Thank you for the very kind introduction, Sophie, and welcome everybody. So tonight we're going to look at some principles of cardiac anaesthesia, and I call this seven principles of cardiac anaesthesia just to give us somewhere to start to make this a digestible topic. Obviously a big part of what we do as anaesthetist is giving drugs, and this I think is where most of the questions are generated.

So we're going to spend a bit of time looking at the drugs that we use, how those drugs may interact with our patient, depending on the underlying disease of that patient. And I'll illustrate that with cases and we'll look at how I would adjust your anaesthetic protocol in certain cases. I think those cases we're going to look at would be dog with dilated cardiomyopathy, case of aortic stenosis, dog with mitral valve disease, cat with hypertrophic cardiomyopathy, and we'll do a dog with atrial fibrillation as well, just for completeness.

And I think this probably covers a broad range of the likely diagnoses we're gonna see in practise, what we're gonna be faced with and asked to anaesthetize. So, moving on to our number one consideration. Really for me, my number, absolute number one is understanding what I'm dealing with.

If we know the extent of the patient's cardiac disease, it makes our life so much easier. So we're gonna talk about understanding what you're dealing with, but. I know we don't all live in the ideal world, and we'll also talk about what if you don't understand the pathophysiology of what you're dealing with.

What if you are constrained by the owner's wishes or finances and we can't work that patient up and work out exactly what's going on from a cardiac point of view prior to anaesthesia. So that leads me on to my first poll question. I have access to echocardiography, a simple yes or no.

So how many of you have access in your practise, either to someone in the practise to do an echo, someone coming in to do echo, or sending your cases to your local referral centre. OK guys, so a small box should have appeared on your screen so you can start to select whether you have echocardiography or not, and then I'll read the answers out to Matt as soon as she'd finished. OK, so about 79% are saying yes and about 27% are saying no.

So I'll end that there. Thank you. Moving on to the next one.

And what percentage of clients agree to echocardiography when you detect a murmur in their dog or their cat? OK, so what percentage of clients agree to echocardiography when I detect a murmur? So nobody has answered 0, 25%, we have 41% of people, and 50%, there's 18% voted, and then 75% we have 41% of people, and 100% is zero.

So there's a tie between 25 and 75%. OK. So at least we've got no one on zero, so that's encouraging, isn't it, I think.

OK, so that gives me a little bit of information to work on throughout the presentation. What I want to just talk about is what does the literature teach us when we do and when we don't have access to to pre-anesthetic echocardiography. Now there's a study that we have been doing in dogs we've just, it's just been submitted for publication.

And we did this over about the past 3 years, and it involved looking at cats documented to have either a murmur or an arrhythmia prior to anaesthesia, and these were 40 client owned cats. And the anaesthetic was actually planned by an anaesthetist prior to those echo results being available. And when I say anaesthetist, there were 3 of us, who were all specialist anaesthetists.

We were given all of the information about the cat, apart from the echo results, the blood pressure, and the, the ECG. So with all of the basic information about the cat, it could have been to do with murmur intensity, it could have been suspected rhythm on clinical examination. So how would we plan that anaesthetic with that basic information?

The cats then went to see the cardiologist and they had an appropriate cardiac workup for their presentation. The 3 anaesthetists then revised their plans based on those echo results. And this was based on the, the same methodology as another human study.

What we were able to show was that out of those 40 cats, 23 had pathology which the cardiologist deemed to be of hemodynamic significance. So it's quite a high proportion, isn't it, out of those 40 cats, if you scale that up to how many cats we see a year, we're talking about nearly 3/4 of those cats with either a murmur or an arrhythmia having something that a cardiologist would say, this is significant, guys, you need to take notes. 17 of those cats, their disease was suspected from the physical examination findings.

So we're not actually detecting as many of those cats, the the significance of the cardiac disease compared to the cardiology workup, which I guess isn't surprising, is it? In 26 out of 40 cases, we changed the plan. And we classified this as either a step up or a step down.

So having that information, did we do something like request that the cat had an arterial line place, or did we request the cat had oxygen after anaesthesia or got transferred to ICU after anaesthesia? Or did we decide that we weren't going to use a certain type of drug? And a step down would have been us saying, well actually I'm less worried about this cat now that I've got these echo results.

And I found this a really interesting study to take part in and even more interesting to actually see these results coming through. What our conclusion is, is that we really need echocardiography in cats with suspected cardiac disease to fully evaluate them prior to anaesthesia. So I hope this information is useful for you when you're talking to owners.

We know that of cats, if a cat has a murmur, probably only 50% of the murmur is significant in those cats. We know that from previous studies. But this study that we've just done now adds weight to that, but when you look at those 23 out of 40 cats that had a murmur of hemodynamic significance, this gives you numbers to go and talk to owners about and say, your cat has a murmur, could be significant, couldn't be significant, cat needs anaesthesia.

The literature would show it teaches us that the best, the absolute best thing for your cat is for them to have an echocardiogram and a cardiac workup. So I hope you can use this information to your advantage. So that's my number one consideration, really knowing what we're dealing with.

Do we have the same information in dogs? We don't at the moment, but watch this space because now we've done this study in cats, it'd be quite easy to replicate. I would say based on my experience, that I think I can do a much better job at planning an anaesthetic and deciding which drugs to use and which drugs not to use in a dog when I have the echo of information compared to when I don't.

And actually don't get lulled into that sense of, oh, this patient has a left 2 out of 6 systolic murmur, it's probably mitral. That picture I showed at the start with the propofol CRI and the ketamine CRI and the outline, that was a setup in MRI. That was a dog that somebody listened to and said, oh it's probably got a mitral murmur.

We said, well, actually we should work that out. That dog actually had a mass in its left atrium that was causing the murmur, and it was scheduled for for spinal surgery. Now knowing all that information, I knew that actually I don't want to use a volatile agent in this patient that's gonna markedly reduce its contractility, compromise our cardiac output.

I could use a. Before getting the infusion in that patient. I know the, the, the dog's cardiac helps to be much, much better.

I was able to plan that anaesthetic really carefully, make sure that I had direct blood pressure monitoring, for example, and that dog had a successful outcome because of that information I was equipped with. So don't just assume that these murmurs are, oh, it's just a mitral murmur because of the breed, because of the age. Let's, let's use the literature and work these patients up as well as we can before anaesthesia.

Number 2 consideration is cardiac output. So let's look at those components of cardiac output. When I say cardiac output, what exactly do I mean?

Heart rates, stroke volume, venous return, systemic vascular resistance, rhythm and valvular insufficiencies all contribute to how our cardiac output can be influenced and how we can manipulate cardiac output under anaesthesia. Obviously, bradycardia can affect your cardiac output. As can tachycardia, but probably quite an extreme tachycardia, and I'm talking more than 180, 200.

These are the kinds of heart rates that are really going to be limiting that diastolic filling, comparing our contractility. The heart just doesn't have time to reject that fraction of blood effectively when we have a tachycardia. Similarly with a bradycardia, how are we gonna tell when to treat a bradycardia, when is a bradycardia significant?

Generally I would say bradycardia is significant when it affects our blood pressure. We look at a mean arterial pressure of more than 60 or 65 millimetres of mercury at all times under anaesthesia. So that's heart rate and we'll bring this in when we talk about the cases that we're going to consider later, how we want to influence our heart rate in those cases.

But I always look at your, I've always look at your heart rate and think how is my heart rate influencing my cardiac cat? Straight volume contractility. We know that this is very pre-load dependent and we've used the term Venus return here we could equally use the term preload.

We know that the more blood you present to those ventricles, the better they contract according to the Frank Starling law of the heart. So we want to ensure a decent preload. In order to stretch the myocardial fibres to see that decent stroke volume, which correlates with a good cardiac output.

And cardiac output is products of heart rate and stroke volume. So these are the two main considerations I'm thinking about when I'm thinking, hang on, how are my drugs influencing my cardiac output? Systemic vascular resistance, this is a measure of peripheral vascular tone.

And if we increase our systemic pass resistance, we increase the afterload and therefore we can reduce caring output through that mechanism. Clearly cardiac rhythm can influence cardiac output. You'll have appreciated the difference when you palpate the pulse in a dog with a heart rate of 120.

Or maybe an idioventricular rhythm of 150, 160, versus ventricular tachycardia of 180, 190, 200. Pulse palpation is one of our main indicators of the efficacy of cardiac output with those rhythms. OK, fantastic, if we can get a blood pressure in those patients, then we can work out if that arrhythmia is having a corresponding effect on our blood pressure.

One thing just to focus on is peripheral flow. Our holy grail under anaesthesia is tissue oxygen delivery. The heart is a pump and the job of the heart is to pump the red cells containing oxygen to our peripheral tissues.

We need to be thinking about peripheral pulses in all of these conditions. So evaluation of that patient, pre-anesthesia and during anaesthesia, I find pulse palpation something that I totally rely on. Valvular insufficiencies, obviously they can have an influence if we have a a severe mitral regurgitation, for example.

We want to alter our pressure dynamics, so we promote forward flow and improve cardiac output rather than reversing flow across that incompetent mitral valve, for example. So these are the things I'm thinking about when I'm thinking about cardiac output. And we'll pick that up again when we talk about monitoring because part of our monitoring under anaesthesia is thinking about how all of these things are influencing our cardiac output and what's the closest we can get to measuring cardiac output.

Number 3 considerations, drugs, you get the impression that's what you're here for, you want to know which drugs you can and can't use, you will go away tonight with that information, certainly. Before we move on to talk about drugs, we're gonna throw a little poll question in there, so which drug causes hypotension. Metazolam, aromazine, meatomidine, ketamine.

There's one answer to this question. OK guys, have your vote, test your knowledge. Let's see what you all think.

We've got a couple coming through. Please do get involved if you're listening. Let's see what you all think.

OK, we've got a fair few in, and this is again another mixed result. We'll give another 5 seconds. If you haven't voted, please do so and then I'll read them out to Matt.

OK, so we've got 50% of people are saying Aceromazine. Nobody's voted midazolam. We've got 44%, same meatomidine, and only 6% voted ketamine.

OK, right, we're gonna work through those drugs and by the end of it, you'll understand which is the correct answer. I said there was only one answer, didn't I? Yeah.

OK, right, so Aceromazine and the alpha 2 agonists meatomidine and Dex meatomidine. So I think we probably fall into two camps if we think about our routine practise primo protocol. We're probably using either Aceromazine and opioids, or we're using it now for two agonists and an opioid.

Most common. I, I think when I ask, when I poll a room of people, it's normally 50/50 in dogs. Maybe slightly different cats, probably more after 2 years in cats compared to aromazine.

Aceromazine, why do we like it from a cardio point of view? It doesn't really cause bradycardia, so it doesn't really affect our heart rate too much. It doesn't really depress our cardiac contractility, so it doesn't have too much of an influence on our cardiac output.

It's said to be antiarrhythmic. Now this comes from studies that use an adrenaline induced arrhythmia model. So they would compare patients that had Aramaine versus patients that hadn't had aromazine, give them adrenaline, see how much adrenaline they need to give to make those patients go into an abnormal cardiac rhythm.

Pretty basic stuff really. As far as study goes, and that's where the work with Ace prosy came from, showing that ACE prey has an anti-arrhythmic effect. Do I think this is relevant clinically?

As much as I'd love to think oh I'm using Arazine for its antiarrhythmic effects, I can't hand on heart say, give a prey to this patient and it's not going to develop a a malignant cardiac rhythm or even an abnormal cardiac rhythm. Aceromazine was the answer to the previous question. Aceromazine causes hypertension.

It's a phasodilator. So this is one of the reasons why I would be cautious about using aceromazine in certain cardiac cases where we're wanting to maintain that venous return, that preload. We don't want to, to cause vasodilation in some of those patients, which would impair our venous return, reduce our stretch, reduce through reduced preload and therefore impair our cardiac output.

So ACE prosine is a vasodilator, just remember that as we go through all of these cases. I'm going to come back to the action of Alpha 2 Agnes because I've got a few slides that we can go through to help your understanding of that, because I saw 44% of you voted that meatomidine caused hypotension. I'll go through and explain why the answer to that question is not metomidine.

Opioids are our mainstay of cardiac anaesthesia. We can use opioids without fear in patients with cardiac disease. Do not be afraid of using opioids of analgies in these patients effectively.

What's the worst that can happen? Methadone can cause a degree of bradycardia. However, I find that that bradycardia is often not severe enough to affect my blood pressure.

So, yes, methadone could reduce my heart rate a little bit, but it doesn't normally have a consequence. If it does, what am I gonna do about it? I'm gonna use glycopyrolate.

The idea behind glycopyrolate, it's an anticholinergic, it increases our heart rate, restores our heart rate back to something more physiologically normal. And to do that, I'm thinking about 5 to 10 mcg per kilo of glycopyrolate. You can start with 5 mics per kilo and increase to 10 mcg per kilo if you don't see a response.

I know most people don't have glycopylate in their practises, but. I think now you've attended this webinar, aware of the importance of bradycardia treating bradycardia, bradycardia as an important factor of cardiac cat blood pressure, you can see a huge wealth of glycopyrolate in practise. We use it day in day out every week.

If you're either listening from the states or you've had any American training, Americans like to use glycopylate in with their pre-med to prevent that bradycardia. You take a slightly different approach in the UK and say, well, OK, if my patient becomes bradycardic and it affects my blood pressure, then I'm gonna give some glyco at that stage. Buprenorphine, other option it's the other opioid that we all use for mild to moderate pain in practise.

Very, very few cardio, adverse effects. I'm pretty confident to say no adverse cardio effects with buprenorphine, and I'm not even, one of the questions I get is, oh, for my cardiac anaesthesia, shall I just go low dose of everything? I'm gonna talk to you about proper doses to use these drugs.

So buprenorphine, I use 20 mcg per kilo, 0.02 mg per kg for everything I do pretty much, and I'd be very happy to use that dose in a cardiac patient regardless of their underlying pathology. Similarly, methadone.

0.1 to 0.3 makes me gig of methadone, I'd quite happily use that for a cardiac patient undergoing some type of painful surgery.

So I'm not shying away from using opioids and I'm using opioids at similar doses to those I've used previously with other patients. So that's opioids for you. Let's not forget the biggest criminals as far as vasodilation and hypotension go, it's the volatile agents isoflurane, superfluorine.

Is one better than another as far as physicalation goes? No, I think they're both just as bad. In combination with aromazine, these are the two big factors causing anaesthetic induced hypotension.

It's his perromazine and the volatile agents. So what do the volatile agents do? They vasodilate and they reduce contractility.

Let's forget that they're a drug. We forget that we're delivering them. If I, I ask one of our interns, OK, tell me which drugs we've given this patient.

The last thing they say, I, they take some encouraging to get to is we're delivering this patient isoflu or Cvofluoride. We forget that we're given this drug, it's just there on the wall that's just going into the patient. We're not injecting it, so we kind of forget about it, but it has some quite adverse cardiac effects.

You saw in that dog with the left atrial mass, I wanted to specifically avoid using volatile agents. And one of the things that we're always looking to do with our cardiac patients is to spare the volatile agent. So we're constantly evaluating that patient, doing everything we can to turn a volatile agent down, whether it's using methadone in our pre-med, whether it's doing a local anaesthetic technique, all of these are aimed at volatile agents sparing, turning the vaporizer down.

Onto the alpha 2 agonists now, so you might be shocked thinking, oh hang on, you're talking about alpha 2 is a cardiac anaesthesia thing. I thought these would be the last drugs you use in cardiac anaesthesia. Well, let's have a look.

Why do we like afterobagonists? They produce sedation, they produce analgesia, which is improved in conjunction with opioids. They have a rapid onset.

I've put a query after able to reverse. The ability to antagonise alpative agonist is not a reason to use in the cardiac disease. I absolutely promise you, when you're knee deep in it and you need to antagonise your alpitu, it will not work.

Do not rely on the fact you can give attiammazole to antagonise meatomy or dexamedatomy to get you out of a hole. It won't happen. Promise you, why?

Once we give these drugs, they are in exactly the same receptors, meatomidine, Atimazole, they work on the same receptors. It's a concentration thing. If your receptors are flooded with meatomidine, that meatomidine has to dissociate away from the receptor in order for the attiammazole to do anything.

So if you've got a patient, you think, oh, I'll give them some metaomy, it'll be OK because I can antagonise it or reverse it with attiammazole. You give them meatomathy, you go, oh, hang on, look, I've got an arrhythmia or my blood pressure's dropped or something awful has happened, let's give some attipamazole, doesn't do anything. I'm not surprised by that.

We need to wait at least 25, if not 30 minutes. After our alte before giving our atti Parmesan. So not a reason to use alpha 2 is the fact that we can reverse them.

I think the important thing with alpha 2 is that we talk about the physiological effects that we see with alpha 2s. This is from one of my absolute favourite papers, and it's a study in dogs. They had cardiac cat catheters placed and it's looking at all the physiological effects that we see with meatomidine in different doses.

This is from back from 1992. They looked at 5 doses of meatomine in the dog, 125, 10, and 20 mcg per kilo. So 1 mic per kilo is tiny.

If you use meatomidine and you take your dose of the dose chart, you're probably using 10 mcg per kilo. 20 mics per kilo, if you get the IV with some opioid, that's gonna produce an amazingly sedated dog that you can do, most things with, I guess, radiography wise, you can, manipulate that dog fairly freely because it very well sedated. This, let's look back, this is the first slide, so this looks at what happens to heart rate.

So before we give the drug, our population of dogs, their heart rates sitting between 120, 130. We give the drug, what happens, our heart rate drops. We're all very familiar with the bradycardia produced by the alpha 2 agonists.

And then we look at the time axis and we can see the more drug we give, the longer that bradycardia lasts. So bradycardia is dose dependent with the alpha 2 agonists. And you can see it drops down to about 30 to 40.

So at the higher dose, this is what we can expect is our initial heart rate. And with our 20 mics per kilo, that's actually lasting 2 hours, and we, we've got a heart rate 60 off to 2 hours. We said before, bradycardia can significantly influence our our cardiac output, and this is one of the main reasons why alpha 2s affect cardiac output, it's the bradycardia that we see.

What about mean arterial pressure? Some of you answered that meatomidine can cause hypotension. This slide disproves that.

When we give our alpha 2s, prior to administration, you can see on the left-hand side here at T minus 15, our mean arterial pressure is between 130 and 140. We give our to agonists what happens, our pressure goes up. But most market increase was in that 20 mics per kilo group where Eminoterial pressure is going up to sort of 175 there.

At those lower doses, it doesn't look like there's a huge amount of change, certainly with 2 mic per kilo group. You can then see over time that pressure starts to come down. But can you actually see, this is mean arterial pressure, can you see any of those bars dropping below 60 millimetres of mercury?

No, 60's not even on that, that axis there. So these drugs on their own are not causing hypotension. We see an initial hypertension.

The bradycardia that we see is in part a reflex bradycardia due to hypertension, but mostly it's due to a lack of sympathetic effect. But the way the alpha 2 agonists work, they reduce sympathetic activity. That's the reason for the bradycardia.

The reflex part is secondary. So our pressure's going up, we're getting our, our bradycardia. Through these two mechanisms.

Over time, our pressure is decreasing, but it's never actually ending up as hypotension. What we may see is if we then superimpose the effects of other drugs, induction agents, volatile agents on our alpha 2 agonists, we may then see as the alpha 2 wears off, we may see the hypotension, but it's generally related to the other drugs, OK? This looks at systemic vascular resistance index, so it's a measure of how tight or vasodilated, vasoconstricted vasodilated the peripheral vasculature is.

And you can see you give the drug, your systemic vascular resistance increases, and then it decreases over time, approaching something normal, but generally, these drugs are predisposed to a vasoconstriction. So as a result of all of those changes, what we tend to see is our patient's blood pressures are increasing, vascular tone remains good, blood pressure remains good after we've used alpha 2 agonist. The bigger the dose we use, the longer the duration of action.

One of the conclusions from this study was actually that if you use 1 or 2 mcg per kilo of meatomidine, so small doses, what people might refer to as homoeopathic doses, you don't really see very much in the way of the overall cardiovascular changes. So if you're looking for minimal cardiovascular effects use lower doses. But above 5 mics per kilo, you see all of those cardiovascular effects.

So actually, if you can use 5, you may as well use 10 or 20 and get better sedation. So actually, personally, I quite like using largerators of alpha 2 agonists because I want the sedation, I want the analgesia, I want that to last as long as possible. What I don't want is the alpha 2 effect wearing off, the volatile effect taking over, and that hypotension developing as a result.

So I think that just clarifies for you what the effect of alpha2 agonists is on our blood pressure, heart rate, and vascular tone. Just as an example here. We always talk about cardiac output monitoring being the holy grail and oh actually we can, we have multi-parameter monitors, we can't monitor cardiac output.

This is all changed, so this is a device called a Moscare up which, Derives some cardiac parameters from an arterial waveform trace. So on the top of this screen you can see that is an arterial waveform obtained from a catheter into a peripheral artery. This was a case that I was anaesthetizing last week.

On the left-hand side of the screen here you can see this is before we give an alpha 2 agonist. So we have a pulse rate of 93, we have a systolic of 100, diastolic of 57, and a mean of 71. When we give our alpha to agonist, you can see the marked difference there, you can see the bradycardia and you can see that that blood pressure has increased.

This was 2 mcg per kilo of Dexedotomidine, so it's quite a small dose of Dexedotomidine. Our mean pressure's gone from 71 up to 93, but our pulse rate's gone from 93 down to 44. So we've got that bradycardia, but that increase in systemic vascular resistance, that vasoconstriction is what's maintaining that blood pressure.

The other thing to look at here is the CI is cardiac index, so this is cardiac output indexed to the patient's body weight. You can see actually cardiac index hasn't changed very much over those two different screens there after that drug. So the bradycardia has been offset by the increased systemic vascular resistance.

And you can also see that it's actually displayed there. We've got an SVRI4 of 1132, and SVRI afterwards a 1596, so you can see that vasoconstriction in action. That's what's going on with our after to agonist.

One of the other things I just want you to focus on is the parameterical DP over DT, that's our measure of contractility. So actually, after giving that alpha to agonists, our contractility is decreasing. This is probably another factor when the effects of our alpha 2s wear off after over time.

Then we have a volatile agent effect as well. What we're actually left with in the aftermath of using the alpha 2 is a heart with reduced contractility. We then superimpose that volatile agent on there and we know how they reduce contractility and we see an overall reduction in in cardiac contractility.

So over time, when our alpitus start to wear off, we do see a decrease in contractility which is undesirable. And that last slide there just shows how cardiac count cardiac index is influenced by those alpha 2s. So as we expect, we give the drug cardiac index drops and that wears off over time in a dose dependent manner.

So that's how fati. If we want to summarise, we've been thinking about how we influence kayak output. Things that increase cardiac output are more pre-loads, more venous return.

We talked about the Frank Starling mechanism that increased hemoid load, stimulates more myocardial stretch, and we get a better stroke volume and cardiac output. Catacular means, you know, if we give adrenaline or no adrenaline, we can increase our cardiac contractility. Yeah.

Any other factor that increases contractility, for example, immobendin, which we may use therapeutically, drugs like dibutamine, we use dibutamine in cases of dilated cardiomyopathy under anaesthesia if we want to improve contractility. Factors that decrease cardiac output would be bradycardia or extremes of tachycardia. Increase after load, so if we markedly increase our systemic vascular resistance index, we're going to decrease our cardiac output.

And also reduced contractility as well is going to decrease our cardiac output. So cases of dilated cardiomyopathy would be a perfect example where contractility is impaired because of the inability of the myocardium to function. Septic patients, another excellent example where myocardial contractility is impaired.

So just a summary of factors that influence cardiac output in a positive and a negative way. He talks about a rosy instead of just skipped over that. Midazolam.

Everyone that was answered correctly that midazolam doesn't have any adverse cardiac. Effects probably at the doses we're using clinically, so 0.25 to 0.5 gigs per gig, we're not seeing any adverse cardiac effects from midazolam.

So this is something that we can safely incorporate into our cardiac anaesthesia, but I would never consider it using midazolam on its own as a pre-med, unless I had a very young or a very old patient. We will say very young or very old. I think you have to be quite young and quite debilitated and quite old and quite debilitated for midazolam not to have that disinhibitory excitatory effect.

In my experience, the first thing that happens when you give midazolam IV to these patients is they just want to eat, and it doesn't matter what it is, it might be their bandage or it might be their vet bed. They just want to eat. They become very noise sensitive as well.

So I don't think midazolam is a suitable thing to incorporate into a primed on its own. And there's a study recently looking at incorporating midazolam into meatomidine pre-med, and they actually showed that when you add midazolam to meatomidine in dogs, it decreases the level of the sedation because of that disinhibit, I can't say it, disinhibitory effect. So we need to be careful about how we use midazolam.

We probably use it more as a co-induction agent. Rather than as a primo on its own per se. Moving on to drugs.

Afaxone or Propofol, which one do we choose for our cardiac patients? Sometimes I think the question is actually more how we use the drug versus which one do we choose. I know personally for me, I have a preference for Alfa loan because I have a lot of familiarity with Alfax loan.

I quite like the work, it was one of the first, probably the first clinical study that came out back in about 2008 after our vaccine was launched in 2007 in the UK. Where some colleagues at the RBC looked at alfaxolone compared to their protocol at the time for dealing with sick patients, and that was fentanyl, diazepine, propofol. And what they showed, these weren't necessarily cardiac patients, but they were sick patients like GDBs, peritonitis.

They showed that from a cardio respiratory point of view, a fain then performed in a very similar manner to what they thought their current gold standard, the fentanyl, diazepam, propofol combination was. Now, before Afaxalin came along, I was using a drug called etomidate for my cardiac patients because everyone said, well, omidate, it has minimal cardio, instability. It doesn't really affect your heart rate, it doesn't really affect your blood pressure.

And actually, as far as I'm concerned, it doesn't really do anything. You give it to the dog and the dog just sits there looking at you. So, I didn't think it it was a particularly effective drug.

And I moved to using alfaxolone once it was launched. And never look back really, so I found Alfaxin to be a very suitable agent for cardio anaesthesia. There will be colleagues who swear byrool, personally, I have more experience with vaccine.

I think the key for me with either of these drugs is that we use them slow, and by slow I mean super, super slow to effect. So we're not working out our 4 mes per gig of propofol or our 2 MBs per gig of alfaxine given the whole lot. We're only giving as much as is needed for a tracheal intubation with no coughing.

So that's our aim with our dogs and our cats. And for these cases, we're looking at a pre-med, which may not be the most sedative premed in the world. We might have pre-med our patient with just methadone.

So we do need to be particularly careful about how much alfaxolone or propofol we give. The slower you give it, the less you need to give, I promise you. Monitoring We're going to apply our monitoring before induction.

If something's going to go wrong, it's probably gonna go wrong either at induction or recovery. So when we say apply monitoring before induction, I'd also say keep your monitoring on instant recovery period. We want to know what's going on with with our ACG.

We want to know what the rate is, we want to be able to glance at that screen and see easily, yes, that rate is still 150, 160, 120. I'm happy, rather than, hang on, that was 150, and now it's 40 and oh, hang on, it's taking me a while to count the pulse on that patient. Having a big screen that we can glance at whilst we're doing something else is recognised to reduce anaesthetic accidents in people.

So I put my ECG and my blood pressure on prior to induction of anaesthesia. Blood pressure, I think it's our most important modality of all. And that can be as simple as a Doppler.

Remember we said about peripheral flow being the holy grail? Our Doppler is placed periphery, we are detecting peripheral flow. There's nothing more satisfying under anaesthesia than hearing that that whooshing sound of the Doppler.

You can be writing on your anaesthetic chart, you can be opening a suture material from the surgeon, you can hear that your patient has cardiac output and they have peripheral flow. And you can hear the arrhythmias as well. If your patient's got a pulse deficit or it's flipping in and out of an idioventricular rhythm, you can see that, you can hear, sorry, the difference in pitch of the flow associated with that change in cardiac output.

So you can actually gain a lot more than you may have previously thought about using Doppler. Obviously our doctor is providing us with a systolic blood pressure in dogs, probably something close to mean in cats, so in dogs we're wanting that to be certainly above 100 if not 120 ideally. Cats, we want that above 80 ideally.

80 to 90. So, blood pressure for me is a really useful modality. If we think about osciometric blood pressure systems, we need to be sure that we get consistent readings, and actually we're probably thinking about using our blood pressure monitor as more of a trend rather than an absolute, and we're gonna keep our mean arterial pressure above 60 millimetres mercury.

You've already heard me talk about these difficult critical cases, and I'm placing a direct arterial catheter in those cases. Briefly on capnography, if you want to know more about Caography, there's an amazing webinar that I did a couple of years back that you can you can find in the archive here. We like catography because it tells us about metabolism, ventilation, circulation, and it can help us judge the efficiency of our cardiac output.

If our cardiac output decreases, our internal CO2 falls because of that lack of circulation. I will leave you to investigate more about catography. Pulse oximetry, measuring our saturation of haemoglobin with oxygen, and any patient we're anaesthetizing if they're on 100% oxygen, their saturation should be above 95%.

It should be above 90%, if not 95%, certainly. So a useful measure, we need to understand when our fossil cemeter has given us the correct reading, but there aren't, to be honest, there aren't many cardiac conditions where patients should desaturate. It's more respiratory conditions where we receive desaturation.

Maybe our patients have failure, but we, if our patients have failure, we're not gonna start a cardiac patient of failure. Reasons for hypotension, mean arterial pressure less than 60 millimetres mercury, would be too much volatile agent, so we need to think about volatile agents sparing as we said before. Reduce volume status if that patient's been on diuretics, maybe they're they're dehydrated, quite possibly.

Poor cardiac outputs may be quite common with some of these cardiac cases we're seeing. Blood loss is blood loss happening on this that surgical procedure? Do we need to replace blood loss?

Do we need to replace volume? You need to think very carefully about blood loss because if we have a cardiac patient, we don't want to go pushing their fluids or putting blood in at a very rapid rate. We need to plan really carefully for these and I think about slow and steady replacement rather than go.

Hang on. All of a sudden, my patients lost 20% of their blood volume. I need to squeeze a whole bag of blood in.

I might be a little bit more cautious than these patients and say, well, actually, this patient has lost 10%. How are we going to be a bit more upfront about dealing with this blood loss? What's my crystalloid rate going to be?

And am I going to intervene a little bit earlier with replacement of, either packed red cells or whole blood? Bradycardia, we've mentioned bradycardia and the influence on blood pressure and we talked about using glycopylate to treat that. And vasodilation as well.

We talked about the difference between Aceromazine and meatomine in this regard. So you can actually see the detection and treatment of hypotension depends quite a lot on the underlying cause, so we need to think about all of these factors when we're evaluating hypotension. And the response to low blood pressure is not always give that patient a 5 or a 10 mL per kilo bolus of fluids, as you can see from this aetiology here.

There's quite a lot to think about. So incorporate all those six factors into your consideration if you have a hypertensive patient. Reaction to surgery, what if my patient reacts to surgery?

We would generally classify nooception, which is reaction to noxious stimulus under anaesthesia, as heart rate, rest rate, blood pressure going above 20% of your baseline, and your baseline would be the heart rate rest of your blood pressure when your patient moves through the theatre and is attitude to depth of anaesthesia. And you can see from this slide on the left, this is before we start surgery. Heart rate is 66, we've got a nice respiratory pattern there.

Our systolic pressure is 133/65. Instantly when the surgeon starts, you can see that heart rate jumps from 66 up to 130 and that patient starts panting. This dog definitely requires further analgesia.

Turning the volatile agent up isn't the answer, because we already said that that patient was suitably anaesthetized before the surgeon started. Our options here, further analgesia, we may repeat our opioid. If we've used methadone, we might get 0.1 me per gig of methadone.

We could use some ketamine I am. We could give 1 mg per gig of ketamine I, we could give half the meg per gig of ketamine IV. Some of you might be thinking, oh, ketamine myocariac patient.

These are low doses of ketamine. We're absolutely fine to use low dose of ketamine in a cardiac patient. And I'm quite happy to use the CRI of ketamine in a cardiac patient.

The whole ketamine cardiac story is related to in vitro experiments in isolated myocardium. So if you have an isolated myocardium, it doesn't have any sympathetic system to it to give a compensatory response. So if you put ketamine on myocardial cells, it decreases their contractility.

But in the real life patient, they have a sympathetic system to deal with that. So that's where the whole ketamine, story comes from. Take home, we don't tend to use ketamine for an induction agent that often anyway.

We're using our faxin or profile, so we're not using our bigger 5 mg per kg dose of ketamine, but we are using ketamine at 1 or 2 mg per kg and the CRI for analgesia. If put there in brackets and meatomidine. If you pre-medit that patient with melaomidine and you may have pre-meded your aortic stenosis or your hypertrophic cardiomyopathic patient with melaomabine, we could repeat the melaomine.

I'll come back to that. Our number 5 consideration, number 4 is monitoring, number 5 is planning. Whenever we anaesthetize a patient, we think about patient considerations, procedure considerations, and general considerations.

So we've got quite a lot to think about under the patient category which we've already talked about. Procedure wise, that's obviously very specific to the procedure that we're doing. And then our general considerations are hypotension, hypothermia and hypoventilation.

So let's plan to make sure we can detect and treat all of these occurrences should they occur. In planning, we can plan according to our cardiac status because hopefully we know a lot about our patients. We're going to use a safety checklist to make sure that we've covered all those considerations.

You may like to download the AVA safety checklist if you're not already using a checklist, and you may like to modify it for certain conditions and for your cardiac patients. Has the patient had the meds this morning, for example? Is there anything else that we should be administering to this patient?

Do we know what the results of the echo or the ECG are? Have we communicated our concerns specific to this patient? Checklists are there as a basis for you to adapt.

Pain, which analgesics should be used. I've already said we shouldn't be cautious about using our opioid analgesics. We should always use our opioid analgesics.

We should think very carefully about local anaesthetics. We should use local anaesthetics wherever possible to reduce that noxious stimulus and reduce our volatile agent dependence. And of course we should use a long story where appropriate.

I think the biggest thing we said for recovery was ongoing monitoring. We've planned carefully with regards to our temperature. We've considered analgesics in our patient, we're not gonna withhold analgesics because we're worried about the cardiac condition.

And we're gonna think about some angiolysis as well, because stress is a factor that can increase stress on our heart and increase myocardial oxygen function. There are quite a few things you need to think about, aren't there? You might like some of these answers onto your checklist.

So let's go and look at some of these cases that we're going to consider. And I think what I want you to take over from tonight is there's no such thing as a card one cardiac protocol fits all. You need to understand the disease, we need to be able to adapt our protocol according to that disease.

In all cases, do they need their meds? Should they be on meds? We should pre-oxygenate those patients.

We should put our ECG and our blood pressure on before induction. Should I just go 9 days, I think I've already answered that question. Failure is not an option.

A patient in congestive heart failure is not suitable for anaesthesia. I don't want them coming anywhere near me. What's gonna happen if I an anaesthetize that patient, it isn't going to end well.

They need to go back to the cardiologist and have their failure fixed. I'm not going to anaesthetize those patients. So conditions, dilated cardiomyopathy, we're gonna consider pathophysiology, drugs to avoid and what a normal approach would be.

For sensible approach. We're going to avoid alpha2 agonists. We already have a poorly contractile heart.

We don't need anything that's going to reduce that contractility even further, and that extends to reducing our volatile agents. We're gonna think really carefully about analgesia, that's gonna be high on the top of our list. We're gonna make sure there's patients.

Treated with Benin. And I know we talk about Pinbendin having a, a very rapid onset of action, but I don't think diagnosis, immobendin anaesthesia 1 hour later gives that heart time to compensate. So I like these patients to be receiving their medication for 5 to 7 days before I think about anaesthesia after a diagnosis of dilated cardiomyopathy.

Personally, I think these patients have a better outcome the the longer they're set up on the drugs. We talked about induction agents, we talked about using induction agents slowly. An opioid would be a suitable pre-med for this patient.

An alpha 2 agonist would be, sorry, an agonist would be an inappropriate choice. Aceromazine would be an OK choice for dilated cardiomyopathy, provided we don't reduce our preload too much, because actually we need this heart needs all the pre-load that it can get. It needs that stretch to gain as much contractility as there actually is in the heart.

We want to monitor blood pressure. If we struggle with blood pressure, the drug we're going to use to treat hypertension in this patient is going to be dobutamine to increase our cardiac contractility. Aortic stenosis.

Those days alpha 2 agonists are actually OK in these cases. What we have, we have an obstruction to outflow. You can see really nicely illustrated on that dia diagram there.

What an alpha 2 does in really low doses is it almost mimics the therapy that we would use, which would be a beta blocker such as atenolol. So we see a slight reduction in contractility, we see a slight reduction in rates that allows more time for ventricular filling and a little bit more time for a controlled ventricular emptying. So actually in that regard, alpha 2s are OK.

But I'd be thinking 1 or 2 mcg per kilo of Dex melatonin or melatonin, so very low doses. Preferably administered IV. If that thought just totally scares you, omit the alpha 2s.

Just give a methadone or a buprenorphine primate, that's absolutely fine. Again, we want to reduce the volatile agent in all of these cases. We want to avoid vasodilation.

We don't really want to drop that pre-load anymore. Again, I'm gonna say this every time, analgesia is the cornerstone of cardiac anaesthesia. This might be a suitable case for a co-induction with propofol midazolam or midazolam alfaxolone.

Something that you might like to consider. Let's think carefully about using local regional anaesthesia for these cases. In my experience, a lot of these cases are boxers presenting for cruciate disease.

So getting yourself a cruciate disease protocol in conjunction with an aortic stenosis protocol that focuses on ensuring cardiac output, but at the same time, optimising analgesia can be really important for these patients. And actually, I find with that, with a very low dose of alpha 2. Alfaxone for induction, a good nerve block.

Methadone, these patients cruise through their anaesthesia very nicely. Probably should have started with mitral valve disease, shouldn't we, because it's the most common cardiac pathology that we deal with on a day to day basis. What we really want to know with these patients is how severely affected they are, and we know that we can further classify those diseases into B1 and B2 now.

So actually, from an echocardiography point of view, this really helps us plan those cases. We want to reduce after loads in these patients, so actually a bit of vasodilation is a pretty good thing. That encourages forward flow, you want flow.

Out of the aorta, you don't want that flow going back across the mitral valve. Normally these patients have good contractility and we want to maintain that contractility. We want to ensure good venous return, so these patients do need some preload.

We need to think about giving these patients fluids. I probably use a lower rate of fluids than I used to use. We no longer think that a surgical rate of fluids is 10 mL per kg per hour.

5 mL per kg per hour seems adequate for most healthy patients. In a dog with mitral valve disease, 2 mL per kg per hour probably is adequate. And the reason for that is because we want to maintain that pre-load, that's the sole purpose for using fluids in those patients, but we don't want to overload them with fluids.

How much easier again. If that patient's receiving an ACE inhibitor, I'm gonna stop that 24 hours before anaesthesia and I'm gonna start it 24 hours later. We knew for several years that this was the advice in people because if you're receiving an ACE inhibitor, you're more likely to develop hypotension under anaesthesia and that hypotension is more difficult to to treat compared to patients not receiving an ACE inhibitor.

And this same study was repeated in dogs a couple of years back, so we now have the information to guide us. If that patient can't survive 24 hours off its ACE inhibitor, I don't want to anaesthetize it. And HCM, so let's give some consideration to those cats that you see.

A little bit of reduction in contractility is not a bad thing in these cats, and a slight reduction in heart rate is not a bad thing. Similar aims to those dogs with aortic stenosis. So actually, in these cases, low doses of alpha 2 agonists are appropriate.

I would kind of caution that I would just check. What I want to know is what is the diameter of the left atrium. So if there's any left atrial enlargement, I'm going to avoid using alpha 2 agonists in these cases.

So really that's where the value of that pre-anesthesia echo comes. Cat has a murmur, does the cat have HCM? Does it have a large left atrium, yes or no.

This is helping me in my decision making. Does it have hokum. So is there an obstructive element to cats, outflow tract?

And is there a dynamic component to that as well? These are all helping me make my decisions over which drugs are used, whether I use just an opioid in those cases or whether I'm happy to add a very low dose of alpha 22 to 5 mcg per kilo. Atrial fibrillation probably doesn't affect dogs as much as it affects people, and people that really .

Impairs cardiac output and makes these people very tired and suffer from atrial fibrillation. I don't think we tend to see that in dogs necessarily. We could maybe use some aces in these patients just to be hopeful about our antiarrhythmic effects.

If that rhythm isn't any worse. We want to maintain a heart rate because actually your heart rate is quite an important component of cardiac output in these patients. We will say that atrial contraction accounts probably for about 15% of .

Cardiac when you think about the whole forward flow component. So there is a component of atrial fibrillation that does affect cardiac output. Obviously it does influence ventricular filling and that therefore influences cardiac output.

If we were to drop the heart rate in these patients, then we may impair that cardiac even further. We want to ensure more attention, we want to ensure our venous return is good. So an Aceros in opioid premed in these patients is appropriate.

Slow minimal amounts of induction agents, you could use a co-induction agent. Alfax midazolam, preform midazolam, reducing our volatile agent, ensuring that analgesia is excellent in these patients, ensuring venous returns, so again, fluids are indicated. We talked about cases where we know what's going on.

What about these undetermined pathologies, what can we gain from history and examination? Exercise tolerance, let's ask the owners, what is that patient's exercise intolerance. Pulse quality, we can gain quite a lot for pul quality.

Is there a respiratory sinus arrhythmia? Because that helps me relax, sign of a healthy heart, respiratory sinus arrhythmia. Murmur location intensity, can we gain any more information for a very careful clinical exam?

And breed likelihood sometimes knowing the breeds can push that likely diagnosis higher up our our differential list. So these basic things we can gain from history and examination can almost help us where we don't have access to pre-anesthetic echocardiography. Drugs to avoid and why.

We want to avoid vasodilation, it reduces pre-load. We want to avoid a marked increase in afterloads, so we're not gonna go using big doses of alpitus here. We want to avoid the deception, so we're gonna do a really good job with our analgesia.

We want to avoid decreases in contractility. So again, analgesia will have a spare of volatile agents. We're not gonna use big doses of alpha.

I wouldn't use alpha 2 agonists in a case of undetermined cardiac pathology, full stop, because we just don't know what's going on. You can see alpha 2s are implicating quite a few of these. They increase after load, they decrease contraactivity, they cause bradycardia.

They're all factors that contribute to cardiac out which we don't want to impair. And extreme tachycardia, and I think we would see extreme tachycardia if we had a poor pre-med, for example. Or a patient that's not particularly well at these times.

He's primaine I'm probably happy to use acepromazine in an undocumented cardiac case. What's the worst that can happen, it can cause a little bit of of hypotension. Alpha 2 agonist I would avoid alpha 2 agonist in undetermined pathology.

I don't think there's ever a reason to say, oh well, I think it's OK to use now for these patients. Induction agents, let's apply the same principles we talked about before with our pray or our our faxlo. For our agents we want to spare them, and we've already discussed what we would do with our ketamine and how we're happy to use ketamine at analgesic doses, so sub-anesthetic doses in our cardiac patients.

Finally, I'm just gonna wrap up with how do I sedate a dog for that cardio exam. So if we've got a patient that's not particularly compliant and they need ECG or echo, what do we normally do in those cases? Dogs, we tend to resort to AC burophrenil.

This is the cardiologist's friend, and generally this will give you a fairly tractable patient, a combination of Aceyburophrenil without causing too many adverse effects. If this is a cat we're talking about personally, I think ACPop is a complete waste of time in cats. The combination I prefer and we use quite commonly for our hyperthyroid cats that either we can't get near them or they need a little bit of sedation for their, their pre-echo pre-anesthetic assessment or the pre-echo before their thyroid disease gets treated.

Alfax in 1 to 2 makes per gig, midazolam 0.3 per cake, and be in a 0.3 per cake all together in the same syringe I am.

That's a lovely combination. And remember our aim for sedating these dogs, all these cats, the end game is always to place an IV catheter and then we can adapt our sedation if we need any more. But it's an iron injection in a calm, quiet environment, placing an IV as soon as we can.

We've got IV access, we've got control, and then we can go ahead and perform our cardiac workup without affecting our echo parameters too much with those combinations of drugs that I've given you. So just to summarise, at the end of that hour, 7 principles, know what you're dealing with where possible. Focus on cardiac cat, but think about those factors that you talked about.

Understand the drugs that you're using and you've got more detail in the notes that accompany this webinar about drugs. Ensure that we use our monitoring effectively so our monitor's turned on, our monitors attached before induction of anaesthesia, and we're gonna keep that right onto recovery until we're happy that our patient doesn't need monitoring anymore. We're gonna plan really carefully so we don't miss anything and we don't add any time to that anaesthetic as well by being well prepared.

Don't shy away from analgesia in these cases, you can analges these cases very, very effectively and reduce stress on our myocardium. And we can be cautious with our patients in recovery. OK, if anyone has any questions, I'm quite happy to take some now.

That was an absolutely brilliant webinar, mass. Thank you very much. I've made pages of notes.

I'm sure our listeners have really enjoyed it too. So we do have a couple of questions so far. So the first one came through around the time that you were speaking about surgical stimulation, and the question is, would you consider buppivocaine?

I would use local anaesthesia absolutely wherever possible. Ideally, we've worked out a local anaesthetic technique that we can do beforehand. But if we haven't, I guess it depends what you're doing, and when you say bpivocaine, I'm guessing you mean like splash or topical.

It really, it depends entirely on the, the surgery that we're doing. So for example, in, let's say any nucleation in a cardiac patient, we often can't do a local block beforehand if there's infection or neoplasia, but buppivoca in that eye socket in a bit of lyre sips, a bit of absorbable surgical sponge is a perfect thing to do prior to closure. If you've got an incision and you haven't done an incision or block before the procedure, do an incision or block on your way out, just infuse some local anaesthetic into that wound once you've closed it.

No consideration, no, no concern for wound healing there and excellent analgesic for your patient. Thank you very much. And the next one is quite long, so bear with me.

So we regularly use mesotomidine and methadone for our orthopaedic surgery and boas surgery. It allows us to use a very low volatile agent while we top up with 0.02 to 0.05 mLs depending on the patient size.

About every 1.5 hours during the surgery as required. Over the years I've noticed that my core temperature of these patients is always a degree.5 or so higher, and it seems easier to maintain.

My understanding of this is because it causes peripheral vasoconstriction. Is this the case? Yes, you are absolutely correct.

A very good reason to use melatonidine versus aceromazine to conserve temperature. Yes. Perfect.

Thank you very much. And that seems to be the last of the questions. So on that note, I'd like to thank all of our listeners for logging in and spending the time to listen to the webinar tonight, and a massive thank you to you, Matt, for educating us all this evening.