OK, thank you for joining me this evening. We've got a lot to get through, so I shall crack on and let's get going. So the first thing we're gonna go over is the cardiac conduction system.
And the first thing we need to remember about this is that it does show us the electrical activity of the heart only. So when we're looking at our ECD trace and we're seeing the waveforms that are produced there, and it's giving us no information about whether the heart muscle is actually contracting or that our cardiac output is there or our pulse is being generated. So we do need to remember to make sure to Monitor our patients as we would with hands and eyes, feeling pulses, auscultations, etc.
OK, so the conduction system in a nutshell, very simply, we all start everything with the sinoatrial node, the sinus node up in the corner of the right atrium. This is the pacemaker of the heart and sets the heart rate and is affected by the sympathetic and the parasympathetic system. So we generate our depolarization waves from here and they come across the right and left atrium, depolarizing the cardiac myocytes as we go and then hopefully producing that contraction and then that movement of blood through the heart that we're looking for.
So as those waves come across the atria, they then come down to the top of the septum, the atrioventricular node, the AV node. Now this is the gateway from the atria into the ventricles, and all the electrical impulses should pass through this point to get further along the system. Then we travel through the bundle of hiss, and then it splits off into the left and right bundle branches, which then depolarize the left and right ventricles.
OK, so that's our conduction system. If we have that in the back of our head as we're thinking about waveforms and arrhythmias, then this helps us to sort of understand what we're looking at and where it's generated, etc. OK, so what we should end up with in leads 12 and 3 is something approximating the picture on the right hand side of my slide here.
So what we've got, just to demonstrate with my pointer, we've got the baseline running through the whole PQRST. And then we've got positive waves above the baseline and negative waves below the baseline. So the first wave we come to is the P wave, and this is the first positive deflection in our ECG wave complex.
And this is giving us information about our atrial depolarization. So our SN node fires, we have our P wave of those depolarization waves coming across the atria. So any abnormalities with our P wave is talking about our atria only.
Then we move on and we've got the QRS complex. Now this is often described as sort of one single thing, the QRS, but it is made up of those three individual waves the Q, the R, and the S. And we can split it down into the Q wave, talking about our septal depolarization, the R wave, our left ventricular depolarization, and the S wave our right ventricular depolarization.
So again, abnormalities within these, we can sort of narrow down in the heart where it's talking about for us. OK, and then we come back to the baseline and we've got our T wave, and this is the repolarization, the reset of the whole system, ready for the next contraction phase and the polarisation. Now in animals, T waves can be positive, they can be negative, and they can even be biphasic, which is a little bit of both.
In human medicine, the doctors get very concerned if our T waves aren't positive, but in animals, anything goes, they don't mind. OK, so here I have a little video for you of a very simplistic recording of lead 2. So this is where we've plotted positive and negative points on our ECG as you can see them here on my picture.
And it just correlates what's happening in the heart along with the ECG trace that you'll see. So we're going to start off in a minute in the right atrium, SA node, boom, there it goes. Depolarization waves across the atria, up to the AV node top of the septum, and then we're coming down the septum with our QRS through the ventricles and then back through to the T wave to reset.
So it's just a nice little video just lets you sort of see and and sort of have that together there. I quite like it. OK, so now we're thinking about when we should do an ECG, and obviously, you know, you can sort of say, well I'll do the ECG every time, 100% of the time I shall do my ECG, but you know, we want to narrow it down a little bit.
It's not always an option, it's not always an easy machine to lay your hands on. So we want to think about those specific times where it really is pertinent to record an ECG, and the first one is going to be in any kind of crash or arrest, situation, isn't it? The ECG and the Capnograph are the two most sort of giving of information, monitoring modalities that you're going to have in a crash situation.
So definitely then. If we have a collapsed or an unstable patient, then I think it's a really good idea to check out the ECG at that point as well, simply because you obviously, particularly if you don't know what's going on and whether, why the patient has collapsed. It could be because, of any sort of cardiac disease, but then again, systemic disease processes which can show with ECG abnormalities as well.
So always worth it there. Arrhythmia obviously is a big one, you know, if we're clinically examining our patient and we're auscultating them and we hear a tachy, a bradycardia or an irregular rhythm for any any reason, then this is obviously a very pertinent time in which to place an ECG to see if you can actually identify what you're hearing on your auscultation as any kind of arrhythmia. Pulse deficits is another one if you're, when your clinical exam, if you're auscultating the heart and feeling pulses at the same time, and you've got a, a non-correlation between the two, so you hear a heart sound, but you don't feel an associated pulse, then again, this is another signification of potential cardiovascular disease, that warrants investigations.
So yeah, a really good time to do an ECG if you've identify that as well. Heart murmurs or muffled heart sounds, again, sort of a big indicator of potential of underlying cardiovascular disease. So again, a time where we want to make sure that our patient is in normal sinus rhythm and not showing any abnormalities on their ECG.
And then with general anaesthesia, it The ECG isn't a monitoring modality that I would skip for a GA. I would definitely always want to have an ECG on if I'm monitoring general anaesthesia for a patient. For me it's, it's just as important to keep your eye on that as it is, your Capnograph or your blood pressure.
OK, so getting a good recording, we want to have that ECG. We want to make sure that we can actually see what we need to on it, that we can actually have a trace that's good enough that we can make an assessment on it. Certainly where I work in my daily workplace, we do get sent ECGs, from practises to, to help with, but if they're not actually of, of sort of diagnostic quality, a bit like an X-ray, if they've not got that.
Diagnostic quality, then we're going to really struggle as as specialists in cardiology to be able to interpret anything the same as you would if you're looking, if you're from a general practise and you're looking at your ECG. So we do actually need to have a really good quality chase here to to make those assessments. So ideally a calm and electrically isolated room.
By that I mean not the prep room where everything is plugged in and beeping and whirring. And whizzing and lab machines are going and the centrifuges running and all those kinds of things. We want to try and calm all that down, minimise all those plugged in, bits of equipment because we want to minimise artefacts on our ECG and electrical artefact is definitely one of those big ones.
For those of you that are allowed to carry your phones with you at work, that's a biggie. Having your phone in your pocket whilst you're running the ECG and you can get an electrical interference from that. So try and adios, all that kind of stuff from your immediate area when you're doing your ECG.
Maybe a consult room is a calm area or the isolation area can also be really calm, you know, any way you can think of within your practise that would, you know, lead you to have that more calm area. We want our patients to be in right lateral recumbency if at all possible. Now this is Because all of those textbook normals that we're going to measure and assess our patients ECG against are driven with those patients in right lateral.
It's for consistency, it's for comparison and correlation. So ideally get that right lateral recumbency for your patient and grab as many people as you need to make that patient comfortable in that right lateral. You might need just one person holding, then again you might need 2 or even 3 as well.
If for any reason your patient is not coping in right lateral recumbency, they've got pre-existing respiratory disease or they're just struggling with their ventilation and right lateral isn't gonna be a great idea for them, then you can perform them in sternal recumbency, that's OK. So we want to stretch out the limbs of our patient and separate them off. We don't want lots of crossover here that goes to the leads as well.
Really take time to undo the knitting, and I've never found a way of keeping the leads separated and lovely. They always bunch up, they're always going to get in a mess. It doesn't matter what you do.
So you just need to spend some time unravelling those leads, separating them out, making sure you've got nice lengths of lead, so that when you're attach them to your patient, things aren't all crossed over. It really does help with the chase. Then you can attach it to your patient either with pads or clips.
Now I like the sticky pads on the feet. I think they're actually really helpful, and so we, I, I like to use those. I do use some micro pore tape to sort of hold them on because as soon as your patient has a fidget or a twitch, sometimes they can just fall off, which isn't so fab.
If a patient has really fluffy feet, which sometimes they do, don't they? Our patients come in with little slippers on, then I will kind of clip that off and, and just make sure that I've got a really good surface on that pad. Similarly with the clips, the a traumatic crocodile clips, they, they're really helpful again because you can place them sort of wherever up and down the limbs again to minimise artefacts.
If you've got a really big breathing artefact from your patient, then you can place them further down the limbs and support those limbs of your patients so they don't have as much interference from those breath excursions. And when we're connecting our leads, we want to make sure again that they're as per our textbook normals. So this means that the red colour goes on the right four, the yellow on the left four, the green on the left hind, and then if you have that 4th lead, the black, it goes on the right hind.
All right, next one is contact. OK, yeah, contact really, really important is to have really good specific contact. That doesn't mean just drown them in spirit and spray it everywhere.
It means sort of being very focused in in getting really good contact. So if you have a very Fur dense fluffy patient, it might mean clipping where you want to place those clips. Similarly for the slipper feet, you can actually just clip that area of the limb where you want to place your clip, and make sure you've got a good clip to skin contact.
I like using gel, particularly for anaesthetics. So if I'm about to go into theatre and monitor a general anaesthetic, I'm placing my ECG. I'll use a bit of ultrasound gel or KY jelly, and put that on the site of my clip to my patient and this.
It really helps. It doesn't dry out through the surgery when you've got your warming device on, the drapes. It's, it's warming theatre anyway, isn't it, etc.
Etc. So I find gel really helpful in that situation. Other than that, really focused spirit spray just to get it where you need to.
And then reapply if you find that your trace is losing contact and it's getting a bit fuzzy or a bit wishy-washy, reapply your contact definitely. The next one is settings, and I've put this one on here, mainly I'm making an assumption that a lot of you will be using a multi-parameter monitor to do ECGs for your patients, which is totally fine. You can make an assessment on a multi-parameter, but you need to make sure that you're getting the best possible trace out of it possible, and settings are really key.
They are for any machine, but particularly for the. Multiparametters, get to know your multiparameter in the ECG settings. So you'll have 3 settings with your multiparameter that you can change.
You can change between your leads, usually 12, and 3, but get used to swapping those leads through. Generally, we're set on lead 2 because it gives you a really good overview through the heart of where the lead is placed. As in my little recording before, we've got the positive and negative electrodes placed across the heart, and that gives you a really good overview.
But for any reason you see anything abnormal in your lead to or you're not quite happy with how it's looking, or it's just not great for any reason, skip into lead 1 or lead 3 and have a check of that and see if you can improve it simply by going to those other leads. The other setting that you will have is your sweep speed. Now this is basically how many complexes you have on the horizontal axis on the page of your screen.
So you can set it usually to 25 millimetres a second or 50 millimetres per second. So again, it makes a difference to what patient you've got, as to how they're displaying their normal sinus rhythm and and just giving yourself the best way to assess those waste forms and how many complexes you want displayed on, on the, on the horizontal. And the third and final setting is the gain or the millivoltage, and this is how tall your complexes are displayed on your screen.
Now for really big dogs or, you know, Labradors, those kinds of guys, they can have really large complexes, and if they're overtaking the whole of your screen, falling off the edge of your screen, and they're not displayed properly, then it's really hard to assess what's going on. So reduce that gain down. To 0.5 and 0.25 millivolts and then you'll be able to make a better assessment.
Similarly, on the other side, there's the cats with the teeny tiny little little always. It's very small QRS is here. Again, if they're really tiny, you're not going to be able to see exactly what's going on.
So increase your gain, make it so that you can view those separate waveforms really nicely on your monitor. It's really gonna help you out, OK. Right then.
So we understand our conduction system. We know what we are wanting to see in our PQRST and where those are coming from. We're gonna, we've got a good recording, how we're gonna read it, what we're gonna do once we've got our recording.
OK, so the first question to ask yourself is what is the heart rate? And the caveat to that is, is it appropriate for the patient in front of me? Now most monitors will count the heart rate for you, but is it telling you the truth?
Oh yes. Now many multi parameters will lie to you, definitely. So I do always check that my, the, the heart rate displayed on my monitor is what actually I'm seeing in front of you.
Now if you've got an irregular rhythm, then this will change beat to beat. So your monitor will compensate for that and it will change your. But you want that ballpark heart rate.
You can simply auscultate, feel a pulse for your patient and do the math, count, do 15 seconds, do the math for you. That's absolutely fine. But we want to know what is the heart rate of our patient in front of us and is it appropriate for what we're expecting to see.
Labrador comes in and I assess the heart rate and it's 32. That gives me cause for concern. Yeah, if a chihuahua comes in and it's got a heart rate of 100, I'm not, I'm that's OK.
Yeah, so we've got to think about what we've got in front of us and what we're expecting to see. The next one is, is there a QRS for every P and a P for every QRS, and a little caveat here as well is, are they relatable? Do they go together?
We want to make sure that we're seeing PQRST for every single complex that's displayed on our ECG. So you want to assess and make sure that those are going together and that they are there and invisible for every single complex. The third question, is it regular or is it irregular?
And then of course the behind question there is, is it irregularly irregular or regularly irregular? And I'm proud of myself for not tripping over my tongue with that one. And then the fourth question right on the back of that, OK, if it's regularly irregular, is it a sinus arrhythmia?
Is this speeding up with inspiration and slowing down with expiration? And you can really see a rhythmical speed and slowing down with that kind of rhythm, and you can certainly obviously just as you're taking your ECG, view the chest excursion of your patient. If you can't have someone shout it out for you.
And then you can make an assessment as to whether this is a sinus arrhythmia. And then the last question that you want to ask yourself is, can you see any abnormal beats or deflections within the ECG that you're taking? So these are the 5 questions to ask yourself whenever you're approaching assessing an ECG.
It's really helpful to take them one at a time and not try to do to try to do too many things at once because you're just gonna get a bit confuddled, and miss stuff out. OK, so let's look at some of those deflection abnormalities that you might see. Just move my little laser down the bottom there out of the way.
OK, so the first one I've got up in the top right hand corner, this is the picture picture here. Let's go through it, shall we? We've got the baseline here, we've got our P wave, and then for this patient, I can see a Q wave.
I can see a T R wave. I don't really see much of an S wave and it kind of slurs down into a negative T wave here and then we're back to baseline. And this repeats 3 times.
So this is pretty standard for this patient. This is what this patient is throwing at its normal PQRST sinus rhythm. So the abnormality that we can see here is a prolonged QRS wave.
This can signify structural ventricular enlargement, so a structural change in your, in your heart chamber sizes, and this is because when we think about our conduction system going back. Through to how we had that with the SA node through to the AV node and then through the ventricles. These are the motorways of the conduction system.
This is everything zipping along 70 miles an hour, getting where we need to go, bish bash bosh, depolarized, sorted, T wave, here we go. Lovely. When we have a disturbance in that conduction system, such as a left bundle branch block, which can be what a prolonged QRS wave signifies, we've got everything slowing down in that conduction system, and instead of the impulses being able to use those motorways because it's blocked, we've got to go back and use the A roads and everything slows down and it takes longer.
Therefore, this can be displayed as taller waves and wider waves. So this gives . The the suspicion that we've either got a ventricular enlargement, so we've got a larger chamber that takes longer to depolarize, therefore our waves are bigger and wider, or we've got a disturbance in our conduction system.
Where the motorways can't be used, and we've got to use the A roads instead, which is slower and takes longer. And this is how it's displayed on our ECG. So it gives us a suggestion.
We can't diagnose from this, but we can make a an assessment, we can make a suspicion from that. OK, the next abnormality down here is the deep S wave. So going through my picture here, we've got the baseline, we've got a wibbly P wave there.
We've got a teeny tiny Q and then we've actually got a teeny tiny R just under my laser pointer there. That is the R wave. For this patient.
And then we've got a really deep S wave, and this is our S wave displayed here really deeply, and then we come back to a bit of a biphasic T wave and then we're back to baseline. And that happens again consistently for this patient, so that is this patient's normal. Now the reason I know that this is a deep S wave, apart from the fact you can see quite nicely our Q and our R as well, which is great, don't always see them all.
Is the fact that my P wave is positive. So I know that I haven't placed my leads incorrectly. I haven't got my patient in a weird position or anything because my P waves are positive, I know that this is actually a deep S wave.
So the deep S wave can signify a right ventricular. Enlargement and then going back to our discussions that we had at the beginning of this presentation about the S wave signifying right ventricular depolarization. So again, with our abnormalities with my S wave, I can extrapolate that that could be a right ventricular enlargement.
It could also be a right bundle branch block. Again, this could be paired with a wide QRS. And then in cats who like to be different, cats, this could be a signification of a left anterior fascicular block if.
We see this pattern in leads 1 and leads leads 2 and lead 3 that's paired also wide. In lead 1, the PQRST would actually be a normal morphology and we would see a nice positive R wave in lead 1. But in lead 2 and lead 3, we would swap to the deep S wave and it would also be.
A wide as well when we measure it. So cats like to be different and it's it's, it can get a little bit confusing when you look into the intricacies of these, but for the purposes of this presentation, I wanted to demonstrate the deep S wave as an abnormality that warrants a little further look into what's going on. OK, for you here now is a deflection normality.
Very, very quickly, it's a wandering pacemaker. Now the SA node is actually quite a large structure in the right atrium and sometimes we can have the the set off for each cardiac conduction to be from a slightly different area of the SA node, and this gives rise to a different look to our P wave, a different morphology, a different. To our P wave.
It can have a varying amplitude so it can be different heights and slightly different look. It's not uncommon in dogs to see it quite very commonly actually in dogs, but it is quite rare in cats. So our P waves on the bottom strip here are depicted by the black arrows and you can see how they change their look.
And this is depending on which area of that essa node has sparked off this particular PQRST. Totally normal. Right, now we're gonna move on to those abnormal beats that we may see, and we're gonna tackle the premature complexes first.
Now if we look at my top strip here, I've got these three beats here. Now these are my premature beats. Now premature is exactly what it says in the tin.
They come early, they're premature. They're, they happen before I'm expecting a next normal beat. So how can I assess that?
How do I really know it's not it's a premature beat? Well, I can simply eyeball my R to R interval of my normal PQRST beats, and on this strip here, I've got 5 quite nicely here together. So I've got my baseline, my P.
I don't really see a Q. I've got a nice tall R. I don't really see an S and I've got a positive T wave.
And this happens nice and consistently for 5 beats. And if I look at my R to R interval, again, it's pretty static, it's not too bad, but then I get this one, and it's much closer here. So this is a premature beat.
I don't see an associated P wave with these beats either. So how do I know that these are atrial premature complexes? They're supraventricular, supra means above, ventricular ventricles.
So these have originated above the ventricles. And the reason I know that they've originated above the ventricles is because the QRS and T look very, very similar in these premature beats to the preceding normal PQRST beats. Therefore, back to my conduction system.
When the depolarization waves come down to the top of the septum to the AV node, the normal conduction pathway has been followed to give a normal looking QRS. The motorways are there, they've been used, it's all zipped along beautifully. We haven't got any wideness or extra tallness.
It looks very, very similar to our standard normal beats. Therefore, whatever's generated these early beats to happen, it's happened above that AV node because the depolarization from my ventricles has followed the normal pathway. Yeah.
Lovely. Right. Conversely to this, we've then got on the bottom strip our ventricular premature complexes, our VPCs.
So going through the strip here from left to right, we've got baseline, P wave, Q wave, R wave, not much of an S, and down to a negative T. And this is repeated 4 times here for my patient with quite a nicely static R to R interval. And then this one happens here.
Now this is early, I can see, I can eyeball it, but it's not where I'm expecting it to. The next beat I'm expecting is about here really, but it's not. This one's happened here.
But look at the size of it. It's twice the height of my normal beat. It's also a little bit wider.
And the T wave for it is also bigger as well. So I know that this beat is a premature beat because it's happened early, but it's not originated from above those ventricles, it's originated from somewhere within the ventricles. And this is because the beat is wider and bigger.
It's not followed the normal conduction pathway. It's taken the A roads and Everything has gone slower. So when we have a ventricular originating beat, the depolarization waves, instead of zipping along those motorways, they take the A rows, they go cell to cell and depolarize the cell next to them.
So it takes longer. So our beat is displayed as wider and taller. So a ventricular originating beat.
We go along the strip and we have a few more normal sinus beats for this patient and then again an early beat arrives and again it is wide and bizarre, it is tall and it so it is originated from within the ventricles. It doesn't look anything like our preceding normal beats. Therefore, the normal conduction pathway has not been followed.
And we've got these two ventricular premature complexes. Right, our next set of abnormal beats that we're gonna look at are our escape complexes, and these happen after a pause. So let's look at the top strip.
We've got our baseline, P wave, little Q, tall R, little TES, and a positive T. And this is repeated 4 times for this patient. So there's our normal sinus rhythm for this patient.
Then we have a nice pause and then we have a beat here, an escape beat here. Now this B doesn't have an associated P wave, so it hasn't sort of gone through the full. SA firing, atrial depolarization, etc.
Otherwise we would see a P wave. But what we do have is a QRS that looks again very similar, if not exactly the same as our preceding normal sinus beats for this patient. Therefore, the origin for this beat has happened somewhere around that AV node junction, but the depolarization from the AV node down has used those motorways and been that normal conduction because it's displayed as like our patient's own normal.
So this is an escape complex. It's most likely to be quite a junctional one. But again followed that normal conduction pathway to depolarize our ventricles.
And then we've got the other example here on the bottom strip, which is our ventricular escape beat. So again, baseline here, P wave, teeny Q, R wave, not much of an S and then not much of a T really, but it is there, there it is just above my laser pointer. And then we've got that 3 times for our patient again with a nice sort of R2 R interval, very static, very regular, and then our pause happens and then our wide and bizarre ventricular beat.
Again, no P wave associated, but it doesn't look anything like my preceding normal beats. It's very wide, it's very long, and we've got a negative depolarization and a positive T wave here, positive repolarization for this ventricular beat. So it looks very different, doesn't it?
So the normal conduction pathway has not been followed. It's originated within the ventricles, no associated P wave. OK, so I wanted to talk a tiny bit more about ventricular complexes because they are a cause for concern, of course they are.
We know that they shouldn't really be there even though sort of most healthy patients, and you and I sat here without any pre-existing heart disease, we'll throw some of these during the course of a 24 hour, but they are a cause of concern when we see them, aren't they? We're like, oh God, there was a, there was a ventricular beat there. OK, so when are we going to worry about them, when there's lots of them.
And I, and I mean lots, you know, if I'm, if I'm doing an hour long anaesthetic and I see 1, maybe 2, I'm not going to write home about it. But if there's 1 or 2 on on every page of my parameter, then OK, that gives me cause for concern. Something's going on here with the patient to actually spark off these ventriculines.
If we have a predisposed breed in front of us and they are throwing these ventricular beads, so breeds like boxers, Dobermans, cocker spaniels, German shepherds, sphinx cats, these kinds of guys, this is gonna give me cause for concern. If these ventricular complexes, the frequency of them is making my patient hemodynamically unstable. And by this I mean that they cannot maintain their blood pressure.
This is a cause for concern. They need to be able to maintain normal blood pressure despite ventricular complexes. And we need to check the systemic disease.
The the culprit for ventricular complex is not always cardiovascular disease. Very, very frequently, it's down to some sort of systemic imbalance, metabolic acid-based disturbances, electrolyte disturbances, and, abdominal pathology. So cancer, go on a cancer hunt, abdominal cancer hunt, splenic tumours common culprit for throwing ventricular complexes.
Two specific instances where I'm going to worry about ventricular complexes when I have an R. T phenomenon, as shown in my top right hand picture here. I've got a baseline, a P wave, a Q wave, an R wave.
I don't really see an S and I've got a biphasic T. And then I've got a ventricular complex here and this one has a negative depolarization, which is pretty equivalent to an R wave in a normal sinus beat, and then a positive repolarization, which is our T wave equivalent. And that happens for this ventricular beat here.
And then immediately after we've got another ventricular beat here. So this again with our negative R wave equivalent. But before it can get to the T, we've got another R on top of it, of another ventricular beat.
So here is my R on T area phenomenon. This R of this ventricular beat is on top of the T wave of the preceding ventricular beat. And it basically means that you've got a really unhappy area of cardiac myocardium that is throwing these beats incredibly closely together and it's not great.
The other time where it's not great are multifocal complexes shown here on my bottom right picture. So I've got a normal PQRST sinus B and another one for this patient. We've then got a VPC, a ventricular premature complex, and this one has a negative R and a positive T.
So. Negative depolarization, positive repolarization, and then the converse happens. We've got a positive R and a negative T.
So this means that there's more than one area of cardiac myocardium that is not happy and throwing off these ventricular complexes. So again, both of these situations are a cause for concern and warrant further investigation. OK, right, moving on now, let's talk about a couple of those arrhythmias that are really common to see, and ones that you want to be confident in, in diagnosing and having a look at.
So the first one we're going to look at is a 2nd degree atrioventricular block. So back to our conduction system, let's remember it again. SA node firing in the right atrium.
Those waves come across the atria and up to the AV node, which is the gateway into the ventricles. Now when we have an AV block, what I like to think about, because I like, I like these little things, these little correlations, these are fun for me. We've got a bouncer on the door and the AV node is our nightclub door, and there's a bouncer there and he's having a look at those waves coming along like fellows coming to get into the nightclub, and he's going, Nah, nah, you're not wearing the right trainers.
You're not coming in tonight, no chance. And he blocks those ways, doesn't let them through. And then sometimes there'll be those waves coming along and the bouncer will go, yeah, actually you're right, we've got room in.
You look nice. You've you've worn the right the right dress code, in you come. That's fine.
On you go. That's absolutely fine. And our waves are let through and it follows the conduction system and we get our standard PQ RST.
So what's happened on my bottom left strip here? We've got the baseline, we've got the P, not much of a Q, it's an R, not much of an S. We've got a big slur down to this T wave here.
But then we've got our 2 in a row here, non-conducted P waves. So again, the waves have come along from the SA node, they've done their P wave, they've done their atria. They've come up to the AV node and the bounce has gone at, no, not coming in, not happy with you, you, you can jog on.
And then we've got nothing. And then we've got another P wave and the same thing's happened again. Bounce has gone there.
You're not coming in. I don't like you either. But then as we go along the strip, we find that we've got again another PQRST for this patient and then another conductive PQRST.
So we've got these two non-conductive P waves in my bottom left strip. In my bottom right strip, we've just got single non-conductive P waves here, but This is what's happening. So for our patients presenting with a 2nd degree AV block, we can sometimes see syncopal episodes or exercise intolerance depending on how many of those non-conductive P waves are happening and how much that's messing with our patient's cardiac output.
We don't really see pulse deficits, and our auscultation is, is fairly unexciting really. Again, depending on how many of those non-conductive P waves. If it's just singular every now and then, you're not going to remark it really, but if there's quite a few in a row or it's very variable, then you might have pauses of varying duration.
So what next for patients with this 2nd degree AV block? We need to consider what's happening with our patient. Now, if it's a conscious patient, the first thing I want to do is check blood pressure.
Because again I want to make sure that my, my patient can maintain that hemodynamic status and keep up my blood pressure. And then I'm going to observe it. Now if my patient's under anaesthetic, I want to think about what medications this patient has been given.
Now, if we've given an alpha to an agonist such as meatomidine or dexedatomidine, then this is a common arrhythmia seen with Alpha 2 administration and it's simply Because we've reduced that heart rate down and we've given our patient a bit of a bradycardia that this arrhythmia can actually come into come into being for patients under anaesthetic. The key here is not to panic, don't panic. Check blood pressure again.
You want to make sure that your patient is hemodynamically stable. Now, if everything's OK under anaesthetic and you're happy, your patient's blood pressures. Maintained, everything's normal, we're cracking on and we're doing a good job.
Don't worry, this is OK. Your patient can handle this 2nd degree AV block that's been set off by your alpha 2 agonist. When your alpha 2 has been metabolised or antagonised, then this arrhythmia will go away and your patient will revert to fall back to sinus rhythm, and you can check that in recovery.
Yes, it's something to check in recovery. Pop your ECG on your patient, make sure everything's OK. Right.
Watch out for this, arrhythmia. There is a risk of degradation to 3rd degree. Now this is when you've got a high grade 2nd degree block when I was speaking about how many of those non-conductive P waves are happening.
And it's about the ratio between the non-conductive P waves versus the sinus beats. When there's a really high ratio there, then there is a risk of degradation into a 3rd degree AV block. OK, right, I've got a little video here for you of a 2nd degree on a multi-parameter, and I'll just play it here.
And what you can see is our patients sort of coming into sort of a a bradycardic state, and you can see the normal PQRSTs displayed, and then every now and then, particularly at the end of this video, you can see a P wave here and then a pause that's non-conducted before another sinus beat. So this can be sort of what you see on your multiparameter when you've got a second degree AV block, and it's definitely something to take note of. It's definitely something to monit record on your monitor and verbalise to your veterinary surgeon.
But again, unless it messes with the blood pressure of your patient, it's not something to necessarily panic about. OK, so let's look at 3rd degree AV blocks. So this is a complete non-conduction of P waves, and a relatable PQRST is not seen.
Our patients mainly present collapsed after exercise or when trying to exercise because they cannot raise their heart rate to deal with exercise. We've got strong slow pulses, we've got no pulse deficits and auscultation's unremarkable other than the bradycardia that's associated. So what we've got here on my strip, we've got these P waves going crazy.
And this is the SA node firing, and we've got regular, regular P waves happening all the time through this strip. And what we've got superimposed on top are ventricular beats. So what's happened is, back to that bouncer on the nightclub door.
That bounces, closed the nightclub, nobody's getting in, nobody's getting through, nothing's happening at all. So in order for your patient to carry on living, the heart is generating ventricular beats in order to produce a pulse and a cardiac output. And these are the ventricular beats that you see superimposed on top of your pee waves.
They are not relatable. What next for patients. Now, sometimes you can try an anticholinergic.
This is atropine glycopyrelate, but it's not usually recommended, it's not usually helpful because what tends to happen is that you speed up your pee waves, but you don't affect that ventricular intrinsic rate that's going on. The best course of treatment for patients in 3rd degree you block is a pacemaker implantation and referral for that if you can't do it in house. Watching out for these patients, a failure of the ventricular beat.
They're usually very, very stable, so it is a question of monitoring them and making that referral if your client is keen, and you have somewhere that that will accept that. So it is a bit of an emergency. You do kind of want same day treatment for this, definitely.
Right, let's look a little bit closer just for a few seconds on the 3rd gravy block because as I mentioned, it's about having that relatable PQRST. So when we look at this strip coming along left to right, we've got a non-conducted P wave. Then we've got another P wave, and this ventricular beat that's here, you could actually, I mean that looks good, doesn't it?
I mean that could be a deep S wave, couldn't it? That could be an R wave, that could be a D S wave. This, this could be working together as PQRST, no?
Sure it could. It that looks viable to me. But if I carry on down the strip, I've got all these non-conductive pee waves, and this one here is much closer to this beat than the preceding vaguely relatable one.
So let's carry on down the strip. We've got this other humpy bit here, haven't we? And we carry on, we've got nonconductive P waves here.
Oh, and then we've got another bit here that looks a bit weird, and then this one straight after that T wave. So what we can see is this one, this one, and this one, these are P waves, and these are buried underneath of these ventricular beats. So we can see.
Now that these PQRs, these are not PQRSTs, these are not relatable. My P waves are regularly happening and my ventricular beats are superimposed on top. So it's just about taking some time, following your strip, looking at more than one complex to make an assessment.
OK, on to SVT supraventricular tachycardia. So this is a tachycardia, that's what it says on the tin, it's fast. And we're looking at rates typically over about 250 beats per minute in dogs.
Now it's patient specific, that's not a hard and fast number to run by, but we're looking for that tachycardia. We can have paroxysmal SVT non-sustained and sustained, and the presentation for our patients, it's usually combined with poor pulses because of the tachycardia. We've often got exercise intolerance.
Our patients are often stressed with this one, man. And I don't know if you've ever had like a palpitation, like a really fast heart rate. It's a bit unnerving.
And certainly patients that I view coming into my clinic. That are in SVT, they are anxious, they're panting, they're dribbling. They, they look worried, yeah.
And when we listen to them, if we've got a sustained SVT it's regular. Yeah, if we're flipping in and out, you're gonna hear that change between sinus rhythm and SVT. And if we look at the strip down the bottom here, we can see our R to R interval, yes, it's very regular.
Can't really discern much P wave going on. I can see the R, I can see the the S and the T, but I can't really see an awful lot out because it's so fast that you struggle to see whether you've got P waves. Is that a P wave there?
And then I've got an R and an S and a a weird bit of T and then you just don't know, do you? It's really hard to assess because of the speed of it. What next for these patients, checking blood pressure.
I'm gonna mention it every time, it's really really important to get blood pressure on these patients. And then they identifying the underlying cause, whether that's a cardiovascular based cause or whether it's a systemic issue. As we go down the line, we can consider doing things like Holter monitor to see how much time our patient spends in SVT and how fast that reaches before we then think about using rate control therapies, which obviously is a concern for the veterinary surgeons.
Watch out for these things. Myocardial failure, if it's sustained and untreated, tachycardias at this kind of rate are not sustainable for any length of time. You know, we can't spend days and days in this kind of tachycardic state.
What we end up with is is such poor cardiac output that we end up with cardiac ischemia, ventricular arrhythmias, and then, you know, progressing on to failures and crashes. So it is an emergency state and we do want to get our patient, referred if, if that's appropriate or treated as soon as possible. So the three things for you to, take away from this rhythm is that it is fast, it is regular, and our P waves are hidden if we're in sustained SVT.
Now my little video I've got for you here is a patient, one of my patients, Labrador patient that was going in and out of SVT very, very frequently. So we start off in sinus rhythm for this video and we can see PQRST at 154 beats per minute. And then we have a little flippy flippy, we have a premature beat, and here we go into SVT.
And you can see that it is regular. I can see my Rwas and T waves, and we get up to rates at 290 there, 296, 292. So it gets very, very fast, very, very quickly from our normal sinus rhythm where we can see nicely PQRST and a rates of 150.
And there we go, flap into SVT again. So you can see the difference there quite nicely. So it's quite helpful when your patient is doing this because you can ascertain the normal PQRST and then see the difference in the SVT.
OK, moving on to atrial fibrillation. Again, this is a tachycardia, not quite as fast often as SVT. We're talking about sort of over that 160, 180 beats per minute in dogs, and we have a total absence of pee waves.
So this isn't just because it's really fast and we can't see them. There aren't pee waves because our atrial fibrillating. So this is usually because we've got some intrinsic cardiovascular disease and it's because our atria are .
Become so enlarged because of that cardiovascular disease process that they start to fibrillate and they can't contract properly, and they don't respond to the normal conduction stimulus. So our patients are often syncopal collapsed with poor pulses showing all those signs of that impactful cardiovascular disease. They're often anxious and panting, often with respiratory pattern changes, particularly if they are in congestive heart failure.
But one of the key things to recognise this arrhythmia is your auscultation. It is chaotically irregularly irregular, and it sounds like trainers in a tumble dryer, and it really does. We.
If you haven't ever heard trainers and tumble dryer, go home and do it. Go on. If you've got a tumble dryer at home, put some trainers in, pop it on for a little bit and and listen, and it really, really is such a good analogy.
I really do love it. It is trainers in a tumble dryer. So let's look at the strip at the bottom here that I've got of atrial fib.
Now when I look at my R2R interval, I can see it's irregular. It's going all over the place. There isn't a sort of a static there regularity to my R2R interval.
And I can see it's really fast, particularly as I start here, I've got QRT, and that's what I can see for this patient and it gets really fast there, doesn't it? But as we go along the strip, we've ended up here with a bit of a wider R to R interval and a bit of nice baseline there, and I can't view a P wave. And as I carry on down, I've got some more fast, very close together, and then I've got a really nice strip here, really nice sort of longer R to R interval, and here's my baseline here.
And now if there was a P wave, I would see it there, and I don't. It is just baseline. Therefore, I can make a really good assessment that this rhythm is atrial fibrillation.
So what next for these patients, again, it's my blood pressure. It's stabilising congestive heart failure first before we think about doing Holter monitors and rate control therapies. Watching out again, cogenic shock is a real figure for this arrhythmia, particularly if your patient is in congestive heart failure, it is really impactful, so we're making sure that we're looking at our patient and making those assessments as a an urgent.
Question. If you've got a feline patient and you're diagnosing atrial fibrillation, it's actually a really poor prognostic indicator in cats, so again, that warrants those questions for your veterinary surgeon and the client as well. So it is an emergency situation, particularly if it's unstable atrial fibrillation, it hasn't been diagnosed before, it's a new presentation.
And the 3 things you're gonna take away is that it is fast, it is irregular, and there are really no P waves at all, particularly when you have those longer R to war intervals and you can assess your baseline. So here's my video for you. This is the Wizzy ECG I have in my practise that shows 6 leads, but I just narrowed it down to leads 12, and 3.
So these are happening at the same time together, along, along the horizontal there, . And one thing I wanted to demonstrate here quite nicely, really, really quickly, I know we're getting close on time, but I wanted to just just have a look at lead two here and you can see this beat here in the middle of lead 2. And it looks a bit weird, doesn't it?
It doesn't really look like anything. It's small, it's strange. I don't know what it, what it's what it's looking at.
But if I look in my other leads of lead 3 and lead 1. It looks much more like a ventricular beat compared to my normal beats going on for this patient. So you can really make a nice assessment, as I was saying, of swapping your leads between 12 and 3 to make an assessment on a beat that you see that isn't quite right.
So let's play the video really quickly. Again, I can see nice irregularities here of looking at lead 2. We've got some particular beats for this patient was not very happy.
And as we go along, we're looking at gaps in our baseline where we can hopefully wait and see if there's a P wave. And this is a really nice one here, and you can see on your baseline there in lead 2 but also in lead 1 and in lead 3 really no P waves happening at all. So this is our atrial fibrillation.
OK, ventricular tachycardia. I know we're really close on time and I do apologise for running over, but we're just gonna spend a very small amount of time on ventricular tachycardia. Again, a tachycardic state.
We can have short runs or sustained, lots of systemic causes and our patients often present in dire straits, don't they? We've got our strip down the bottom here, we've got two sinus beats for this patient, a short run at VTA here with our big, wide, tall, bizarre beats of ventricular origin. A little sinus beat in the middle there for posterity, and then a nice run.
A VTEC and we can see that there's hardly any baseline, definitely no pee waves, it's big, it's wide, it's bizarre, and it's causing issues for our patients. We need intravenous access, we need oxygen therapy, we need treatment with lidocaine. Watching out, we need to watch our patients for low output failure and shocks, particularly if it is sustained and degradation, into ventricular fibrillation and crash procedure.
So definitely an emergency. The last slide that I've got here for you is just a little mention on cats because they don't read the textbooks and they like to do their own thing and they like to be weird if at all possible. It's thinking about heart rates.
Again, appropriate heart rates for your cat in the clinic is less than 160 beats per minute. Bradycardia could well be, you could have the smoochy smoo cats that are so relaxed in clinic. They are, they do exist.
I have seen them, where their heart rate might be 120, 130, but generally we're looking at having heart rates for our cats in those high 100s and even early 200s. Their QRS complexes can look isoelectric, which means they're just as negative as they are positive, and those QRSs can be really small. There's no minimum R wave height documented for cats, so they can be really tiny.
And each of my three pictures here on the right side of my slides are normal for these cats. Potassium imbalances are a common culprit of ECG abnormalities. Sinus arrhythmia is not normal in the cat, wandering pacemaker is rare, and cats in 3rd degree atriaventricular block actually tolerate it really well.
And I'm not sure it's just because they have less exercise requirements, or whether their intrinsic ventricular rate is more likely to be sort of 100 beats per minute or so, so much faster than in dogs where it can be as low as 30 to 40, but cats seem to cope with it really, really well. So that's my last little mention of cats. Here is the summary slide for you.
So take a screenshot, but the five questions to read the ECG are ones to take home for you today, the deflection of normalities are suggestive of cardiac enlargement or a conduction disturbance, but you can't diagnose, you need some further imaging to make that diagnosis. Worry about those VPCs if there are lots of them, if they're multifocal, if you see R on T phenomenon, or if your blood pressure is affected. Your alpha 2s can give rise to a 2nd degree AV block, and you can antagonise that if it's required, if it's messing with your blood pressure.
Check the blood pressure. Check the blood pressure. And then your atrial fibrillation is fast, irregular, with no pee waves at all.
Your supraventricular tachycardia is fast, regular, and your pee waves are hidden. Cats like being weird, watch them for their bradycardias, and your emergencies are 3rd gravy block, atrial fib, ventricul tachycardia, and SVT. So thank you very much for listening.
I do apologise for running over time. Hopefully we've got enough time still for some questions. Thank you for joining me.
