flow one way so that they protect against flow going back the wrong way. If those valves allow blood the wrong way, typically that flow vibrates the valves structure, and just like a reed in a wind instrument, that creates sound or it creates vibration which we hear as the heart of.
Then we've got holes in the heart. So after flow murmurs and leaky valves, we have holes in the heart, and this is a, a ventricular septal defect. You're looking at the heart, it's upside down and what you're seeing is a big green jet entering the right ventricle from the, what's called the perimmembranous region.
So it's where the aorta attaches to the left ventricle. There's a little hole and we get a jet of blood squirting through that ventricular septal defect. And then finally we've got extra cardiac shunts, the most common of which is one we've already mentioned is that's a PDA patent ductus arteriosis, and that's a, a, a tube that connects, the two great vessels, allowing blood to flow through all the time.
So we know what causes murmurs, where and how do I listen for murmurs. I know this is basic stuff, and bear with me. I hope it will be useful, even if you've been doing this for 30 years.
There's always stuff you can learn. And if we take a a a rational approach to to listening to auscultation, we can get a lot of information. So the first tip, actually, I'm listening to murmurs is before you get your stethoscope out, palpate.
And I, I try and teach students palpate before you auscultate. It doesn't exactly trip off the tongue, but it's a useful thing to to to try and remember to do. When you're palpating.
Use the palms of your hands, not your fingertips. People think that the fingertips are the most sensitive part of the hand to vibration, but it, it's usually not actually, it's usually the base of your fingers on your, on your palm, underneath your knuckles if you like, the palm side of your knuckles, and you'll find that it's probably more sensitive to vibration. Feel both sides carefully.
The best way to do it is to, is to wrap your hands around either side of the apex beat and just feel, what's going on. Especially in puppies, you can pick them up. I do this routinely, you just pick them up and cuddle them, you can pretend that you're, you're cuddling them for fun, but actually you're palpating for a thrill.
If you detect a vibration, a thrill, that's really important information. And that's, that's the key is palpate over the apex beat and around the heart, especially in puppies and kittens, they're small, so you can get your whole hand, whole palm round the area of interest. Because you can palpate the apex beat which gives you a lot of information and detects thrills.
This gives you a quick heart rate, so palpatingapic beat allows you to just quickly ascertain the heart rate before you stethoscope and count it properly. It gives you some idea as to the strength of the heartbeat. There is obviously some variation, the difference between a fat Labrador and a thin whippet's going to be dramatic.
But if you put your hand on and notice a very strong apex beat or concurrently an absent apex beat, that can be really useful. I've diagnosed intrathoracic masses purely on the presence of an absent beat, on one side, and then when you listen, you can't hear the heart sounds on that side either. There must be something in the way.
So it's a very useful, quick thing to do. I can give you an idea of the size of the heart, because if you can feel the heartbeat over a large area of the chest, like in a cavalier with advanced, with a loud heart murmur or micro advanced mitral valve disease, if it's got significant cardiogaly, the heart's bigger, it's pumping more blood, so you get an idea of the size of the heart, so it's useful, useful clues. Most importantly, thrills.
A thrill is just a vibration that you can hear. Sorry, the vibration that you can feel with your hands. The, the, the, the murmur is so loud, it's now vibrating.
I tell owners it's a bit like when you turn the speakers up so loud that they actually vibrate, because they're rattling with the sound, and that's exactly what a thrill is. So a thrill is an extremely loud murmur, one that you can feel. And these are important.
Never neglect a thrill, never ignore a thrill, never say that a thrill, er, is nothing to worry about because they're always important. They might not always be dangerous, but they're always important. My next top tip is to use a medical instrument and not a child's toy.
I get fed up of seeing stethoscopes like the one on the left in practise. You can't hear anything with them, throw them in the bin or give them to your kids to play with. You need a decent stethoscope, I think for small animal practise.
Most of the time you only need a paediatric head. You can have the adult head as well, it comes with your stethoscope, but, mine comes with two, and I took the adult one off, and I honestly haven't used it, in 10 years, apart from once or twice listening to horses. Alright, so we've picked up our stethoscope.
Let's remind ourselves of a bit of cardiac anatomy. So there's our dog, and that's roughly the position of the heart, and you know that because you're used to taking chest X-rays. So just imagine a lateral chest x-ray sort of superimposed over that dog's thorach, and that will help guide us on the, the location of where all the cardiac structures are.
So if we take this diagram of the heart, it's a human, obviously it's a diagram of a human heart, it's upright and labelled superior and inferior vena cava. But actually this picture is quite useful because it's roughly aligned with the shape of a a a canine heart on a lateral radiograph. We call it the left ventricle, but actually it really is, should be called the caudal left ventricle.
And we call it the right ventricle, but it really should be the cranial right ventricle. So the, the right ventricle is actually cranial, and to the right, the left ventricle is caudal and to the left, unlike in a a a human. So this really helps us with a radiograph is to orientate ourselves where we are.
So the left atrium actually is cordo dorsal on that radiograph. It it's it sits does sit to the left hand side, but it predominantly sits caudal. The left ventricle sits right underneath it, so that forms the er the apex of the heart from this view.
The right atrium sits cranial to the left atrium and also wraps around it on the right hand side, so. It's not, it it almost covers almost the top of the, the whole top of the heart, left a and poking out slightly further cordially. And then they've got the right ventricle, overlying the left ventricle and wrapping up and around and into the pulmonary artery.
And this is all useful because it helps us know where we're listening for murmurs. There lots of ways to remember this, this is the way that I remember and teach. I use an ABCD, approach.
So we start at the apex, that's where you feel the apex beat and in especially in normal dogs, the apex beat, you'll be listening over the mitral valve. As the heart enlarges things can move and they can get less distinct, but if you've got, for example, a, a, a quiet left, apical murmur of mitral valve disease, you will hear it just directly pretty much over the mitral valve, and that's the apex region on that diagram on the left. The base is above it, it's not usually directly above it, it's above it and slightly cranially because the heart is tipped on a slight angle.
So you've got apex base, you've then got cranial, which is one, at least one if not two rib spaces further forward from your basal position, and then you lift your stethoscope directly up from there, dorsally from there right underneath the scapula, really cranking into the armpit of the dog. And that's the, that's the ductal location A, B, C, D. On the right side, you've got 3 locations that mirror the 3 on the left, so you've got ABC apex, base, and then cranial.
Now when you're doing an auscultation. It can be a little bit overwhelming to think you've got 7 places to listen to, but if you just put this diagram in your mind's eye when you're listening, start the apex on the left. Always start in the same way, always do your auscultation in the same way.
Start the apex, lift cranial for the base, very cranial for the cranial position, and then lift up again for the ductus. Do that on the right hand side. As well, you, you can forget the ductal location on the right hand side, and if you just have a, a wave of your stethoscope over those locations, you will detect, all pretty much all the cardiac murmurs there are.
If you've also palpated first, so you've put your hands on, you've felt for any thrills, remember to always listen over where you felt the thrill, because that is clearly where the murmur will be loudest. And that can really help you if you then aren't sure where it is, start at your apex and move around until you've located the murmur. It gets a lot easier with practise.
So if we just look at the left side of views, A, B, C, D, where do they er correspond to? So if we put the heart diagram up again and and sort of place it over the, the murmur location, at the apex, we're we're looking at the mitral valve. So we're towards the back of the heart and we've got mitral regurgitation.
The reason we hear it there is that the, the vibration through the valve translates down the cordi tender and sort of rattles the cordi, the valve structure itself, and that's where it's loudest, the sort of the ventricle and the atrium turns the echo chamber and and create the sound. So that's our mitral murmur, mitral over the apex. As we then move dorsally and cranially, we go over to our aortic valve.
That's our base position, our left base corresponds to the aortic valve. Move cranially and as you can see on the diagram, we've got the pulmonic valve. The pulmonary valve is cranial to the aortic valve on the side of the chest, and we're approaching it on the left lateral side, so that gives us our, our, pulmonic location at the left cranial point.
And finally we've got the duct test, the ductus sits between the aorta and the pulmonary artery just above the heart, and that gives us our ductal location. Often the sound will vibrate along the aorta, and so that's why you hear it quite highly, high up in the chest. This is where probably a lot of you will have learned your PA map or PAM acronyms for remembering murmur locations, but I much prefer A, B, CD because you've got to remember to listen to the doctor.
If we move on to the right hand side. We've, we've got the three locations VAT VAT, so you've got Palman VAT. On the right hand side, the.
Apical location is tricuspid, so on the left it's mitral, on the right it's tricuspid. The basal location is aortic again. If you listen cranially on the right, that's where we listen as we hear most VSDs.
So most VSDs are right cranial location. So now we've located it, we need to describe how loud it is. And this is a, a point of contention for certainly for me, I think for other cardiologists as well, and I'll tell you for why.
Now you can grade the murmur and the most commonly used system and the one that cardiologists advocate, is a grading system, from 1 to 6. Often we'll use Roman numerals for reasons I don't understand, but probably something to do with trying to look clever. .
Grading system with 1 to 6 is, is that standard, I guess. I don't like it, and actually I just prefer to describe what I hear. I like to use terms soft or quiet.
Moderate, which means the same as the heart sounds. Loud, which is louder than the heart sounds and thrilling or palpable. Why don't I like the 1 to 6 system?
Well, it, it's inconsistent, so we know that cardiologists disagree with each other, about when grading, and we know that we disagree with ourselves when grading. If you take dogs out of the room and listen to them again, you will grade differently a proportion of the time, so clearly that's not a very good system. It's also confusing to people because they quite often forget the grades, and I see a lot of the time people using, mixed grades, they'll say oh grade 2 to 3 or 3 to 4.
Well, the way that the system is supposed to work, that can't happen. It's supposed to be a mutually exclusive system, and it isn't. We're listening to a sliding scale of volume, of course you can't just arbitrarily put it into 6 categories.
We're just trying to make it a bit more sciencey. Also, it confuses owners. We've, we've done research, showing that both with mitral valve disease and with congenital heart disease, grading out of 6 serves no useful purpose and you can grade out of 4 using a descriptive scale, without losing any clinical information and simplifying it.
So I'd always rather simplify if possible, . It, it stresses owners out because you describe a number, you give them a number, and they don't know what that means because you haven't got time to go through and explain what it means. You, you say, oh, it's a grade 3, well, last year it was a grade 2, what do I do?
What does that mean? Or I, I get them coming in every week, I'll get an owner say, well, one vet said it was grade 2, but this year it's a grade 4. It's got twice as bad and and they don't know what that means.
They just hear a number on an arbitrary scale and are scared by it. I'd much prefer to say, well, your dog's got a soft heart murmur. Soft means this, this is what we're talking about.
I can feel your dog's heart murmur. It's so loud, it's important that we do these tests. It, it allows us to simplify things and explain things in a much better way, er, rather than just relying on these, these daft arbitrary numbers.
Anyway, that's what I do. So as well as describing the location and the loudness of the murmur, we also describe the timing, using typically three descriptors, systolic, diastolic, and continuous. Here's a systolic murmur.
And the clue to that is it occurs during the heartbeat when you feel the pulse. It's short and the murmur lasts about the same amount of time every time, and there's a gap in between. So this is what you're used to listening to day in, day out, because the vast majority of murmurs in small animal practise are systolic.
If in doubt, guess systolic. Diastolic moments are much, much less common. I hear probably fewer than one a year.
And diastolic moments occur only during diastole. Here's one actually from a horse with aortic regurgitation. Lovely.
And you heard that really long one, that's because the horse had a little pause and during diastole the the leaky aortic valve continued to leak. You can hear them in smaller practise, but they are very, very rare. So don't really worry about diastolic murmurs.
The continuous ones are not that common, but they're important and you don't want to miss them. Here's a continuous murmur. So continuous murmurs, you hear all the time, you hear a usually a peak during systole, but they're present all the time.
It can be tricky sometimes to tell, especially in a fast heartbeat, if a murmur is continuous or just very loud systolic, because a very loud murmur overlaps so much that you don't really hear the diastolic component. But if you listen carefully over the all locations and you really locate the murmur, you'll usually be able to hear the, the pause between systoes in the moment if it's, if it's systolic only. Now you can use other descriptors on top of these, so you can start to say things like hollow systolic or pansystolic or late diastolic, early cyst, you know, and so on and so on.
I, to be honest, I find it gets confusing and doesn't really add much information. We've already got the important descriptors location and loudness. It's likely to be systolic or continuous, so that's a helpful thing to say.
Starting to get fancy using other descriptors, personally, I think it's a waste of time. It's something we've borrowed from human medicine and we, we act like we know what we're doing with it, but I wouldn't worry about it too much. So we want to describe the location, the loudness and the timing.
Is it soft, moderate, loud, or thrilling? Is it on the left or the right? Is it on the apex, left apex, right apex?
Is it the base, is it cranial, or on the sternal border, and in er er in young animals or any animal really is, is there a ductal murmur? And finally, timing systolic. Brackets diastolic because they're so rare or continuous.
So if you describe those, that gives us a huge amount of information to work with from the auscultation. So aside from the auscultation, what else can we be doing? The, the other key components of the cardiac examination, well I've already said the first one, palpate, palpate before you auscultate, palpate the apex beat, get the clues that you can from the apex beat as well as for feeling for any thrills.
Listen over where you feel the heart's strongest, that's typically the apex on the left-hand side. But make sure you do the methodic listen over all regions, just to make sure you don't miss anything. And this will take you a whole minute.
I know that feels like a long time when you're listening, but it's a good, minute that you don't have to listen to the owner, which is helpful. And if you're not sure, which is absolutely fine because this is not easy, ask for a second pair of ears. You know, if you're, if you're, you hear something but you can't quite, quite get to grips with it, ask for a second pair of ears because that can help just to, to, to be a bit more certain about what's going on.
Don't just worry about the terminology, don't worry about the numbers, the grades, all that stuff. Just describe what you hear. Even if you just write down what you, you know, I, I heard it on the left hand side a bit above the apex, and it was as loud as the heart sounds.
That's useful because we can work with that. It's much better than using a bunch of, quite frankly, outdated terminology. Make sure as well as listening that you record the heart rate and the heart rhythm.
You know, it's no good saying fast or slow because your fast not might not be the same as my fast. My fast in a heartbeat's 300. My slow is 40.
But I would write the number down because that's much more useful. And describe the rhythm. Again, don't get too technical, just describe, oh, it was fairly regular, it was a bit irregular but probably sinus arrhythmia.
It was very irregular, it was chaotic. I heard a regular rhythm with an occasional early beat, stuff like that. Stop worrying about regularly irregular.
I can't even really say it properly, it's a mouthful, so don't worry about stuff like that, just describe regular. Irregular, chaotic. So that's our cardiac auscultation, as well as that, er, as well as obviously using your hands and your stethoscopes, don't forget, look at the, the gums, look at the colour, look at the jugulars, because that tells you about right right heart pressures, and feel for ahemeral pulse, because that can give us clues about heart function as well.
Obviously there's lots of other components to clinical examination, but I'm just focusing on the cardiac aspects of it in this talk. So now let's think about the most common causes of murmurs in young animals. If we take dogs, and we've got pretty good data behind this, if you look at all the studies, that have studied prevalence of, of congenital heart disease in puppies or dogs, these four crop up most commonly.
So we've got pulmonic stenosis. We've got sub-aortic stenosis or just aortic stenosis. We've got a patent ductus arteriosis, PDA and ventricular septal defects, so they account for nearly 90% of canine congenital heart disease.
Just for reference, hence the title of this talk, tetology of fallow is about 1% of cases. And I guarantee that if I've got students and I ask them the cause of a murmur, tetralogy will nearly always crop on the list. Because it's fun and it's interesting and everyone takes time to remember those four lesions and all the rest of it, but it is rare.
If you have a couple of to allergies in a career, in practise, you'll have had a busy, general practise, and if I've had maybe 20 of these in a career, I'll have had a very busy cardiac practise. They're not common. What about cats?
The problem with cats, as always, is they're cats. They have no rules to follow or or, certainly fewer rules to follow than dogs. The four most common defects are, ventricular septal defects, patent ducts arteriosis, PDA, tricuspid dysplasia, and mitral dysplasia.
So the valves dysplasias are a bit more common in cats than they are in dogs. Those 4 lesions account for about half of cats, . Disease, cat congenital heart disease, again, interestingly, tetra allergy, actually about 7% in cats, so cats are more often get, what we call the cola trunkal defects, so problems at the centre of the heart with all the plumbing.
The problem is that cats can get practically anything, and they're very difficult to tell apart. So we're gonna use some rules or some guides in dogs, we'll talk about cats after that. The other one that's missing from the list of course are flow murmurs, which I mentioned earlier.
Flow murmurs are super important, because they're common, very, very common, but they can be a bit of a minefield. So first let's talk about flow murmurs. They're also known as innocent, functional, physiological variety of of names for them with different causes.
But I just like the term flow moment because it's easy to understand and remember. another way of thinking them is, is pathological or non-pathological, and non-pathological are flow murmurs, and pathological is everything else. It becomes important, particularly when I'm seeing cases with low murmurs, because I've got to reassure an insurance company that, although the dog has a murmur, it doesn't actually have a disease.
There's a good er paper summarising these, and this table gives a nice summary of, of the way to try and tell the difference, but typically, . Flow murmurs are soft. I, they can be musical, which means they can have little squeaks and sounds within them, not just a but a whoop whoop, or things like that.
And they're usually short duration, so they don't usually last the whole of Sisterly. More importantly, they are never loud or thrilling. And they are never continuous, so you cannot have a continuous flow murmur, you cannot have a thrilling flow murmur.
Try to avoid calling them puppy or kitten murmurs because a puppy with a PDA has a murmur, but it's not a puppy murmur, it's a PDA murmur. So I don't like those terms because it confuses people and I think sets people at ease a bit too quickly. Romas are a diagnosis of exclusion.
You can't ever be certain just by listening. You can have a good guess if you're experienced, and I'll, I'll usually have a guess, but they are a diagnosis of exclusion, not 11 to be made just with a stethoscope. And again flow moments, it's just that laminar flow turning into turbulent flow for some reason.
Now I said not not to believe your stethoscope, and you can never diagnose a a flow murmur, just with a stethoscope, but that's true even with cardiologists. I thought both of these, on the left is a dog, and on the right, we've got a cat. I thought both of these were flow murmurs.
The one on the left, I, I confidently predicted to the owner, which is always a way to, completely set yourself up for a fall, isn't it? But I confidently predicted to an owner. The echo was a waste of time, but we'll do it just to be safe, cos it sounds like a flow murmur to me, don't worry.
Turns out the dog has no atrial septum. And so it had a very soft murmur, sounded like a flow murmur to me, but it's, actually got no a septum. So that was an embarrassing one to get wrong.
And on the right, I've learned my lesson by now. I said, I think it's a flow murmur, but I think we should do the echo to make sure because this, this cat just, you know, it's a cat, you can never tell. And lo and behold, it had toy of fellow.
So you can't tell with a stethoscope for sure, not even experts with a stethoscope can tell for sure. OK, now so let's think about the the four diseases that we see in dogs. First one, pulmonic stenosis.
So here I've got the, the. Disease in images. So if you look at the top left we've got a normal heart, we've got the, the, the valves in position, you can see on the diagram.
With pulmonic stenosis or pulmonary valve stenosis, which is the most common form, what happens is you get a, the, the valve fails to form correctly as the, the heart is developing and so it causes an obstruction. So the valve doesn't open properly because the leaflets are stuck together. And or the pulmonary artery is is narrowed with various types of obstruction.
And if you look at the top right hand panel, you've got 4 different types of pulmonic stenosis there. And those all show this kind of, I, I describe it to her as it's, it's a bit like a very short wind sock. So you have this tunnel-like structure, with an opening at the end, and it should be opening wide, allowing blood to flow through unimpeded and clearly in all of these cases you can see, that it won't do that.
The one bottom left panel C, sorry, on, on still on the anatomic diagrams, that one actually, they're very thin leaflets, and that's one that I would fancy a go at ballooning. And D is also one I would fancy a go at ballooning, although I might expect less success because there's valve leaflets are thickened, but at least I've got something I can try and open and stretch. You can see that the, the top two, A and B, they're just so thick, a balloon is probably not gonna do very much there, and that's more of a surgical candidate or possibly something for a stent.
Now the echo images at the bottom are left and right. I'll get these to play. They show the these results of pulmonic stenosis.
So, on the bottom left echo image, we've got right ventricular concentric hypertrophy, so really thick right ventricle. The right side is much bigger than the left actually compressing the left heart. And that's the change that we see on, on right, right, parental long axis view.
And on the right we've got the image of the valve itself in cross section. So when you're looking at this, it looks a bit like a pair of clappy hands or a, a sort of misshaped seagull as the pulmonic valve, and you can start to with your mind's eye, use the images directly above that, the the pathology images to, to sort of envisage what's going on in three dimensions and you've got this structure, it should be three very thin leaflets that fold out of the way and instead, they are thickened and distorted and they're not opening properly. So that's.
Pulmonic stenosis in a nutshell. So what's the clinical approach to pulmonic stenosis? Well, from a history point of view, they may show signs of exercise intolerance.
In severe cases they'll have signs of weakness and collapse, on exertion because they can't push blood out and round. So they get what we call forward failure, but often, most often, they have a normal history. It's amazing actually the number of cases that we see that have a supposedly normal history, no problems at all, and then we do a balloon and the owners report that they're much better.
So I think often the owners don't notice the difference. Sometimes they only only notice the difference if they've got two puppies and they've got one much faster than the other, one much brighter, one much more active. But they may come in with a completely normal history.
They'll have pink membranes, they may have jugular pulse or distention, and they'll usually have a normal femoral pulse quality. From a murmur perspective, the murmur of PS is left cranial. So ABCD, it's the cranial one using your PA acronym, it's the pulmonic valve.
So the murmur of pulmonic stenosis is left cranial. You would think it would be on the right because it's the right heart, but that's not how it works, that the pulmonary artery wraps around, and on the left and that's where you hear it. You need to go quite far forward, especially in well muscled breeds, particularly the bulldog breeds which are prone to pulmonic stenosis.
So Frenchies and English bulldogs, listen really far forward underneath that muscled forearm. For the murmur of pulmonic stenosis, and they'll often be thrilling, OK, they'll often have a thrill, and that's where you need to be putting your hands to feel for that vibration. They're usually loud, even quite mild disease, they're usually loud murmurs.
And they only systolic. And that's a murmur of pulmonic stenosis in a French bulldog. And when you get used to listening to them, you can, you can hear they have quite a harsh sound.
They sound subtly different to something like mitral regurgitation. Why does all this matter? Because we can manage and really make a big difference to some of these cases.
We take these dogs to theatre, we catheterize, usually the jugular, and we slide a wire up into the heart. And over that wire we can pass a balloon and stretch the valve. So this is balloon valvularplasty.
And I'll play the three angiogram images. So here is the contrast injection, so we've just injected dye round. And that gives us a look through this pulmonic valve, allows us to measure the size and and work out what size balloon to pass.
We then slide the balloon, you can see the start and end of the balloon, there's the two black dots on that wire, and that's the the, the black dots being passed across the valve, and if you compare that image to the one next to it on the left, you can see that the, the valve, the balloon, it's just sitting across the valve itself now. And then we inflate. So stretch and it pops open.
There we go. So that was a balloon inflation of pulmonic er er a narrow pulmonic valve or pulmonic stenosis. And we stretched it open, allowing more blood to flow through and hopefully making a huge difference to that case.
They clearly they don't all respond, there are risks to this surgery and it's expensive. In our hands, this kind of surgery costs about 4500 pounds. But we expect it to be, certainly.
And you can't say curative, but we can give some dogs back a normal expectation, normal life expectancy, normal quality of life, and we will expect to help the vast majority of dogs who we operate on. So it really is a worthwhile thing to find and to do. Next on the list, we had PDA or patent ductus arteriosis.
So the PDA is a vessel, it's a congenital blood vessel connecting the aorta and the pulmonary artery. So there it is in our diagram, top left and on the right you can see a path specimen where they've sliced open the aorta and the pulmonary artery and you can see the vessel between. And they it it most of the time in dogs they're shaped a little bit like a cow's teat.
So you have the sort of the body of the teat and it narrows down to this little little hole and that's the jet, that's the er sorry, that's the osteum. Of the duct, like a little opening into the pulmonary artery, and that's what, and, and that's what allows the blood through, because it's a small hole, it's a bit like the thumb over the hosepipe trick, and you get this jet of blood squirting through. But because we get a shunt, we get blood flowing from left to right.
The left heart ends up having to pump more blood, so the left heart enlarges, and if you leave these long enough they get huge hearts and they can go into congestive heart failure. What about our examination? Well, history wise, they are, they can be breathless, and they can be exercise intolerant if they're in heart failure.
Again, often they have a normal history, particularly in the young puppies. It's rare to see a young puppy in heart failure with this, but, er, if you leave it long enough, they will go into heart failure, usually in the first year of life. They'll have pink gums.
They'll have normal jugulars and they'll have a strong or tall femme ephemeral pulse quality, various names for this, but I like tall or strong. So you put your fingers on the, on the femoral, oh gosh, that's a, that's a good pulse. And if you're thinking, gosh, that's a good pulse and you, you pick up a a a murmur, you should start to think, ah, this could be important.
The murmur I think is easy as long as you practise good auscultation habits. We, you need to go over the ductal region, so that's how high in the left axilla, go really far forward and really high up. They are often thrilling.
They're usually at least loud, but I would say the majority that I see are thrilling as long as you feel in the right location for the thrill. And they're the continuous murmurs. So they sound like this.
And my pro tip for you is that PDA murmurs sound nothing like washing machines. If, if your washing machine sounds like that, you probably wanna get a a washing machine, er repair person out to investigate. Please stop using the descriptive term washing machine murmur.
It means absolutely nothing. Er, it's not helpful, and it annoys me. And why does this matter?
Well, again, we can whip these patients into theatre and we can pop a plug er across the across the hole and cure these dogs. So bottom left, we've got er a catheter, it's gone up the femoral artery, and it's in the aorta and it's called a pigtail catheter cos it's got a curly end and we're gonna inject some dye and we'll see the ductus. .
There we are. Quite fast, you get this flash of blood through the ducts that tells us where we go. We push a wire forward and through that we feeder this this plug, this one's called an ACDO or an Amplatz canine ductal occluder, and it's a a sort of hat with a a top on it, and that is specially shaped to fit across, The, the cow's teat of the PDA, the, the flat end pokes out into the pulmonary artery and the cup sits within the, the umpola of the, the duct itself, and it blocks flow, and these will usually block flow within 5 minutes of putting them in, and we will scan these dogs an hour or two after waking up from surgery and their hearts will have shrunk in size.
We can also, and tiny dogs like this little one, who was only about 1.2 kg when we operated. We can use a, a double-ended device called an AVP, an Aplatz vascular, plug, and these are really helpful in the little dogs because we can go down the jugular, or the femoral vein.
So we can close dogs that are absolutely tiny and absolutely massive. Our, our biggest is about 60 kg, I think, . And we would expect to cure most dogs as long as we get them in time.
The saddest thing in the world is when you get one of these dogs who is a year old in heart failure with myocardial failure, and there's a good chance that even if we close it, it's too late and it will die. Finally, . Oh sorry, not finally, but next is aortic stenosis, or sub-aortic stenosis if you want to be technical, but don't worry about the sub bit, just call it aortic stenosis, and that's a narrowing underneath or in or around the aortic valve, the left ventricular outflow tract.
There's various types depending on the breed, but most commonly we see it as a subaortic ridge of tissue that runs partway around the outflow tract and and stops flow. Now in severe cases, it will cause a pressure over the left ventricle, so the left ventricle has to thicken in response to that pressure. And because it's not meant to do that, you end up with damage to the muscles.
So if you look at the bottom left echo image, what you can see is a thick left ventricle looks like a cat with HCM, but actually that's a puppy. And it's got these bright areas which we, presume to be myocardial fibrosis, so damaged because the heart muscle, that thick area of heart muscle can't get enough adequate coronary supply and it scars up and that's a substrate for arrhythmias. On the right you can see the colour Doppler image of the obstruction at the aortic level.
What about the history and examination with these cases? Bad cases will have exercise intolerance or collapse, but again, often normal, so don't expect clinical signs with these necessarily. They'll have pink membranes, they'll have normal jugulars, but they'll have a a normal or in bad cases, a weak femoral pulse quality.
The location is. Basal, so it's usually left base, occasionally, well, it's often you can hear it on the right and occasionally it'll be louder on the right bases. So just listen over your apex beat and then just a little bit above, a little bit further forward, and that's your murmur of aortic stenosis.
They can be any grade, and they can be soft, they can be thrilling, they're always systolic. So puppy. Left basal murmur, weakish pulse, especially if you're an excited wriggling puppy, and you think that pulse is a bit weak.
You should be thinking at, could this be aortic stenosis? And that's what it sounds like. So again, different to your typical mitral murmur, they sort of, they have this, they described as crescendo, decrescendo, which isn't very helpful, but outflow or rejection type murmurs and they just.
Now it's important to to figure out . Which, how bad the disease is, because mild aortic stenosis cases usually will live normal lives. They shouldn't be allowed to breed because it, we know it's hereditary in certain breeds, so boxers with evidence of aortic stenosis shouldn't be bred from, for instance, or Rottweilers or Newfoundlands, any, any dog shouldn't be bred from if it's got congenital heart disease.
But we expect mild cases to live normal lives. To be honest, for serious cases, for severe cases, there is not much we can do. People have tried.
Doing, surgery on these, but the dogs usually die. They've tried ballooning them, something called a cutting balloon valvularplasty. It looks exciting, it probably is exciting to do.
There's no evidence it actually prolonged life. It might palliate signs but not for a huge amount of time, a year or two. It's expensive and dangerous surgery, so honestly, my dog had this, I wouldn't operate, and do that, but some, some would, but I wouldn't do that.
Finally For dogs, ventricular septal defect, VSD hole in the heart. These are common. Fortunately they're usually nothing to worry about, but they are a hole in the ventricular septum, allowing blood to flow from the right left side to the right side in most cases.
They can be in any location, but the most common location is this, this region we call perine permembranous, which is just underneath the aortic valve, entering into the right ventricular outflow tract. On echo, they look usually pretty normal from a long axis perspective, and then use colour and you'll find this little hole, with, with blood flowing across left to right. They're usually normal on history because the vast majority of VSDs are, are mild.
They're small holes, they don't cause any problems, so they're usually normal puppies. They'll have pink membranes, they'll have normal jugulars, and they'll have normal femoral pulse quality. When you're listening, this is when we get to the right side now, so the murmur of a VSD is usually right cranial.
That's because of the location where the hole is and where the blood flows to. It flows out into the right ventricular outflow tract right cranially. They, they can be other locations, but that's most often where you will hear them.
And they can be any grade, but most are small holes, so they create very turbulent flow, and they're usually loud or thrilling. So a thrill on the right, systolic thrill on the right, thinking BSD. And that's a VSD in a dock.
Most of the time, as I said, we don't need to worry about them, they are small, they're not relevant. Most are small, restrictive, which means they, they don't allow much blood through them. Perimembrane is just underneath the aortic valve.
Large ones can be closed. We've got a possible case at the moment that we might close, but that's the first one we as a group of 8 cardiologists have had in upwards of 10 years, so they are extremely rare that they actually need to be closed. So trying to put this all in summary, there's no way you can summarise all of congenital heart disease in dogs on one slide, but I'm gonna try and summarise the commoner presentations.
So if it's soft, a flow murmur's likely, but you can't diagnose it with the stethoscope alone, and some of the really bad heart diseases only have soft murmurs. So if it's soft, it's a flow murmur's likely, you've got options, you either monitor it, or you, have it looked at by a cardiologist. If it's moderate, loud, or thrilling, you need to examine carefully.
Your clinical examination really matters because it can help guide you. And the four things to think about are the location of the murmur, the timing of the murmur, what do the jugulars look like? And what are the femoral pulses like, and if you have those 4 bits of information, you can, you can have a good guess as to the big 4, the top 90% of cases in dogs.
So murmuration. Left base is aortic, left cranial is pulmonic, left axilla is PDA and right cranial is VSD. Anything else, any other locations, or a mixture, you need a cardiologist, and even then we may not be able to add much more.
But those are the classic ones to, to remember. Timing AS, PS and VSD are all systolic, and the PDA is the continuous one. Again, anything else needs a cardiologist.
Jugulars, if they are pulsing or distended, it's likely to be pulmonic stenosis or other significant right heart disease, so you shouldn't be seeing jugular distention in a healthy, especially young animal, . And then finally, femoral pulse, if the femoral pulse is weak, think aortic stenosis. If it's normal, depending on what else you've found, it could be a VSD or pulmonic stenosis.
And if you've got a strong or a tall femoral pulse, think PDA. So again, soft, it's likely to be a flow number but you can't be certain. If it's moderate or louder, you need to examine carefully, it is not a flow murmur, it will not go away, it should not be ignored, and please, please, please don't miss PDAs because they're the ones that we can fix.
And this is why it matters because this dog had a thrilling left axillary murmur. Her vet had told her it was probably just a puppy murmur and she grew out of it. They documented the thrill.
They said it had a thrill, but they, and they wrote in the notes, probably a puppy murmur, nothing to worry about. And we saw her at 11 months old when they changed vets and the damage had been done. We tried to, to close it, we tried closing this PDA, it's a huge duct.
But she died the day after surgery, we think from a, a ruptured duct. It was just too late. The heart had just failed.
The duct had been left too long, and when we closed it, she died, and it's obviously she was the nicest of dogs with the sweetest of owners, fully insured, so there's no problem ever doing surgery. We just should have done it when she was 3 months old, not, 11 months old, and I never want to do this again, and I know sadly that I probably will because this is what happens. All right.
What about cats? So I've mentioned already that the four most common, the VSD, PDA, and then tricuspid and mitral dysplasia, but they only account for about 50%. So the cats can have a, a lot, they do, they do have a much more varied spectrum of disease.
And as always applies, the only rule with cats, there are no rules. You know, here are 4 cats, all of whom had left sternal murmurs. We've got What have we got on there?
We've got a tetralogy of haow, bottom right, we've got a tricuspid dysplasia, we've got a reverse VSD and we've got something called an atrioventricular septal defect or AVSD. These are all hideous diseases, they're all very serious. We haven't got treatments for these, so you could argue academic in all of these cases, but they all sounded pretty similar.
You can't tell with cats. A cat or a kitten, especially with a murmur, especially a loud murmur needs an echo. That's the rule.
Alright, back to our quiz. So here's our puppy. Came in Monday morning, lovely owners.
What do we do? We don't panic, that's what we don't do. We have a careful listen, take a bit of history, have a careful listen and decide what's next.
So when you do your, your careful examination, we find a palpable thrilling left axilla continuous murmur. The puppy's got quite strong pulse quality. But normal jugulars So What's he got?
Yeah, that's right. It's a PDA, see? Told you, wasn't that difficult.
So If you hear any murmur, do a thorough cardiac examination and document what you find. A soft murmur in a young animal with no signs, it is reasonable to wait. It's best to offer echocardiography, ideally specialist echocardiography with someone who's used to seeing and diagnosing congenital heart disease.
Especially if the owner's got any concerns, because it's better to come to us and we say, nah, good news, don't worry about it than to worry about. That's fine. And most insurance companies will actually reinsure that pet if we've documented no disease.
What you don't want to do is miss serious heart disease and fob them off. But if the murmur's moderate or louder, it's potentially important disease, not always bad news, but potentially important disease, and it needs to see a cardiologist. Although it often is bad news, there are some conditions that we can effectively cure and certainly manage with prompt treatment.
So it's not an academic process we can make a big difference. And here's again, finally why it matters. These are my two dogs, Dovey and Betty.
Dovey's the Border terrier, and Betty is the Labrador. The Border terrier had a PDA, which we fixed when she was a puppy. She's now 8, nearly 9, still a pain in the arse, but we love her.
And on the right, that's Betty, our gorgeous Labrador, who came to me from the Dogs Trust because she had bad pulmonic stenosis, and we've ballooned her and she is still going strong. She's now, I think 7 or 8, and she goes, they both go running with me, they're much faster than me, and they're absolutely gorgeous, and we've killed them with, with treatment, so that's why it matters. OK, thank you very much for your attention.
I hope that was useful and if you enjoyed it, and especially if you've got any connection with motor neuron disease, I'd really appreciate a quick visit to our just giving page with fundraising to er to try and help this awful condition. Thank you very much for your attention. Hope you've enjoyed those two sessions.
I think they were really, really good, . This is the end of the congress. If you're like me, you'll want to go over those heart sounds again so we can obviously sort you out with recordings.
Dawn has put that back in the box. I think we'll put it back in again, so it's right near the top. Just a little comment from the previous talk.
At which, you know, I would say with all the information that we pass, it's really important, you know, to make your own research on it as well, so there is a disclaimer on all of our webinars, but Liza's made the point, just to say that anticholinergics are contraindicated in patients who have received alpha 2s. It was really good, I think on Wednesday we had a talk by Karl Moseley talking about premedication and trying to reduce anaesthetic gases. And I think there's been a movement away from ACP to more of the meatomidine type products.
So if you've got a bradycardiallier who was saying, I, I do that, that you have hypertension, then you need to antagonise the alpha 2, not give anticholinergics. This wasn't said in the lecture, but most clinics I know are more likely to get alpha 2s as a pre-med. So just a little note there, obviously for something for you to go back and study and research, all of our webinars do have a disclaimer, but having said that, I think they've been two fantastic webinars, as has the whole series, and if you would like the recordings, they are available from next week, but you could buy now.
Of course, if you'd like a membership, then look at that. Just like to thank everybody who's been involved in the virtual congress, all of you for coming, for the sponsors, for all of the team at Webinarett for making this such a fabulous conference. There's been many, many thousands.
Of hours watched by you all over the last 5 days. If you've enjoyed it, give us a little mention on social media with the hashtagVC2023, and hopefully I'll see you on a webinar very soon. Take care, good night.
