Good evening everybody, and welcome to a Thursday night members webinar. My name is Bruce Stevenson, and it is my honour and privilege to be with you tonight, as we go through the presentation on conquering your fear of the ECG. I don't think we've got any new members tonight, so not a lot of housekeeping.

Usual rules apply. If you've got any questions, just click on the. Q and A box, pop them in and we will discuss them at the end.

One little thing I do just want to highlight to everybody is, don't forget our virtual congress. Very exciting, a whole week of CPD 100 hours free to members, but you do still have to register. So that's the 22nd to the 28th of February.

So really exciting there. So without further ado, tonight's speaker is Kiren Bogart, and he is the clinical lead in cardiology at Langford Wits. He's a diplomat of both the American and European colleges and an RCVS recognised specialist.

He was published widely, was of particular interest in feline echocardiography, canine cardiac biomarkers, and interventional procedures. Kieran treats all species with heart disease, and they've spoken all over the world on cardiology and interventional radiology. Kieran, welcome back to the webinar vet and it's over to you.

Thank you very much. I'm gonna just warn you up front that my cat is sitting next to me here, so who knows what's gonna happen. Hopefully, he's not quite at the point of advancing slides, but he can certainly shout loudly enough.

He's 1515 and, and kind of angry. So, forgive me if he butts in. We are gonna review the very basics of ECG, because this is something I think is super important for people to try and overcome their fear.

I. I'm not sure whether a lot of people's fear of the ECG is because it's quite an abstract concept, looking at the electrical activity of the heart, or whether it's just the fact it's on graph paper. So it reminds people of, of, you know, being in, you know, GCSE maths or whatever, and, and, and having trouble with.

That. So I'm not quite sure where the fear comes from. I think if we approach the ECG in a very basic, very logical, very methodical way, which we'll discuss this evening, then hopefully we can overcome those fears and actually start using this as a very important diagnostic tool in our clinics.

This is the first veterinary ECG patient that ever existed. This is Jimmy the Bulldog. And Jimmy the Bulldog, I always honour him at the beginning of any of my ECG lectures, because back in the 1880s, he was a bit of a, a sort of phenomenon really, because his owner was a physiologist.

And as you probably know, In Victoria in England, there was a big thing about science and, and the popular enjoyment of science. And Jimmy the Bulldog would travel the country and do evening shows where he was stood in a petri dish at either end, and, connected to a galvanometer. And this generated a trace of the electrical activity that was going on in his body.

And his owner was actually present in the House of Lords. He was a very well to do scientist, probably the science was a hobby I imagine. And he actually was part of the first ever debate in the UK Parliament on animal welfare because somebody raised the concern, they believed that Jimmy was being electrocuted by being connected to this machine.

And his owner correctly pointed out, actually Jimmy was doing the electrical activity. He was creating the trace. He wasn't subject to the electrical activity.

And this was happening in all of us. So, that was the very beginning of veterinary ECG and then people forgot about it for maybe 60 or so years, and then people started getting very interested in it again as veterinary medicine, became more of a technical profession back in the 50s, 60s, and 70s. So, cardiac conduction, let's think about the very basics.

If we try and understand the events that are happening, the anatomy, the physiology, then I think actually making the leap to understanding what's happening with the ECG and with arrhythmias is a little bit easier. So we're gonna review the very basics. Let's think about cardiac anatomy.

We've obviously got the sinoatrial node and the atrioventricular node. And the sinoatrial node is the dominant pacemaker of the heart, that generates the pacemaker rhythm, and that's what causes the P waves on the ECG. We're gonna review each segment segment, yeah, segment of the ECG trace in some detail.

The AV node. Is the gatekeeper of the ventricles. All the electrical activity in the atria has to pass through the AV node in the normal heart to depolarize the ventricles.

Now. It's very important to remember that the atria and the ventricles should only be connected at the AV node. Because there's a fibromuscular plate of tissue between the atria and the ventricles, and this atrioventricular plate is impervious to the electrical activity of the heart, apart from at the AV node, which means the AV node is a particularly important point.

In the heart, because not only does it allow electricity to pass from the pacemakers in the atria down into the ventricles, but it also slows conduction down, which, if we think about it, is good because it allows the atria to depolarize with electricity and contract and empty. Into the ventricles, which then fill and that primes them ready to increase stroke volume. So if we have a normal conduction through the heart, we have normal atrial contraction, ventricular filling, ventricular contraction.

If we lose that normal synchronicity, cardiac output drops about 20%. So it's very important that timing of that delay. There are different levels of conduction tissue in the heart, and if I just highlight with a laser pointer here.

We have some Pathways which connect the nodes directly, so we have the sinoatrial node connected to the AV node via 3 pathways, and a 4th pathway connects the sinoatrial node across to the left atrium. So the right atrium will be polarised a little bit earlier than the left. But this fast conduction tissue, this wiring from the right atrium to the left atrium, allows the left atrium to sort of keep up with the right and therefore maintain that sort of emptying of the atria at almost the same time to fill the ventricles.

It passes down into the atria ventricular node and then below that is the bundle of hiss. And this bundle really is what penetrates the fibromuscular plate. And the bundle splits into left and right bundle branches.

So the right bundle branch is very superficial, it actually hangs in a tiny thread of muscular tissue and crosses the lumen of the right ventricle. So this is actually very easy for us if we're doing cardiac catheterization or procedures to catch the catheter on and damage. Sometimes you see dogs with an ECG that suggests this has been damaged through some event in the past, and it's completely irrelevant, it's relatively common as an incidental finding.

The left bundle branch here actually spreads into a spider web of fibres across the left ventricle and it's much deeper within the myocardium. So getting damage to the left bundle branch is actually much less common and suggests there's more likely to be heart disease present. And at the very tips of these fibres are the smallest fibres of the conduction system called the Pikinji fibres.

And they penetrate deep into the ventricle to carry that electricity as close to the myocardial cells as possible, to allow the myocardium to depolarize. And the last little bit of depolarization is cell to cell. So there are different levels of conduction tissue in the heart, the higher up tissue.

Is capable of actually generating pacemaker currents similar to the sinoatrial node. So all of these cells in these fibres can generate pacemaker currents. In fact, that's true all the way down the heart.

There are different levels of these intrinsic pacemakers all the way down the heart. The reason the sinoatrial node is the one we call the pacemaker is it's the one that depolarizes most often per minute, so therefore it's the dominant pacemaker. So any cell in this conduction tissue can act as a natural pacemaker of the heart.

Tissues higher up, closer to the sinus node have a higher intrinsic rate of depolarization. So this is why the cyan neutron node dominates because it's got the highest rates, but further down we've got lower rates which will help us if we've got arrhythmias, if we've got blocks. Now what's slightly annoying I guess, but does explain why we get arrhythmias, is that if you take a normal myocardial cell, which doesn't have pacemaker activity, or a pacemaker cell from low down in the heart, say down in the left ventricle here, which shouldn't be doing any pacemaker activity unless there's a block somewhere.

If you make that cell hypoxic or damage it in some way, so make it ischemic, put it in an environment higher in potassium or aidedemic, then what you can do is actually make those pacemaker currents change. You can make them faster, you can make them slower, and you can take a cell that shouldn't have pacemaker currents and generate pacemaker currents by making that cell unhappy. So these are various mechanisms of arrhythmiagenesis.

So the intrinsic rate of the sinal node, I, I've written here 80 to 120. That's the kind of resting rate in a dog. I know cats are higher, and I know humans are a little bit lower.

I also know that if you take that dog and take it for a run, that will increase way above 120, OK? So there is a sympathetic effect to increase that, intrinsic depolarization rate. And there's the parasympathetic effect of vaal tone if the dog is sleeping, say, we often see on on hold at 24 hours.

ECGs, sleeping heart rates in dogs dropped down into the 30s at points. And that's a normal sinus rhythm at that rate. So clearly, dogs have a big effect of the, sympathetic and parasympathetic nervous systems on that heart rate.

I'm saying it's 80 to 120 for your average dog trotting about the house, trotting about the vets. The AV node has an intrinsic rate around about 60, and it doesn't vary much. It will be depressed by vagal tone, it will be increased a little bit by sympathetic tone, but nowhere near as much as the sinoatrial node, which is the most flexible and responsive of the pacemakers.

If we go even lower down still into the bundle branches, then we'll see that the intrinsic rate drops to about 40. And down in the Pikinji fibres it's 20 to 30. So this is how the sinoatrial node maintains dominance, it's because it depolarizes more often.

But if we were to chop off the sinoatrial node, that would be slightly unfortunate, but if we were to do that, the AV node would take over. And if we were to remove the AV node or damage it in some way, then these fibres down here would take over. So when we have these heart rates, 2030, 60 a minute, and they're these slow heart rates because of a block or something, we call those escape rates.

So this is the heart relying on its backup pacemakers. And that's really important for me as a cardiologist because these are the things that keep the dog alive, whilst I can get involved and and provide some treatment to try and help the patient. So, let's look at an ECG of sinus arrhythmia.

You've all seen sinus arrhythmia, you've all heard it, you hear it every day. This is actually on a halter ECG. This is a normal trace.

We've got a normal PQRST. It looks a bit weird cos halters look a bit weird because they're on the chest. They're a bit more like equine ECGs.

They're not on the limbs like we see in dogs, . What I'm trying to show you here is the phasic variation in heart rate we see that often is associated with breathing, not always, but often associated with breathing, so sometimes it's referred to as respiratory sinus arrhythmia. Each strip here is 30 seconds, each horizontal strip.

So you can see this is a dog at 1:30 in the morning through to just gone 1:36 in the morning. And you can see what happens is the heart rate speeds up, and it slows down again, and speeds up, and it slows down again. And you can see the patterns that this generates over the course of a full 5 or 6 minutes here.

So it's not just, when you're auscultating in the clinic, this happens, this will happen at rest, and, especially during sleep. So that's because of vagal tone, and vagal tone causes this association between the breathing and the rate. If we think about vagal tone, often there are pulses in vagal tone, it's quite a an irregular thing, so slow heart rates are normally irregular.

For example, here, we've got a dog who's under the influence of vagal tone, this is a strip of sinus arrhythmia. And here we've got another strip of sinus arrhythmia, and this is on a halter, this is on a 24 hour ECG. The software is marking these longer pauses as red, because it's suggesting that these pauses shouldn't be here, that these are problematic.

It's actually not the case, it's just that it's a dog ECG and dogs have longer pauses than humans, which is who the software is calibrated for. So we can see this phasic irregularity at lower heart rates. That is normal.

Slow and regular is bad. So if we have a heart rate less than 100 beats a minute, there should be a phasic variation. You can use the term regularly irregular.

I just don't like it cos it's hard to say and can confuse people. So slow and regular is bad, you should have the phasic variation brought about by vagal toning dogs. If you have a heart rate of 60 and it's regular, that is not reassuring.

So I've seen it written sometimes in clinical notes of a dog that I'm about to put a pacemaker in. Someone has written, maybe 6 months ago even. Heart rate 60, regular, good.

And I think, no, actually that's not true, it should be irregular. Now I know what that means, but slow and regular don't go together, and make me feel comfortable. Normally, if you have a slow, regular rhythm, that represents some sort of abnormality.

If you see that in the clinic, just try to stimulate some excitement or some stress. So I tend to give a little clap or whistle or me or something and try and stimulate a bit of sympathetic drive. And what that should do is it should increase the heart rate and make it more regular, but you should see that nice response to the catecholamines that you generate.

A good way is to try and open the door, reach the door and touch the door handle and the dog might want to leave, and the heart rate often goes up. If you don't observe that response to that little burst of sympathetic drive, that suggests there's a problem. So I said we're going to talk about basics.

We've got the normal ECG. On the left we've got a dog, on the right we've got a cat. And let's go through the basic morphology.

Both have a P wave. These are to scale, I should say. So the P wave is the first positive depolarization we see.

We tend to look at these in lead two. So we're gonna look at different leads tonight. I, I'm really looking at lead 2.

That's where the measurements are standard. The other leads are just different views of the heart and looking at the electrical activity from different points of view. So the P wave is the first positive deflection.

It's followed by a QRS complex. Now let's take a look at that. We call it QRS and we think the Q is negative, the R is a large positive, and the S is a small negative.

But actually in most dogs, they have a very small Q wave. The R wave is nice and tall and predominates in this trace. And the S wave is negligible.

You may see a little bit of an S wave, you may see more of a Q wave in a deep chested dog. So dogs like Dobermans, Dalmatians, wolfhounds, they'll often have quite a prominent Q wave. In humans, they don't really have a Q wave at all.

So any of you who've got family who are who are doctors or you know anything about human cardiology, yourselves through personal experience or family experience, Q waves tend to mean you've had some sort of myocardial infarction if you're a human, but in dogs, they are normal. And even deep chested dogs have very deep ones. The Swave should be a very small wave or non-existent as in this trace on the left.

In the cat there's really not a Q and there's not an S. So it's OK just to call that an R wave. I'll still use the term QRS complex cos if you can magnify that enough, you'll see there's something there, but there's not much of a Q and not much of an S in a normal cat.

Following the QRS complex we have the T wave, and the T wave can be positive, it can be negative, it can be biphasic. The important thing is, that it is less than 1/3 the R wave height. Or R wave amplitude.

So it shouldn't be the same height as the R wave, it shouldn't be nearly the same height as the R wave. And here in the cat ECG trace on the right, you can see that's a negative T wave. That's OK.

Again, in humans, they worry a bit about T waves, meaning something different, meaning old infarction or ischemic damage. But you know, first of all, that's not really something we see in cats, and secondly, we're looking at the heart quite differently on ECG in dogs and cats, because we're looking at them in a very different recumbency, and we're looking at the heart in a very different manner to how they would in a human being. So we can't compare those rules about the T wave and about Q waves and things, between the species.

So the P wave represents atrial depolarization. So this begins in the sinoatrial node, and when we leave the sinoatrial node, we start activating the myocardial cells of the atrium. So the electrical activity starts causing these cells to depolarize.

And what we're seeing here is the wave of electricity which is causing the activity within the cells of the atriary themselves. So if we have a bigger P wave, we probably have got bigger atria because there's more myocardial mass that we will see on the ECG. Next we see this interval in the PQ segments, the PQ interval, and that's a pretty flat baseline on the ECG trace.

This is where the electrical activity is sitting in the AV node. The AV node is an area of naturally slow conduction, so it's slowly sort of diffusing through the AV node. It's not really depolarizing any of the myocardial cells.

Therefore, we don't see anything happening on the ECG. The electricity's there, it's travelling through the heart, but it's kind of shielded, it's not in the myocardium itself, and remember we're seeing the myocardium here, we're not seeing the conduction cells. So when it exits the AV node into the bundle of hiss and the bundles and the branches, we get the QRS complex.

And this generates the the ventricular depolarization. OK. So this is where the ventricle, the ventricular mass will depolarize and at the same time it will contract.

I don't like using the term contractions about an ECG. So some people will say, . VPC means ventricular premature contraction, but actually that's not always the case, because obviously you can have electrical activity without a contraction.

That's how we get the rhythm pulseless electrical activity in an arrest situation. So try to avoid the term contraction about an ECG and talk about complex instead. So after the QRS complex, we have, sorry, during the QRS we've got the Q is the septum depolarizing, the R is the left ventricle, and the S is the right ventricle.

Now that's quite important because I said there's not much of an S wave. We don't often see that in in dogs and cats so well. If you see a big deep S wave, that suggests your right ventricle is big.

If you have a particularly tall R wave, that suggests your left ventricle is big. The deep Q waves don't tell us that much about the septum, but they often tell us about breed. So after the QRS complex we have ventricular repolarization, which is the T wave.

And this, the reason this doesn't look so narrow and so organised as the QRS complex and also the reason that it can be quite variable in appearance between individuals, is because repolarization happens cell to cell. Instead of going on this very defined conduction system where the electricity travels in a very organised manner, it just happens cell to cell and the electricity sort of fades away as the cells return back to their resting membrane potentials. We're gonna talk about two different morphologies of beat.

These are both from a cat ECG and the ECG trace on the left is is actually from a normal cat, but the ECG looks a bit strange because of the position the cat was in. So forgive me, that, the T wave looks very tall compared to QRS. But we can see here we've got the P, the QRS and the T.

If you look at the trace on the right, that ain't normal. There's no P wave. There's what looks like a big negative deflection in this case, and then a T wave here.

So this is the QRS, very abnormal looking and a T wave. So this is a ventricular beat and the way to remember it. Is that the ventricular beats are wide and bizarre.

They usually are followed by a pause, not always, but usually. And again, they most often have no P wave. If they do have a P wave there, it's not related to that.

It just happens that the heart was trying to generate a normal beat at the same time as the VPC happened, that can be a bit misleading. So The reason that we've got this nice positive P wave here is because in lead two, we're looking at the axis of electricity across the heart from the right hand to the top right of the heart, if you like, to the left leg. So, the top right of the heart to the bottom left.

So, when the electricity passes across the atria from the sin of atrial node, it's passing towards lead 2, which is what we're looking at. And we're looking at lead 2 here, we see a nice positive P wave. Then we go down to the ventricles as a nice positive QRS complex or a positive R wave because it's coming down towards the positive electrode of lead 2.

The ventricular beat looks the opposite. It's a negative wave and then a very bizarre looking T wave. And that's because it's probably starting somewhere down the left ventricle and going in the opposite direction, which is why it looks negative in lead two.

So the, the, the negativity or positivity of the wave tells us about the direction of conduction in the heart itself. So if you have a beat that's negative, next to a beat that's positive, they have to come from different places and they have to be coming from probably opposite sides of the heart. The reason it's wider than normal is because this is not going within the normal fast conduction system.

The QRS complex is narrow because this electricity is travelling on this superhighway, a very specialised conduction fibres. The ventricular premature complex is wide because it's travelling on the back roads. It's not travelling on the motorways, it's travelling cell to cell between the cells themselves, the normal myocardial tissue, rather than on the specialised conduction tissue.

So it just takes longer, which is why the complex is wider than normal. So when you're looking at an ECG, there are 4 main steps to interpretation, and I promise you that if you follow these very basic rules every time, it will stop you becoming overwhelmed by what's going on, cos there's a lot of information in the ECG. And secondly, it will allow you to be super methodical and not miss anything.

So the first step is look at the heart rate. I used to have nightmares before my board exams that I would be in the board exam, presented with an ECG, and I didn't have nightmares about it being horribly complex. I had nightmares about me being so confused that I couldn't work out what the heart rate was.

And actually, I have had cases before where we're discussing with students or, or interns or vets in practise, and I said, what, what do you think of this ECG? And they're telling me about blocks and brady arrhythmias and things. But the heart rate's 200.

So of course it's not a Braddy arrhythmia, that's a tacky arrhythmia. So start with the heart rate, that's gonna set you up straight away for thinking, OK, it's too fast, or it's too slow, or it's normal. So it'll give you differentials if you like, just based on the heart rate where you can begin working out what's happening.

Next, look at the regularity. Is the rhythm regular or irregular? So if there is an irregularity, is there a pattern to it?

Does it look like sinus arrhythmia? Or is it just chaos? And think about that in terms of the heart rate as well, so remember I said slow and regular is bad.

Next, look for the P waves, look for the QRS's and try and establish a relationship between those two waves. So is there a P for every QRS? Is there a QRS for every P?

If those are both true, are they reasonably and repeatedly related? So when I say reasonably related, I don't mean that there's just a ratio of 1 to 1, but they're at random intervals from one another. Are they, are they, you know, a, a normal physiologic interval?

Do they look as if they're connected, and is that relationship repeatable throughout the whole trace, or does it change? The 4th step is then to try and make a rhythm diagnosis. So is it supraventricular or ventricular?

Are the complexes upright and narrow in lead to, or do they look wide and bizarre? And that can help us then say, do we have a normal background rhythm with some abnormalities on top, or do they all look abnormal? Is it tachycardic?

Is it not? Is it regular? Is it irregular?

So suddenly, from answering these four questions, looking at these 4 steps, we've managed to achieve quite a complex description of what's happening in the heart. Calculating heart rate is a real bugbear for some people, but actually it's very easy if you have a 15 centimetre ruler or, in fact, a big biro with the lid on. The lid on is an important calibrating step to make sure that this measures 15 centimetres.

Now, ECGs will print out or be on screen cos many of you will have digital machines, I suppose. And it will have a rate of the paper speed. So generally, there are two main paper speeds, 50 millimetres per 2nd and 25.

You can get machines that will run them at 10 millimetres per second and even at 100, but 50 millimetres per 2nd and 25 are the standard ones. So if you take your BIC biro at 50 millimetres per second, so that's 5 centimetres per second, that means your 15 centimetre biro is 3 seconds long. So you can count the number of complexes that your pen touches when you put it on the ECG and multiply it by 20.

That will give you your heart rate in 60 seconds to your minute heart rate. And at 25 millimetres per second, because the paper speed is slower, it means that that's now 6 seconds within your pen. So you just multiply by 10.

So you count in a row of complexes and multiply by 10. So we're gonna look at some interactive ECGs. I will give you either a 15 centimetre bar and a paper speed.

If I don't give you a paper speed, I'll give you how long that 15 centimetres represents. So here's an example. This is an ECG from a dot.

It is not totally normal, but it is not totally abnormal either. So we're just gonna look at it as an example of how to calculate heart rate. So looking at this, I would just eyeball it and say, yeah, it looks pretty regular.

I can see a P. QRS T Fine. So this is probably a sinus rhythm and it looks regular.

OK, what's my heart rate gonna be? So, I need to look at the paper speed. So on our machine, when it prints, it comes out at the bottom 50 millimetres per second.

This is the amplitude. So 20 millimetres per millivolt. So that's measuring the height of the QRS complexes.

I don't want to get bogged down in that, that's, that's generally not that important, certainly not as important as the rhythm diagnosis. So our paper speed of 50 millimetres per second. So if we lay our BI biro on top of the ECG, that's a 15 centimetre marker there I've put on, which is to scale, that's 3 seconds.

So I'm counting 1234567 complexes in 3 seconds, which means there's 70 complexes in 30 seconds, which means in 1 minute there is 140 complexes. So it's 140 beats a minute. So this is probably a sinus tachycardia.

So what's happening here, let's apply our our rules again in this example. Trying to remember, do I have a poll question associated with this? I don't think I do.

No, you don't. I don't. Good.

And I'll give away the answer. So applying our rules to this ECG, what's the heart rate? Well, the heart rate's actually about 60 per minute.

I've not calculating it on here cos it's a very short strip of ECG. We've got a P, QRS, quite a deep Q. Maybe it was a deep chested dog.

P. QRST OK PQRST. OK, so straight away we can see we've got a rhythm that's slightly irregular.

If this is representative. Have we got a P for every CRS? Yes.

Is there a cureS for every P? Well, no, if that's a P wave, that's a positive deflection with no QRS afterwards. So that's interesting, .

The heart rate's pretty normal, kind of low end of normal. Are the P waves and CRS is reasonably and repeatably related? Well, that looks normal to me.

That one looks a little bit longer than this. But it's still kind of normal. This one looks pretty normal, and obviously this one hasn't conducted through.

So are they reasonably and repeatably related? They are reasonably related, but there's a little bit of variation in that repeatability. And the rhythm looks super ventricular, it's upright and narrow in lead two.

There's nothing wide and bizarre, and all the complexes look reasonable to me. So this is probably a normal sinus rhythm, but we've got this block. How do we classify that?

Well, that's an atrioventricular block. So we've got a P not followed by a QRS. So this is a type of AV block when you get occasional pes that are blocked, and that's called a second degree AV block.

And actually we often see this type of block where we have a variation in PQ interval like this before a block in dogs who have got high vagal tone. So actually, this is probably a dog who's had some opiates, and is quite relaxed or sedated. Maybe it's a very brachycephalic dog, or maybe it's just a super relaxed dog in the home environment, because they will sometimes get blocks like this as well.

So this is not the sort of block that concerns me. Is it human dynamically significant? Well, heck no, not if this is happening, you know, very occasionally.

We've got, you know, normal beats around it. This dog's blood pressure hasn't even noticed that there's been a block. So, arrhythmias, tacky arrhythmias, braddy arrhythmias, I think ECGs are super interesting.

They tell you a lot about what's going on. I worry that most of you are kind of switched off now, you're doing a homer, and we've all been there, and, most of us have been there in an ECG lecture at some point, so I apologise for that. I think these ground rules of how to look at an ECG are super useful.

We are gonna go on. To look at some interactive ECGs. This is what Jimmy would have wanted, he would have wanted to leave this legacy of us enjoying ECGs and talking about it for the session.

So, here is your first case. What I'm gonna do is just give you a moment to take a look at that ECG. Before I ask the questions.

So remember, think about the heart rate. Think about the The rhythm And think about Whether the morphology of these complexes is normal. These are the things we're gonna talk about.

So, your first question is what is the heart rate? I'm a kind person. I've got a paper speed there at the bottom and you've got a 15 centimetre marker.

I don't know if the pole is covering your slide to see the 15 centimetre marker. It can drag it, yeah, I just realised that. So if, if it is covering your 15 centimetre marker on the screen share, you can just drag that poll out of the way.

This is anonymous, I can't see who's voting for what. So, you can vote what the heart rate is there. You've got an MCQ, so answer A is 40 beats a minute, answer B is 80 beats a minute, answer C is 120, and answer D is 160.

Folks, all you need to do is simply just click on the answer that best suits you. And as Karen said, it is anonymous, so nobody will know. There's no repercussions.

Exactly. And the best way to learn the ECGs is to do ECGs. So yeah, I mean, you, up until now, you've made it sound absolutely simplistic, and I can't ever believe why I've battled with ECGs before.

It's about putting it in practise and that's where, where it becomes a problem. So, come on guys, give us a vote. We, we have We don't have many, many, answers in yet.

I normally would end the poll by now, but I'm gonna give it a little bit longer because I do think it is important. I'm gonna remind people, so don't forget, this is, this is 3 seconds because we're on 50 millimetres per second if we look at the bottom of the screen there, 50 millimetres per second. And this is 3 seconds that we can see here.

So in 3 seconds, just count the number of complexes that touch the pen or touch the bar. OK, so I'm counting 1234. So 4 by 2 is 8.

8 by 10. We know that Yeah, we got a whole lot of answers coming through. Let's poll and And share those results with you.

So, it's a, always a, a tough one. The first interactive poll, I think, because people don't want to put themselves out there. But you're not, you know, you're not raising your head above the parapet, you're not going to get shot at or anything.

And, and, I have a little thing above my desk to remind me every day. It says, every expert starts as a beginner. And I think that's true, you know, we can be a beginner at a new subject, we don't have to be inexperienced as vets.

So yeah, this is an 80 beats per minute heart rate, as I, calculated as I, as I sort of read out there. The ECG is, is abnormal in other ways. There's some other stuff going on for sure, and we'll come on to that in just a moment.

So, What's the main abnormality that you're seeing here? So remember, look at The rate, is it regular or irregular? Sorry, the rhythm, is it regular or irregular?

Is there a P for every CR? Is there a CRS for every P? Are they reasonably and repeatedly related?

What's the rhythm diagnosis? Are there any abnormal beats in the background of normal beats? Does everything look weird to you?

And how would you call that? So think about, you know, is that ventricular or supraventricular, is there a block, is there a chaotic irregularity? So I've just put 4 answers up here.

What's the main abnormality? Answer A is atrial fibrillation. Answer B is atrial premature complex, and C is ventricular premature complex, and answer D is atrioventricular block.

Now, I know that there are some, there's more than one abnormality here, but there is a, a primary abnormality which should be leaping out at you, as you look at this. So don't think, oh, it's I'm probably guessing something that's too easy. I, that's not the case.

We're just using this as a talking point and an example of sort of jumping off point for discussion. Once again, Kieran, I'm going to extend the question waiting time a little bit just because we do need people to, to really look into this and understand it to get the greatest benefit out of it. Remember, folks, absolutely anonymous, so don't feel embarrassed.

Look at it, work it out, and then make your selection and just click on the relevant answer. I'm, I'm gonna walk you through what I see. You're gonna give the answer again, aren't you?

Probably, that's OK. That's not, I mean, there's no, there's no prize, you know. It's your presentation you're entitled to it.

I'll, I'll do less walking through as we go. This is only the first case, so the . You feel free to vote or not vote.

I don't mind, but you know, vote, vote for what you are gonna go for, rather than what I tell you, because otherwise everyone's going on to the same thing, and that's a bit boring, isn't it? So I'm walking it through. I, I always look at lead two.

I, I look at other leads, if I think, oh, can I see a P wave? Oh, I'm not really sure. I look at and look at another lead.

Can I see it there? Yeah, all right, it's probably a P wave. So I use the other leads to validate what I'm seeing in lead 2.

OK, so don't get distracted by these, these other 5 leads. Look at lead 2. So here we've got a positive flexion, and then a big wave in the middle.

And then another wave. This is, this is a PQRST morphology here. Could that be a P wave?

Because it's quite short, isn't it? Well, look in lead one, yeah, it's present. It's there as well.

It's there as well. That suggests it's real. If we're seeing it in multiple leads.

So it validates what we're seeing in lead two. So there's P. QRS.

T In the second complex we've got another P wave that's a little more obvious, isn't it, a little wider, a little taller. QRST P QRST. P QRST.

The QRS is funky looking, isn't it? It's a little wider than it should be. There's a little notch in it.

Yeah, OK, so that's a bit weird. And when I see things like that, where you've got a normal rhythm, but the QRS morphology looks a bit weird, I worry about heart disease. Obviously as a cardiologist, I worry about heart disease more than most, but I think here I, I think, oh, I wonder what's going on in that heart to make it look so strange.

But the rhythm is normal, so we're starting from the sin atrial node, we're depolarizing the ventricles and the ventricles re-polarized. That's fine. I'm, I'm OK with that, that's a normal rhythm.

I'd expect a normal pulse from that. I'm not worried I need to do anything about that. We walk it along, we've got 4 normal complexes.

Are they regular or irregular? Well, there's a little irregularity, isn't there? But the heart rate's about 80, so it's less than 100, so it's, it's expected to be a little bit irregular.

Then we have this complex here. So this complex is not the same as the others, and therefore we can call it bizarre. It's a little wider, although these are a bit wide, but this is wider and it looks different to us.

It's negative compared to the positive deflections we're seeing here. OK. Can I see a P wave associated with this?

Well, I don't think so. I can see the T of the previous complex, but I can't see anything else there. So this looks like we've got a QRST that's wide and bizarre looking compared to the others.

So I'm gonna call that a ventricular beat. Good. So we've got the majority of people coming down on, on ventricular premature complex, and I, you know, obviously that's absolutely what I would agree with.

Atrial fibrillation, we've got, I think 10% of people staying at AF, 5 saying atrial premature, and 10% saying AV block. So I can't see any non-conductive P waves here, and non-conductive P waves would be the hallmark of an AV block. So I can't see any non-conductive P waves, so that rules that out for me.

Atrial fibrillation, there's no good looking P waves. We just have a baseline that's really strange looking, fibrillation, it's just fine, electrical activity, little undulations, and it's highly irregular. So we have got irregularity here, but because the heart rate, is less than 100, it's allowed to be irregular, it's expected to be irregular, and there are P waves in front of all those QRS's.

So I would exclude there being atrial fibrillation based on that. I don't think I can see an atrial premature complex. It, it's difficult because when you've got sinus arrhythmia, some beats come a bit early, some beats come a bit late because of that irregularity caused by vagal tone.

But nothing here looks like it's crazy early to me. It doesn't really break a rhythm, it looks like this is, this is sort of ticking along nicely. So for me, the main thing that I'm concerned about here is a ventricular premature complex.

And that's where I've highlighted it here. So I would describe this ECG. When I describe an ECG like this, I would say the predominant rhythm or the background rhythm is sinus rhythm or sinus arrhythmia, OK.

The heart rate's 80 beats a minute. We used our a BIC biro to do that. And there are some VPCs.

Now here we just have one VPC, but if we took the ECG for 1 minute or 3 minutes, you'd probably have a few more VPCs. And also there's this notch in the R wave in the QRS complex. I'm just gonna say that's a notch.

It's a little splintery, you know, appearance. I'm not gonna worry too much about that, because the rhythm is still being driven by the heart's predominant pacemaker. So for me, the major abnormality is the ventricular premature complex we can see there.

Here's the 2nd case for you. So take a look at this. This is also from a dog.

They're all dogs, I think you see cheese. And this is lead 2. So have a look So the first question is what's the heart rate.

So this is at 25 millimetres per second. I can't tell that by magically looking at it, although, you know, I'm pretty good, I'm not that good. But I've given you a 6 2nd marker there.

So remember when you've got 6 seconds to obtain your minute heart rate, you multiply by a factor of. Do. I think Most people have very smart pens now with sort of rubber grips and I don't know, highlighters on the end and all sorts of fancy things from drug companies.

But I still like the really cheap big biros because they, they just do me so well for ECG analysis. I'd recommend you carry on with you at all times. It does change the heart rate quite significantly once you start adding rubbers and highlighters on the end, doesn't it?

Yeah, it does, yes. Makes for some interesting diagnosis, if nothing else. That's very true.

Suddenly everything's just 10% more tachycardic. Right, folks, another 15 seconds, . And then we will end this poll.

Right, Kieran, I think you're going to be pleased with the results on this one. There you go. Ah, very good.

So, 120 beats a minute. Absolutely. Is that OK?

Yeah, it's fine, isn't it? It's a dog in the consult room. You know, we're not too worried about that.

If the dog was asleep at home with a heart rate of 120, that would probably be quite gravely. Concerning. So always remember the context of the patient, you know, think about how worried they are to be there, think about their age.

Breed is not important in heart rate. Big dogs, so Great Danes, don't have a massively different heart rate, heart rate to Chihuahuas. It works out about 10 beats a minute.

So, you know, often people are told that big dogs should have a lower heart rate, small dogs, higher heart rate. It's just not really clinically important. So, you know, if you've got a Great Dane that's got a heart rate of 120, that's really worried to be there, I bet you wouldn't worry about that in a chihuahua.

I wouldn't worry about it in a Great Dane, because they're not different. They're the same species. And what we do see is that juvenile dogs have a higher heart rate than older dogs, probably just because it's all new and exciting or worrying for them.

So what's the major abnormality? So have a look again, remember, is the rhythm regular or irregular? Have we got a P for every QRS QRS for every P?

And are they reasonably and repeatedly related to one another? Is there any rhythm problem? Is there any ventricular beats, or anything else that we can see?

So remember these questions as you're looking at ECG because these questions are super important for picking up all the things. The question for the poll, has got the potential answers. A, atrial premature complexes.

B ventricular premature complexes, C, atrial fibrillation, and D atrioventricular block. We've got some very fast answers coming in, which is great to see. People are flying there.

Yeah, some people are just spot on the mark. But folks, take your time. This is about understanding and reading and listening to what Karen explains to us and how he explains it afterwards.

So, please don't be shy, don't sit on the fence, have a look, make a judgement, make a call. Doesn't matter if it's right or wrong. If it's right, fantastic, you've got the understanding if it's wrong, it's great.

We're recording this and we can go back and watch it over and over and get it to sink in, so that's fantastic as well. In the notes that I've provided, I've given you the the ECT strips so you can, if you want to watch it back, you can annotate the ECG strips as you go and make notes on there. I thought that might be useful, more useful.

I'm sure it will be. Fantastic. Right, so let's end this poll quickly and share those results with you.

Fabulous, yes, so we've got a majority coming down on atrial premature complexes. A couple of people saying atrial fibrillation, AV block, and VPCs. I, I would say absolutely this is is atrial premature complexes.

You can also call them supraventricular premature complexes. So if we walk through the rhythm. We've got P QRST P QRST.

Again, again, then this is the T wave. And suddenly we have another upright narrow complex here. So it's got a QRSMT.

So it's not wide or bizarre, it's a tiny bit shorter, but that's not that big a deal. That may be related to respiratory motion, cos you see there's a bit of motion on the strip as we move along. It may be related to some other facts as well.

I can't see an obvious P wave, but actually the complex looks to all intents and purposes, the same as the rest. So it's not wide, it's not bizarre, and therefore it's not fulfilling my criteria for for calling it ventricular. So this looks like a beat from the atria.

So we're gonna call these atrial premature complexes or supraventricular premature complexes. And we've got one. 2 And even a 3rd 1 here.

So they're fairly frequent, bearing in mind that this is about 7 or 8 seconds of ECG we're looking at here. So they're fairly frequent. So when you're auscultating, you might hear this and think, gosh, quite irregular.

So on auscultation, it would be quite difficult to identify that it's not atrial fibrillation, which is highly irregular. But what we can say is that with atrial fibrillation, you do not have nice obvious P waves. And here we do, we've got nice P waves for every other complex apart from the prematures.

OK, so this can't be atrial fibrillation, because you don't have atrial fibrillation that lasts for one beat. If you do have temporary atrial fibrillation, which is quite rare, but normally it lasts for several minutes before it goes back into sinus rhythm, and they're very hard to pick up those cases. I've seen a few, but they're only detected on 24 hour ECG.

So what's the major abnormality? Well, these are atrial premature complexes, so let's look at the difference here. We've got the ventricular premature complex at the top, so it's wide, it's bizarre, it's by bizarre I mean it, it looks different to the other complexes.

OK, versus the atrial premature complex, which looks pretty much the same as the other complexes. So with the VPC my differentials would be heart disease, of course, heart disease causes arrhythmias, predominantly disease of the ventricles would cause VPCs. Most heart diseases for the ventricles, so that doesn't really narrow it down.

But VPCs we see with lots of different systemic disorders. So we see them, strangely, we don't quite know why with splenic masses, we see them with things like gastric dilation vvulus. We see them with septic foci, any severe inflammatory disease, hyperthyroidism in cats, sometimes just the stress of being at the vets.

We will sometimes put a a 24 hour ECG on a dog, send it home. And you get your results back, and all the VPCs happen in the car park of the vets and in the car on the way home and they get home and they never have any for the rest of the day. So, you know, these halters, these 24 hour ECGs can be very revealing in that regard.

Atrial premature complexes generally are non-cardiac in origin. Mostly they're caused by stress, fear, pain, inflammatory disease, systemic disease, especially patients who are behind on fluids, things like that, and, and under the influence of catecholamines or painful, atrial dilation can cause atrial premature complexes, absolutely, but. When I see them in a dog who is in the vet's for another reason, I focus on the other reason.

I don't focus on the atrial premature complexes. Ventricular premature complex is is a little bit more of a flag for me, there might be something going on with the heart. So, got 2 ECGs here.

We're gonna have a couple of questions about this, but these are, these are sort of in contrast to one another. You've got two very different heart rates. So the top here, we've got an ECG strip with a heart rate of 280 beats a minute, versus at the bottom, a heart rate of 160 beats a minute.

So I'm just gonna give you a moment to look at these traces and sort of compare and contrast them, have a little think about what we're seeing. These are all traces that I've. Recorded over the years in patients in my clinic, or clinics that I worked in.

So, you know, there's little wobbles, there's little marks on the ECGs, that's just it's just life. They're real traces, they're not idealised. Hopefully they, they show what we want to see.

So my question Which relies on you thinking about what arrhythmia we're seeing is do you treat this arrhythmia? We're focusing on the top ECG here. So do you treat this arrhythmia that we're looking at?

So the heart rate is 280 beats a minute. Walk through what we're seeing on this trip. You may see to do like this fairly frequently, depending on what sort of practise you work in.

The answers are coming in nicely, so very good. It's . This is an easier one to answer.

Good. All right, 5 more seconds and then we'll end this poll. Feel like we need some sort of musical countdown.

Let's get those results up. Ah, I, I love it when there's a sort of a bit of a split, 70/30. So 70% of people would treat the arrhythmia, 30% of people would say no.

So, I, what am I gonna do? Let's see what, whether people would treat the bottom one. First, and then I'm gonna discuss them both.

OK, so the bottom one, the heart rate's 160 beats a minute. Again, the question is, would you treat the arrhythmia? We clearly have some strong opinions on this one, Karen, they're coming in thick and fast.

I like a strong opinion. Who thought vets had strong opinions, hey? Yeah.

Not, not the, the, the strong A-type personality that you would expect to just answer things straight off, is it? You would do that. Right, folks, we're gonna give you another 15 seconds on this one.

We've got a lot of numbers in already, but I'm just gonna give you a little bit more time. Just for the stragglers coming through, another 5 seconds. And then we will reveal the answers.

Right, so let's do this quickly. So 76% say yes. So more people, a greater proportion of people would treat the bottom one versus the top one.

Super interesting. I often worry that I enjoy these interactive polls more than the people who are doing them. But they are revealing of what the audience is thinking, so that's always, yeah, and I think, I think it's important to say that, I'm just gonna wind it back to this slide.

It's important to say that actually, you know, there are some things where there's just no consensus amongst the experts. So, if, you know, I, I'm saying, oh well, you know, I would never do this, and I'd always do this. Well, actually, you know, there's probably another cardiologist or critical care specialist or anaesthetist or, or whatever out there who's like, oh no, that guy's talking rubbish, I would definitely always do this.

. So, you know, the fact we've got some disagreement amongst our peers here is, is, is normal, and really to be encouraged. So, I'm gonna walk you through what I'm seeing in these traces, and I'll give them names, because you saw I popped up a couple of names there, but I want to be able to see the trace, which is why I've backtracked. So here, my trick when I see an ECG like this, first of all, I think, oh my goodness, what's going on?

I want to look for the normals. So over here, I can see some normal complexes, so I can see a P. QRST P QRSTP.

So I'm looking at this and thinking, OK, well that's reassuring, that's my benchmark for what normal is. So what the heck is going on here? Well.

If you take one of these complexes, it's wide. It's bizarre, looks different to the rest. It's wider.

Therefore, this is a ventricular complex. So we have a, a, a run of ventricular complexes here. I don't know how many.

I mean, I'm just gonna guess the length of my thumb. You, you know, this is really technical here. We've got 12345.

We've got about 35 ventricular complexes, maybe 32 in a row there, at least. And actually, I can tell you this is from a long strip where this dog had about, 20 or 30 seconds of heart rate like this, at around about 280 beats per minute. So, that is worrying for me.

Because if we have a ventricular rate that that's that fast, when is the heart filling? Because normal heart rates in dogs, you know, they, they'll go up to 200 under duress when they're exercising, when they're very worried, they will go to 200. But that's in sinus rhythm.

So it's a bit more coordinated, your, your emptying's better, your filling's a bit better when it's more coordinated. With ventricular beats, it's not as efficient, the filling, the emptying of the heart's not as efficient. And the way the heart rate gets higher is not by making systole shorter, or at least not much shorter, diastole gets shorter.

So therefore your filling time in diastole reduces. So with a heart rate of 280, your cardiac output will be really, really poor. And actually, if you feel the pulse, the pulse rate might be about 50 or 60 per minute.

But the heart rate would be closer to 300. So that's telling you, electrically, that heart's moving frequently. But it's not able to generate enough pressure to open the aortic valve to get blood out because it's filling so poorly, the rates so high.

So actually, the top 10 yeah, I would treat that. I mean, in my head I'm looking at it and I'm reaching for the lidocaine at the same time, OK? So that's a real worry to me.

Even if it's only sustained for 10 seconds, it's very fast, and if that became sustained for longer, that could be a lethal arrhythmia. The other thing is, rates that are that high can be quite electrically unstable. So when you see, I'm just following the laser pointer here on the left, when you see the second complex in a row coming right off the back of the of the first, so you see here we've got a little notch of baseline.

R. T And there's hardly anything, there's really no baseline before the next R wave. So this is often referred to as R on T phenomenon.

There are some different definitions of that from human cardiology, but most veterinary cardiologists will call this R on T phenomenon. And when you've got the R coming off the T of the previous beat, electrically, that's very unstable and actually can cause ventricular fibrillation, which nobody wants to observe. So I would, I would definitely reach for treatment in this particular dog.

And I imagine this dog looks rubbish. I imagine it's panting, it's sort of focusing on what's going on, it's not really very happy. The bottom one is a very different creature, because the heart rate here is 160.

So with a heart rate of 160, actually it's pretty normal. It's a little high for a resting dog, but, I'm not so worried about fitting being compromised. It's not electrically unstable because there's a big old baseline between the QRS complex and the T wave.

It's the T wave of one, CRS of the other. And actually this is the sort of rhythm at this rate where I tend not to reach for treatment. I don't tend to start worrying about treating ventricular arrhythmias till they're over 200 beats a minute.

So 160 beats a minute, especially when it looks very regular and these morphology of the complexes look pretty much the same every time. I'm not so worried about it. In fact, look at the sinus rhythm to the left.

The rate of that is not dissimilar to the rate of this. So if we give this a name, I'd call the top one ventricular tachycardia, or maybe even fast ventricular tachycardia to be as descriptive as we can. The bottom one, I'd call it accelerated idioventricular rhythm.

I, I hate that term. These are just sort of confusing terminology, but at that rate, most people don't call it ventricular tachycardia, because actually for a dog it's not that tachycardic. So we call it accelerated ido.

Ventricular, I don't know why it's ventricular rhythm. Often these are associated with systemic diseases. So these are the sort of arrhythmias we see in septic patients, patients who are behind on fluids, patients who are really painful, you know, with a rhythm like that, I will often.

Try and give a fluid bolus or assess analgesia, or, you know, look at the patient holistically and not really think about treating with antiarrhythmics. So I guess my question was quite vague. Would you treat the patient?

I guess I would treat the patient, but I wouldn't be treating the arrhythmia. So, Here's another ECG. We'll look at this one and then we'll skip forward to a final case, because I know things are, it's getting late a little bit, so we'll wrap it up fairly soon.

So take a look at this ECG, and have a think about what we're seeing again, focus on lead two. And you can probably predict the first question is gonna be about heart rate. So be thinking about the 50 millimetres per second or 25 millimetres per second, it's down the bottom of the paper.

So I'm gonna give you 15 centimetres and your first question on the pole is what's the heart rate? Remember to think about the rhythm, not only from a, a sort of, is it supraventricular or ventricular, but think about is it regular, is it irregular, if it's irregular, are there patterns to it? So think about these other things too.

Right, folks, again, you know the story by now. Click on the answer that best suits what you believe to be correct. And once again, it is still anonymous, so I can see the rate that they're coming in, but we don't know who is answering which answer.

So, what is the heart rate? Option A, 75 beats per minute. Option B, 100 beats per minute.

Option C, 150, and option D, 200 beats per minute. We're just going to give this another 10 seconds cause we've got some stragglers coming in. And Let's reveal that quickly.

There you go, Karen. Great. So people are coming up with a heart rate of 200 beats a minute.

So we just count the number 123456789, 10. Multiply it by 20 because we're at 50 millimetres per second, so that's a heart rate of 200. OK, good.

So, it's tachycardic, that's for sure. So you see straight away we're thinking, OK, well what, what could be causing tachycardia, what rhythms can be, can be associated with a high heart rate? So just have a little think, there's no poll associated with this.

Have a little think, what other abnormalities are you seeing on this ECG cos obviously it's not just the rate that's too high, there's something else going on too. I think With our students who come to the clinic at Bristol Uni, On a Monday, I always say, well, what do you want to learn this week? You know, what, what can we do to make your, your lives in cardiology easier?

And they all say ECG. So we have some pre-prepared resources now for them, to review and to look at, and we have a wrap up session on a Friday, where it's like a Q&A, we review some traces. And on Monday, people are, they say, oh, I just, I never thought I'd be able to look at an ECG.

I felt so. Worried out of touch, but actually we just give them 6 ECGs, we give them this same framework, thinking about them, and then they go away and reflect on these ECGs over the week. And on a Friday they come back and they're talking like experts, you know, you feel like these even vets who've been in practise for a few years, you've got good knowledge, they've seen these cases, really just spending time thinking about what they're seeing and trying to relate it, and just discussing it with their colleagues makes a big difference to them.

They come back on a Friday and they say, oh yeah, ECGs, no sweat. I feel like I could deal with those. So, you know, if you're feeling a little bit overwhelmed at the moment, that's OK.

Take a look at the notes, take a look back at the recording, make some annotations and review things. And I bet the second time you go over things, stuff will click, you'll feel more confident about it, because it certainly happens for our students of all different learning preferences, of all different backgrounds. So what abnormalities are you seeing?

Well, I'm seeing a few things here. I'm seeing, first of all, a highly irregular rhythm. So there's no pattern here, is there, to the irregularity.

Look at the QRS's, we've got a long gap here, shorter, even shorter, somewhere in the middle, super short. There's nothing that's repeatable. OK.

So that's highly irregular rhythm. You could call it irregularly irregular, if you like, I hate those words, or you could call it a a chaotic irregularity. There's undulations of the baseline.

It's quite hard when the complexes are very close together to see that. But if you look here, where the complexes are further apart, it's really crazy looking baseline, isn't it? And because of that, I can't see any regular repeatable P waves.

So, therefore, I can't really answer the question, you know, is there a relationship between Ps and Qs? Because I can't see any Ps. So, this is, these findings are very characteristic of one particular type of arrhythmia.

So that's the question, what is your rhythm diagnosis? Kieran, I'm afraid there are no more polls, loaded, so I don't know. That's a bit.

Think, think about what your rhythm diagnosis is. Reflect upon your learning process. And, so I, I would look at this and say these three things are characteristic for atrial fibrillation.

You know, I said previously, oh, well, it can't be AF because I can see P waves. Flip that around. I can't see any P waves here.

I've got this horrible, irregular, undulating baseline and therefore, that means this is a fibrillatory baseline, OK? So I would call this atrial fibrillation. And the one characteristic that that stands irrespective of your ECG settings or the quality of your ECG trace or interference in the background or whatever, is that this is super irregular.

So most arrhythmias are not this irregular. If they are, they might be a sinus rhythm with APCs or VPCs. But then you will see normal beats and then clearly abnormal beats.

And here the beats all look the same, but they're superimposed on this sort of chaos. There's nothing else that does that. It has to be atrial fibrillation.

So this is the final ECG and looking at this ECG, this, I'm just gonna walk you through what we're seeing again, so we've got. These positive deflections and he's bigger. Much more obvious deflections, and again these positive deflections, bigger, much more obvious deflections.

So let's think about the heart rate, this is a 6 2nd run here. So in 6 seconds, I've got 123. Yes, I know it's somewhere between 3 and 4 in real life, but let's just take it as measuring this simply.

We've got 3 in 10, sorry, in 6 seconds. So multiply by 10, the heart rate's 30. So straight away, can't be a tachy arrhythmia, it's definitely a rowdy arrhythmia.

And a heart rate of 30 suggests to me there's some block just from the rate. So what could be going on here? Well, we're seeing the block, aren't we frequently, we've got a P that's blocked, another P, P, P.

There's a little P. So is there a P for every QRS? Well, I guess so.

There's a P in front of it. Are they reasonably related? Yeah, that P falls at a sort of physiologic interval before this QRS.

That one's too close. That's not reasonably related. Let's look at the next one.

That's way too far away. That's not reasonably related and it's not repeatable. So actually, are there Ps and QRSs?

Yes, are they related? No. We've got two separate rhythms here, and the P waves just march on through those QRS's.

So this, this Brady arrhythmia, is also associated with a very high grade block. So. This is an atrioventricular block, and this is a 3rd degree atrioventricular block which is defined as a complete AV block.

Bonus points, what's going on here to cause this? We've got no P waves. Heart rate's 30.

Now that's the same rate as the AV block. But it's not the same appearance, is it? Look, there's no P waves here.

Very flat baseline in between the complexes, slow, regular. These QRS complexes are really short. These T waves are tall and spiky.

This is a classic hyperkalemic ECG. And this, this is really important to remember, you know, don't forget to check your electrolytes. When you see ECGs that look very strange, especially if they're bra bradycardias, think about your electrolytes, because this was a dog in an Addisonian crisis.

It could just as easily have been a blocked cat or a a a patient post RTA that's got a ruptured bladder. Just for funsies, I wanted to show you this, sinus rhythm on the left. 21 seconds of no complexes at all.

This is a really high grade atrioventricular block, and this is a dog that was pretty much rushed into the operating room to put a pacemaker in. It's amazing sometimes what you come across. So, We're gonna wrap it up.

You may feel like you've been through an ordeal, you may feel like you're a little bit overwhelmed by some of the things we talked about and some of the things we've seen, especially if you started this session not feeling very confident about ECGs. But trust me when I say, if you spend time going back over the notes, testing yourself on the ECGs that I've given you, I've given you all these examples here, and then maybe reviewing the presentation again and just going through our discussion of those cases, actually it'll be a super, super useful learning experience for you. So don't count it as just, oh I watched the webinar and I left feeling a bit miffed.

Actually, go back and and put in a little bit of time cos it will make a big difference to how you approach these cases in the future, I promise. Thank you very much for, for paying attention, sorry to run a little bit over. We may not have much time for questions, so I'm happy to do that.

If anyone wants to contact me, they can ask me questions via Instagram. I've got an Instagram, thing where I put pictures of pacemakers and stuff up on there, and the handle for that is at vet_cardo and I'm always happy to to answer a question after a presentation on that. So thank you very much.

Kieran, thank you very much, and I think you're selling yourself short. That was an absolutely fascinating presentation and You, your, your method is so simple, yet so effective. And I think you're right.

If we go back and, and re-listen to it and, and, you know, watch those, take the notes and, and, and look at those ECG tracings again, I think, the learning from this is going to be absolutely immense. And I think we, we get to claim a couple of extra hours because there were so much packed into one. So, well done, and thank you very much.

Thanks, thank you. I did want to say though, you know, that last ECG you showed, I think you say, if you're feeling a little bit of a stress or, you know, you're overwhelmed, I think if I put an ECG on a dog and saw that, I would be a little bit more than stressed. And it wouldn't only be the dog that needed a pacemaker after that one.

Our first reaction, when we, because we watched it come out of the machine, obviously, and, our first reaction was, Wow, that's a long pause when it was at 3 seconds. And as the time ticked on, we were thinking, oh my God, is he, is he OK? And the dog's limbs became a little bit rigid.

But then he sort of, you know, came back in and looked fine, and, and was very happy. So we were quite pleased, and then quickly contacted anaesthesia to get into the operating room. Yeah, and, and, and the vet went outside to go and have 6 cigarettes at the same time.

Couple of questions. I know we've run over, but it's been fascinating. It's been worth every second of it.

Leticia wants to know, would you always sedate and what do you recommend sedating with? I would almost never sedate because it will affect the rhythm. So I, I, oh hello, my cat's just come to say hi.

Sorry about that. I was about to say not even cats when I sedate, but he chimed in. So, yeah, I, I, I would always do them conscious.

You know, you see these photographs in textbooks, and I'm guilty of it myself in textbooks and lectures, putting photographs up of these sort of very calm looking patients in right lateral recumbency with the ECG electrodes perfectly placed. You know, I, I had a cat a couple of weeks ago that was hyperthyroid and and crazy arhythmic, . And to, it was like playing Buckaroo.

We put the ECG clips on the cat who was sat in his carrier, but he was so noise responsive. We actually put the lid on the carrier and I put the lead in through the door and sort of carefully clipped them onto his elbows and his knees, while my resident ran the ECG in the dark, you know, away from the cat and it. It was very, very difficult to do, especially getting the spirit on.

We had several things where he just jumped and all the clips fell off. But actually, with a bit of time and persistence, we, we could get it. And then we could see that actually, this cat, was having sinus rhythm with frequent APCs.

And as I said before, stress, and other hormonal states and things can cause that. So this guy was really hyperthyroid and really worried. Actually, I saw the ECG, having heard it, I thought, oh, maybe it's got atrial fibrillation or ventricular tachycardia or whatever.

And I got the ECG, it was well worth spending the time, because I could say, oh, you know what, I'm not that worried about him, actually, let's give him something for anxiolysis. So, you know, I think, I think that's a really important thing to do. Just, just spend the time and take the time doing it and really try, do try to avoid sedation.

Yeah. We've got loads and loads of comments coming through about how fantastic and people agreeing with my sentiments of, of, your fantastic method and thanking you and everything else. So, just one more question before we, we wrap up here, and I don't know who it came in from, but somebody anonymous says, how can you tell the difference between atrial fibrillation with rapid ventricular responses, and a true ventricular tachycardia?

So yeah, it can be a little challenging to to do that. I think true ventricular tachycardia is normally metronomically regular. And yes, it might speed up a little at the start when it gets going, and it might slow down a little at the end if it before it breaks, but generally it's regular.

AF is highly irregular, so if you, if you can watch that long enough, you will see there will be longer gaps in those RR intervals with atrial fibrillation. So again, it's the irregularity I always come back to with AF. Excellent, excellent.

Again, follow your four-step process that you gave us in the beginning. Yeah, that's fantastic. Kieran, it has been an absolute honour and a pleasure tonight and thank you so much for your time and sharing your knowledge with us.

Thanks, everybody. That's super good. Thanks very much for for participating and, and asking some questions.

That's great. And thanks to everybody for joining us as always, to my controller Dawn in the background. Thank you for making everything run seamlessly and from myself, Bruce Stevenson, it's good night.