Hi, thank you, thanks for joining me. So today we're gonna talk all things about ECG so we're gonna go through the basics of what you see in your machine, what your trace, what each part of that trace means in regards to that electrical activity in the heart. We're then gonna kind of dive into tachy arrhythmias, looking at supraventricular arrhythmias, looking at our ventricular arrhythmias and the kind of traces that we're gonna see with that as well.
And we'll talk a little bit about what I'm kind of sign, presenting signs and things and then we'll see with those patients. So first up, we are gonna talk about the actual machine itself. So I'm gonna mention paper and traces quite a bit through this but I obviously I'm accounting for the people that just use multi parameters more more often than not these days.
So I, what I would say is that if you are using a multi parameter and you notice an arrhythmia and you're not sure whether that arrhythmia is true or not, then it would be best to to print a paper trace and whether that's putting on a a paper trace like electrocardiogram. With a separate machine or whether you're multitra has the ability to print off paper traces, some, some do, particularly those that have defibrillators on them, you're able to print off the trace. So when we're thinking about our ECG machine, we think about three kind of things, but mainly two things when we're trying to look at what, how to get the best, trace for us to, to read.
So the recommended settings suggests that we have a philtre turned off. So if you're using the manual, ECG machine, the one that just gives you paper traces and this little box that you see on this picture. This little window, then you turn the philtre off because unfortunately the philtre often philtres out some of the arrhythmias.
So the paper speed should be set at 25, so you can see here, that's pointed to the number 25, so that's 25 millimetres per second, and the gain or the sensitivity, as it's also known as, this sensitivity adjusts the size of the complexes. So if you can't see the complexes, they're very small, they adjust your gain. So again you can do this on the multiple parameter.
Often the touch screen, or you can use the dial to go to the ECG settings and often on the multi parameters it will gain rather than sensitivity. So if you increase your gain, you're gonna increase the sizes of those complexes, so you'll be able to see your PQRST and identify them more easily. So we're setting these to optimise our recordings, so we want the complexes that they're big enough to be identified, but not so large that they overlap with the other leads, which we'll talk about the different leads in a minute.
So the heart rate's fast, we might increase our paper speed to 50 millimetres per second, so at the minute, as you can see in this picture, it's on 25, but if we had a tacky arrhythmia, then potentially we would increase our speed to 50 millimetres per second. As this spreads, the complex is wider and that allows for an easier interpretation. So we all know that if there's different colour ECG leads, it will depend on your machine on your multi parameter or if you're using a a paper trace ECG machine.
There's many different ways to remember it, so more often than not they are red, yellow, green in the UK. So, you remember the traffic lights are red, right, for en, yellow, often I say Leo, left forelen, and green left hind limb. The other way that you can remember is that you have right, red for right and then lemon over line.
Black sometimes is found with these with these leads and to make up 4 leads and that is your neutral so that again goes on your right hind limbs. If you remember your your traffic light, then you remember that the black will just go on the one that doesn't have a doesn't have a lead on it already. And some other machines, so particularly I'm on some multi-premises like the Surve or in the US I know and also on the paper traces as well that it uses this white, black, red, green, so the green is neutral and it can also be brown in some machines as well, .
There's no way that I remember the white, black, red and white, right, and then black over red. So unfortunately, sometimes they have on the actual leads so they have little dots and they'll say which ones they need to go on so. It's recommended that in critical patients, as I said, potentially those that we might be defibrillating so we'll talk about indications for defibrillation later on in our ventricular arrhythmias, that we use a conductive gel rather than use alcohol.
And if you're using alcohol, you do have the ability to use a defibrillator, you are potentially gonna be . Opening that patient up to burns if you start to use the defibrillator. So what are we looking at when we look at our traces, as we call them?
So the bipolar triaxial, lead system that we use today, so the lead 1, lead 2, lead 3, that was developed by a Dutch, physiologist in about the early 20th century, and as well as that, he also developed the PQRST complex terminology that describes those ECG wave forms. So lead generally consists of electrical activity that's measured between a positive electrode and a negative electrode. So you can see I'm on our, I'm on this picture here, I'm on the, let me get the pointer, sorry.
So you can see here we have negative, we have positive and negative and then 2 positives. So what we're measuring is often between a positive and a negative electrode. So when we look at our lead two, we're going from this right arm, this right limb for limb right through to .
All left like, I'm. And so the electrical activity goes from positive to negative through the heart, those electrical activity. And so when we look at this electrical activity, the orientation of a lead, with respect to the hearts of the one I just discussed is lead 2, that we look at the lead axis.
So electrical impulses with the net direction towards the positive electrodes, so as I just seen with that lead to, . This will generate a positive waveform, so we can see this in our lead two. We have our QRS, our PE and our QRS both have a positive waveform.
They both go up above the baseline. And those directed away from the positive electrode. So for example, I'm lead one, I'm Or lead 3, sorry, 3, I will have a negative wave formal deflection.
So when we're thinking about this, we have different, so. We also have, when we have our paper traces, we also have a 6 lead ECD trace. So we have leads 12 and 3, so you can see where they clearly are on this heart.
And lead 2 is looking at the electrical activity from the tip of the heart to the base of the heart. Lead 1 is looking at the electrical activity from that sinoatrial node across the atria, and lead 3 is looking at the the activity from the base of the heart to the top of the atrium. But now when we get these lead 3, we also have AVR we have AVF and we have AVL.
And so these arrows are just, I'm showing you the direction that they're going in as well. So AVF goes directly through the heart, AVL goes across. I'm kind of in a similar fashion to lead 3 and AVR goes backwards up through from the base of the heart to the top.
When we look at our choices, they're slightly different, but what we can see and what we should be appreciating with all our patients is that although we have a different point of view on the heart, we are still seeing the PQRST it just might be that some of them are negative waveforms rather than positive waveforms. So we're using these paper traces, it does actually allow for that further investigation into things like conduction abnormalities, cardiac chamber enlargement. But for the most part what we're gonna be looking at, when we are looking at our multi parameter monitors, and as nurses we often look to lead to, to make sure that your multi parameter is set to lead to, .
Because sometimes it will automatically set to lead 1 or lead 3. So lead 2 is the most common. It provides the most normal sinus looking beat, which we're just gonna talk about in a second.
But if you are struggling with League 2, you can switch to lead 1 or lead 3, just remember in which direction they're going, and the, and the view that that's potentially gonna give us. So in our, I'm. When we think about where our beats are originating from, so what we start with is electrical impulses that are caused by the sodium ions, and they rush into the myocytes in the heart, you know, the heart cells, and the potassium moves out, causing a depolarization.
So atrial depolarization, that whole atrial depolarizing and the potassium moving out, is caused by an electrical activity that starts in the sinoatrial node that lives up here in that . In the left ventricle left atrium and that then causes an electrical impulse to travel across the atria, and depolarizes those atrium, and that causes, a depolarization from right to left. Sorry, it's on the right atrium.
And a prolonged PR interval, is usually caused by. Things like a highbal tone. So think about your brachycephalic breeds.
Think about, patients that have gastrointestinal disease, thoracic, pathophysiology, anything that's causing the high bal tone might cause a prolonged PR. So that, from that P wave through to where that R is, we'll look at that in a second. However, if the PR is shortened, that's usually the AV node is missed.
And so this is where the next BBCR atria, and now what happens is we send an electrical activity to the atrioventricular node, the AV node. And once we get to this AV node, which is again kind of on the right side of the heart. The electrical impulse will then travel through the, bundle of his to to help depolarize these ventricles.
So what happens is, we get an initial depolarization of the intraventricular septum, the middle bit, and that's a negative that we see with that. Waves. So we'll talk about this in a second.
And then, so what happens is the hypoundry system, so the bundle of his that goes through the middle of the ventricles that causes that negative deflection in Q, and then as that, electrical activity spuns up through the kanji, fibres. And up through the ventricles through the right and left bundle branches, we depolarize all the bazilla portions so right to the base of the heart and that's why we then get that negative S deflection so. The P wave is attributed to our sinate atrial node, not atria, and this is why when we think about the size of our atria in comparison to our ventricles, our P wave is much smaller.
So when we have our QRS, it's much bigger because think about all those muscle fibres, all those myocytes that are involved in that depolarization, which causes ventricles to push the blood out to the body, out to the lungs, . And so when those large muscles in the ventricles repolarize, what happens is we get a small positive or negative deflection, and that's our T wave. So obviously with the P wave it's so small and then when the atrial repolarized, there isn't, there's basically just a baseline.
Whereas in our ventricles, that's why we have the T wave. So if we, have a shortened PR, so I mentioned that lengthened PR if we have a shortened PR, it's usually because the AV node has been missed, and that's often a characteristic of our ventricular rhythms, so we'll talk about that in a second when we come to look at our actual rhythms. So we've just talked about the electrical pathways that that that the heart takes.
And now you can see our typical signs beat on an ECG that's showing the two. So it usually has these three distinct waveforms, there's P wave, the QRS complex, which is actually 3 waves in close relation to each other. And then the T waves that we've said that P wave reflects that atrial depolarization.
So number one, it begins at the sin atrial node. We get the mass depolarization number 2 and then repolarization 3 and that AB node being triggered. Once we have that AV node triggered, we get the.
Bundle of hiss down the middle of the ventricles and then that ventricular septum that causes that Q negative deflection because those the myocytes in there are depolarizing. Travels up the lungi fibres, left and right bundle, bundle branches, so number 5, and causes that massive R wave because now we get those ventricles right from the bazilla portions are depolarizing, through down to that S wave. Now we come to our ventricles, repolarizing and this is where we see our T wave.
So when we understand which area the wave is coming from, we can better understand our ECG traces. So abnormalities in the conduction system lead to those arrhythmias and they're represented on the ECG and so when we look at that normal size rhythm, we're looking at a representation of the normal conduction. So several principles that are important to remember when we undertake ECG rhythm assessment.
We need to remember that all normal cardiac cells are capable of depolarizing when they're stimulated by a neighbouring cell, and that's called excitability. So they kind of jostle around, and it's kind of like a domino effect. So once one cell gets excited, the rest of them around it become excited and that's when you get that depolarization.
And this capability is termed conductivity, but there's only certain cells within those myocytes that are capable of auto automaticity. So that means just beating on their own, so they just beat their own drum, and we'll talk a little bit about those in a minute, but what we want to do is when we're thinking about our ECGs, we want to ask some questions. So we talked about that normal trace and that normal conduction system.
So now let's think about the reasonable questions. So first, what is that heart rate? So we, if we determine our heart rate, we can determine whether it's fast or slow or normal, and that's gonna help us to work out if there's a problem or not.
Most machines will give you that heart rate on the screen, and but in some cases you might need to do it manually or double check it and this is relevant on our paper traces which we'll talk about a kind of cheat cheat how to do that, using a ruler or a big pen. So once we've got our heart rate, and let's, we're talking about tachy arrhythmias in this lecture, so let's say we've determined our heart rate is fast. Now what we need to ask, is there a P wave for every QRS complex.
Now this kind of seems obvious, doesn't it, the way that we've just talked about the conductivity, it should have a P wave for every QRS, but unfortunately some, for some rhythms, and we'll talk about specific ones in a bit. Oh. I'm But for example, this one, this is an atrial fibrillation.
What we see is normal QRS complex and I say that in age, but what we don't see is any P waves. There's no P waves for any of those QRS complexes. Potentially we might say that some of those little waves are P waves, but they're not associated with that QRS, so what happens is that QRS is just showing up.
As and when it, you know, it feels it needs to, and there's just no P wave associated with that. I'm Question number 3 is, is there a QRS complex for MVP waves, so that kind of just sounds like the same question as the last one, but. Equally, what happens, particularly in our AV blocks is that we see regular P waves, but what's happening, so if you think about the name atrioventricular block, so what's happening is our sinoatrial node is firing, our atria are depolarizing as they should do.
So we see those P waves in a regular fashion. And what happens now is, is that potentially there might be some messages getting through. But for the most part, there is no message going into that atrioventricular node and therefore there's no message going down to this bundle of hiss to depolarize those ventricles.
And so what we see is we see tall narrow complexes of our, there were some message has has gone through or that the ventricles have decided to be on their own to try and catch up and so. What we see and what we can see here is that we have these regular P waves, but there is no QRS associated with each P wave. We see a QRS and so I'll just get my pointer out again.
So you see P wave and there's a P and yes this QRS kind of looks like it's next to the P wave, but as you can see here, it's kind of spread a little bit further. This one's a little bit closer to this QRS complex. This one is kind of on the QRS complex, each one is spaced differently to the QRS complex to the last one.
So once we kind of worked out if there's a P wave for every QRS and if there's a QRS for every P wave, we're now gonna be looking at whether they're consistently and reasonably related. So this is kind of just what I talked about in terms of so again I'll check my pointer. I'm, so you can see the P waves.
But the P wave here is kind of on the QRS. Again, this one's spaced a little bit further. This one's kind of close, this one's a little bit further away, this one's further away, this one's close, so they're not reasonably related, which means that those P waves don't belong to that QRS.
So they're just, you know, they're, they're going to the same place, but they're not me either the ships in the night basically. So the only examples of where PQRS complexes might be seen but are not related, we'll talk about but like where we just talked about with our atrioventricular blocks, and so our 1st, 2nd and 3rd degree AV blocks. We'll also talk about junctional, rhythm, like a junctional tachycardia, because sometimes what we see with this is that the P waves are hidden, and so it can kind of be deceived into thinking that there's no, related, P wave for every QRS.
And then finally, what is a QRS morphology? So is it tall and upright or wide and bizarre, so this is gonna give you clues as to where This electrical impulse has originated from. So if it's originated within the atria, the QRS is usually tall, upright and narrow.
If the impulse is originated in the ventricles, what we see is this wide and bizarre complex. And that's because the impulse hasn't travelled through the normal conduction system. And what's happened instead is I just kind of briefly mentioned it on the last slide, but we'll talk about it more in a couple of slides, is that the myocardium, has had to depolarize cell by cell, which takes much longer than that conductivity where they automatically all get excited and depolarize all at once.
So it makes that complex wider to think about the, the size of your ventricles, there's much more myocardium, to, to initiate a cell by cell process, whereas the atria, they, you know, they're quite small, the muscle is, you know, is thin. So think about that. So if you have a tall and upright and just think about the fact that they look quite small, and they represent atria, wider bazaar are your ventricles.
So then again, we look through our, all these questions, and then what we also want to do is look at the underlying rhythm. So we kind of want to look at the rhythms. So is it regular, and does it have relationship among the complexes?
So is it regular or is it, this is where I start to get tongue twister, regularly, regularly irregular, with consistent repeating pattern, but a variation in the rate. Is it irregularly irregular, so the rhythm's chaotic, there's no pattern to the irregular nature of the rhythm. So for a good example is our atrial fibrillation.
So what's happening is you do see those tall wide complexes for our QRS morphology, but there's no rhythm, so I'm just gonna pop back to that picture. So you can see actually, I'm We don't have a regular, like it's not one square apart. These are a little bit closer, then there's a wider part, then there's some beats here that may be a little bit more regular, but then again, less less regular.
So that would be considered an irregular, irregularly irregular rhythm unless it's chaotic. It kind of sounds like shoes in the tumble dryer when you listen to them. And then finally we have our paraaxol, and that's just a sudden outburst, and often we see this with like our accelerated idioventricular rhythm with our, ventricular tachycardia, often we get a sudden outburst where we get these rapid series of Rapid ectopic beats, these VPCs, and they begin and end abruptly and they go back to, say, maybe their heart rate's 120, and all of a sudden their heart rate goes up to 200.
They've got massive entry to the tachycardia with the, with our VPCs, and then it goes back to 120. So it's called paraoximol. And that can last as many as 3 beats, but it can actually last minutes to hours, but then all of a sudden it will just stop.
So it's just an example of a ventricularrhythm you see is wide and bizarre, so it's actually ventricular tachycardioverging on ventricular fibrillation. We'll talk about that in a little bit, but this is a, this is kind of a trace if you see this, make sure you, make sure your ECG leads are run properly. Make sure your patient's looking OK, but otherwise be rushing for the lidocaine and potentially if you have the defib, get your defibrillators charged.
So we talk about measuring our trace, if we're talking about paper traces, we'll just go through this very quickly. We can, determine our heart rate on an ECG strip that's recorded at 50 millimetres per second in our, ventricular like tachycardias. So we count the number of complexes in 15 large boxes, so 75 millimetres and multiply by 40, or if you have it at 25 millimetres per second, your, your trace speed.
And then you multiply by 20. And so, These are the larger boxes and within that they have these little boxes. So I like to use the big pen sheet, which is you place a big pen with a lid on from the first R wave that you see.
And so for a 25 millimetres per second speed, the pen will equal 6 seconds. So you can see on the right here that there's more complexes within that smaller frame, but it's actually 6 seconds. So you count the number of R wave intervals between the first one and the end of the pen.
And then you multiply it by 20 if your paper speed is 25 seconds, 25 millimetres per second, or by 10 if it's 50 millimetres. Per second, I'm not gonna be patient's heart rate. I'm Sorry, wrong way around.
So 20 by . 20 if it's a 150 millimetres per 2nd and 10 if it's 25 millimetres per second. So you can see there's 3 seconds and this gives us 160, and this one gives us 170.
So other things that we might look at just kind of see if our patients have regular rhythms, so we talked about that regularly irregular, regularly regular. Irregularly irregular, we can measure these things the PR interval is the interval between that SA node being depolarized through to our bundle of his. So that kind of looks at how long it takes that contractility to to occur.
We can look at our Pwave and amplitude and duration. So again, then we're looking at how our HR are depolarizing, and, and re-polarizing. The QRS, complex duration.
So again this is looking at how long it takes for our ventricles to fully be polarised, and then our QT, segment duration, so or our ST segment. And that will look at how long it takes from the from the ventricles to depolarize through to to starting to repolarize. So again looking at the contractility and and the systolic and diastolic, .
Of the, of the hall. And then the R to R interval is the one that's gonna help us with looking at heart rate, whether we have regularity between our complexes. And so if we have rhythms that originate from a single site in the ventricles or in the atria, they're often regular, whereas if there's rhythms originating from the sinus node, they're often irregular due to variations in adrenergic activity.
So for example, the atrial fibrillation. So we came here to talk about, atrial tachycardias. So we're gonna talk about where these tachycardias come from.
So you said that we have that excitability. We have all, all of those cells being excitable at once, is that conductivity, which we talked about the conductivity pathway in our heart. But there's only certain cells that are able, able to be on their own.
So these pacemaker cells can undergo spontaneous depolarization, and that happens when the resting potential becomes less than negative, and that's during diastole, and that's up until that threshold is released. So what we get is this change in speed of spontaneous depolarization. And that happens over a couple of heart cycles, so the, the, the charge becomes more and more of our heart cycles and what happens then is that then we see these ectopic beats.
So tachycardia that's associated with pacemaker cells, these ones that beat on their own. They gradually gradually speed up over several seconds because if you think about they've got to reach the threshold potential, so they've got to do that over a couple of diastolic systolic cycles. So tachycardia that, originates from rectopic foci that often accelerates abruptly.
So we have these specialised cells in the sinus node, AV node, the Hy system that are able to do that automaticity. But under normal circumstances, the pacemaker cells outside of the SA node don't usually reach that threshold potential because what happens is our, you know, the whole heart is at some point depolarizing automatically. And so that means that the pacemaker cells distal to the sinus node, the subsidiary, pacemaker cells, they have a slower depolarization rate than the sinus node.
So they're less excitable. So if we start to see these ventricular ectopic foci, that means that there's cells that are reaching that threshold potential outside of that sinoatrial node. So first up is our supraventricular tachycardia, and as the name implies the arrhythmia occurs above the ventricles or supramenian above, .
So this means our atria, so our sin atrial node, our atrium, and most common is, atrial flutter which happens around the tricuspi annulus, so where it's circled here, and so this is caused by those ectopic foci within the atria, so the complexes can be tall and narrow. And often it's really hard to to discern between P waves and T waves. You can actually in the atrial fibrillation.
So with our fibrillation we see kind of a wiggly line or a flutter it's more of a sore tooth, . So there's often a single wave between the QRS that encompasses kind of the P wave and the T wave, and so it's really hard to tell what's what, and this is again why we get paper traces if you are struggling to see this on your multi parameter. So this can be an extremely rapid rate, it could be up to 200, potentially even higher than that, and that's caused by those bursts of premature atrial contractions, these APCs, and these contractions of the atria triggered by the atrial myocardium.
So they haven't originated from the sinoatrial node. The sinoatrial node is trying to do its job. It's trying to trigger that, conductivity.
But what's happening is little ectopic foci within the atria are kind of like having their own little party, and setting off, the, the atria flutter, so I'll look at a video of that in a second. And these can be transient or sustained. So again this is the this is the one that your patient might come in, lethargic, weakness, exercise intolerant.
When you start to listen to them, they sound like they've got shoes in the tumble dryer, they have pulse paradoxes, so they have odd pulses, they don't match the heart rate. And these patients, their cardiac output is gonna be severely compromised. That's why they're lethargic, they're exercise intolerant.
You know, we're looking at their physical parameters, their pulses aren't matching their, heart rate and therefore that's, you know, potentially a result of poor cardiac cat posts, severely compromised because of these atria not doing their job, depolarizing and sending the blood into the ventricles. This actually can be broken by increasing the vagal tone. So you can do these vagal manoeuvres, and there's carotid sinus massage, or, more commonly seen is that we can put pressure on the eyeballs so shut the eyelids and put pressure on the eyelids to increase our vagal tone, and that sometimes can right that that conductivity.
If we're not able to do that, then we're gonna start to think about calcium channel blockers. So, most commonly it potentially it's gonna be MR diltiazem, so benzothiazepines. We might use phenol alkalines, so verrama pill.
Roma pi milk, and then things like amlodipine, most commonly that we use our dihydro pyridines. And they're used to break that, supraventricular tachycardia. So the calcium antagonists block those voltage dependent channels.
They stop calcium rushing into those heart cells, and they allow the blood vessels to relax and open and stop that, threshold potential reaching the, the point where those ectopic foci can suddenly start triggering the atria to to be. So anything above the AV node is also a supraventricul tachycardia. So just as an example, this is a supraventricular tachycardia, with our supraventricular premature depolarizations.
So this can happen from our atrial myocardium or AV junctional tissue. So like I said, it's just above the AV node. So often with these the R to hour interval is constant, and they can occur for prolonged periods, but for some dogs in particular they can have short runs with this, a super ventricular tachycardia.
So most of the time, just with our normal supraventricular tachycardia, the rhythm, is rarely irregular unless we start to see atrial fibrillation, atrial, flutter, but atrial fibrillation in particular. And that's because I'm in most of these cases, the QRS complex are are typical of superventricular complexes. .
But as we've talked about, there's no Pwis that are attached to that. So examples of these supravented tachycardias are gonna be atrial premature complexes, atrial tachycardia, junctional tachycardia, atrial flutter, atrial fibrillation. So it's just a nice little picture of the normal conductivity in the heart, so we said that our atrial fibrillation, results when many folk are rapidly fire.
In the atria and that gives that an undulating baseline. So you can see here that those atria kind of just got that undulating conductivity, but the AV node is still trying to do something by sending some electrical activity to the ventricles, and that's because the activity of the atrial cores is in increased ventricular firing, and this is where we start to see our tachycardia from. So, atrial fibrillation is the, the definition is that it should be a a higher heart rhythm 100 beats per minute.
And as I said, it's characterised as an irregular, irregular, irregularly irregular rhythm, both in its atrial and ventricular depolarizations. So what we see with our atrial flutter. Is this you can actually see this undulating kind of wibbly wobbly line, and I said that tennis shoe, the the the shoes in the dryer is the thing that we're gonna hear on these, .
Atrial fibrillation is often seen in patients with atrial dilation so cardiomyopathy and dilated cardiomyopathy and in particular. I've mentioned junctional tachycardia a couple of times, and this is the junctional tachycardia produces a heart rate of more than 100 beats per minute, so. It's not necessarily super, tachycardic, but that you will have a heart rate of more than 100, and that has a relatively narrow QRS complex.
So this is characterised, it has AV node involvement. So we have our normal, sinoatrial atria AV node, and what we see is we get this, it's slightly different to our atrial tachycardia. And that's because, intrinsically, the AV junction has a, a, a rate of about 40 to 60.
So if it was left to its own devices, as you saw with the last slide, that AV node is still sending electrical impulses. And so if that isn't blocked that normally has a heart rate of 40 to 60 beats per minute, just that AV node. So anything over 100, is a junction, well, anything over 60 implies a junctional tachycardia that that AV node is beating too fast.
And so on ECG what we see with junctional tachycardia, we have P waves that are hidden, so you can see in this first one here. That the P waves are actually hidden, even though we have a normal QRS complex and T complex, so actually the P waves are probably underneath that QRS. We potentially sometimes have, inverted P waves for the QRS, or retrograde or short upright ones, or sometimes the P waves appear after the QRS or they seem to be a .
To appear after the QRS. So I'm especially in lead 2 or 3 in ADF, this is where these junction or these hidden or weird P waves might appear. And it can coexist with other, scular tachycardias, and that's because of that disassociation between the SA and the AV node.
So just another example, again, we've got inverted P waves and now we have this tachycardia as well. So just watch out for these. If you have a normal QRS complex, and then these inverted, this is often a sign that something's going wrong at our AV node that we, that AV node is beating too fast.
So let's talk about ventricular premature complexes. These are the things that we're most often gonna be seeing and when we think about our tachycardias, we often go hand in hand with our ventricular premature complexes. And these are premature beats that originate from the foci within the ventricles.
So multiple foci, will lead to ventricul premature complexes in a different structure. So multifocal we'll talk about this in a minute when I put the, the examples up. So what happens with these BPCs is that they often, they occur and what we get is a pause after that before we get the next sinus beat.
So the R to R of the sinus beat from the BPC to. The next sinus beat, I'll just get my pointer up, is longer than the, that sinus beat to the next BPC is often shorter. And that can be caused by a lot of things.
So often, heart pathology, myocardial hypoxia, so think of any trauma patient, anything that's had gastrointestinal disease, myocardial trauma, so following the hit by cars, they can be associated with pain, asidemic states, so a lot of our patients. That we have in that we're treated in the hospital. They can be because of the use of some drugs as well.
And then, so typically these drugs, they are, they are treated by lidocaine, but lidocaine can also induce BPCs as well, like very contrary. So when we see these, we, we might not be able to differentiate between our superventricular premature complexes and our ventricular premature complexes. So the treatment of these two actually differ, so it's quite important to make sure that we have the right one.
So what we see, is this aberran conduction. So they have this wide, think about big Vs, but again, so for example, these ones down here are multiform. So you can see that we have our typical looking VPC here, but what we see here now, that is a VPC because it's wide and bizarre, even though we look like we kind of have a normal QRS complex.
And so. Again, it might be because we have right or left bundle branch blocks, and that can alter the QRS duration and morphology for a similar reason. So if the conduction through one of those branches is blocked at the left or the right ventricle, then the depolarizing, isn't gonna happen the same way that it normally does, and so that, that waveform is gonna look slightly different.
I'm And so This is just another example of our uro complexes. These are single VPCs, but what we can see as well sometimes is our bigemini and our trigemini. So that's when we have two VPCs together, 33 or more VPCs together.
And the treatment for these, so this is an example of a trigemini and then a a a a bigemini and a trigemini. And what we see with these is we start to see more and more. So this is when we're gonna start to think about the criteria of treating them, and the, and the treatment is gonna be your lidocaine bolus followed by CRI if it converts or procanamide.
Again, these patients, just going back to our mentary premature complexes, often they seem kind of nauseous, we might feel, you know, changes to our pulses, they, they're often, You know, we might have pulse differences to our heart rate, and our patients seem nauseous. Sometimes there are patients that are that have had like gastric surgery or they're in pain and we've had them on pain relief and they're, they're having runs with these VPCs, often if we get them up and move them around, sometimes they can convert these as well. So sometimes we kind of get a little bit confused with accelerated idioventricular rhythm and ventricular tachycardia.
So an accelerated idioventricular rhythm actually occurs more than we probably think and it's a slow ventricular tachycardia, so it's a unique form that's typified by slow heart rates, so it's like 70 to 150 beats per minute. And the rate of this accelerated idioventricular rhythm is usually between 10 to 15 beats of the normal heart rate of that patient. And that, the control of that rhythm alternates between two sites.
So we have the sino atrial site and then just these ventricles. So this is why we see these BPCs that we, see in the accelerator in your ventricul with them. And because the rate of the idioventriative focus is slow, there's little hemodynamic consequences.
So these patients generally remain asymptomatic. So just thinking about these ones like I just said, these painful or post-gastric surgery, they might seem a little nauseous, but for the most part, you know, you might have your ECG on them and be really worried because they have a heart rate of 130 and you're seeing some BPCs. But otherwise your patient looks fine.
This is often because it's accelerated idioventricularhythm. There's no hemodynamic consequence that we're seeing with this. So commonly seen with non-cariac disease, things like trauma and also with dogs with traumatic myocarditis, not a neurological disease, we see this as well.
And so treatment for this is rarely indicated. However, our ventricular tachycardia is, is needed to be treated, and this is when we have a, defined as a run of 3 or more VPCs in a row, with an arrhythmia, of over 150 beats per minute, so often they're between 150 to 300. And we should really just be really familiar with the centri in tachycardia, these VPCs that we see.
So ventricular tachycardia is characterised by these wide bizarre QRS complexes without an obvious P wave. So you can see here, actually I'll just kind of point it out, these kind of look like normal complexes. You might say that this is an inverted P wave, but it isn't, and these are the wide QRS complexes.
So occasionally you might still have a normal beat, but what we start to see, as this ventricular tachycardia. Progresses is that we start to lose these normal beats. And so with this we get a marked reduction in our cardiac output.
These patients are really sick. They're tunded, they're nauseous. We have poor peripheral pulses, fast heart rate, respiratory effort.
Because think about now if we have a reduction in cardiac output, our body is now trying to meet up with that metabolic oxygen demand, and therefore it is increasing the respiratory rate and potentially respiratory effort to get as much oxygen as possible. This is particularly if you've ever done a direct arterial pressure, you can see the pulse wave is starting to disappear altogether. So really important to be monitoring on mean arterial blood pressure of these patients as well.
So several criteria for treating BTEC, and some, runs of BPCs and slow BTEC might go untreated. But it's really important, so, we start to look if our patient is symptomatic, so if they have markedly decreased cardiac output, they have syncope or organ dysfunction as a result. If you have a rhythm that's at risk of becoming ventral configuration, which we'll talk about in a minute, or if we have a sustained tachycardia greater than 160 to 180 beats per minute, so this is when we start to think about our, our, antiarrhythmics, so lidocaine and procanamide.
But we have to consider as well that, as well as being antiarrhythmic, they are also pro arrhythmic. So as I said, too much lidocaine can actually cause BPCs because it's a pro arrhythmic as well. so there's actually been studies that have.
Done that have found that treated BPCs and BTA might actually cause increased mortality. So we do want to be cautious with treating these. So again, recognising those that are in accelerated idioventricular rhythm, making sure monitoring signs to see if they are symptomatic or not as well.
However, obviously we know that untreated forms of ventri for the tachycardia can move into ventricul fibrillation. So this is just an example of ventricular tachycardia that is probably heading towards our . Heading towards our BFI, this is a, this is one that is more than likely this patient will be symptomatic.
They will potentially be having episodes of syncope, they will have organ dysfunction, markedly decreased cardiac output. There's a sustained retak of over 160 to 180. And this is almost becoming this R&T phenomenon.
So, what we saw in the last one, you can kind of see that there are at least little kind of ledges in between them each beat, and then so with this one what we start to see. And where it's pointing out with those arrows is that you is there a loss of this ledge and this is where our QRS and so R now is just backing onto the, so the depolarization is backing straight onto repolarization and depolarizing immediately and then what happens then is that there's no, there's no time for repolarization and so. As with atrial fibrillation, there's ventricles and now having that undulating wave and nothing is getting out to the body or to the lungs.
And we get this extremely fast rate. So on that previous slide, there's a rapid VTA, but all the complexes are the same. On this one we start to use R2 phenomenon.
If you see this, make sure you tell that immediately and this patient needs treatment. One yesterday. So ventricul fibrillation, when we start to see this ventricular tachycardia, as you can see, as we start to get faster and faster, as the heart starts to get tired, as it starts to have less time to repolarize, therefore, no time for sodium and potassium to so sodium to refill and your potassium to depolarize, we start to get this kind of wiggly line.
And it is a very interesting rhythm, so it's actually, when we have our, when we think about our CPR efforts, when we're doing our CPR, what we're hoping to do is kind of induce some kind of rhythm, so if you have a ventrico fibrillation. We defib these patients into asysto so we can create a new rhythm. But in dogs it does rarely occur spontaneously, so there's only about 10% about over rest for, compared to 50% in humans, that's why you're always in Grey's Anatomy and ER, you know, they get the defib straight out they defib in their patients.
Obviously we're not doing that in our CPR patients. So it's completely erratic, no discernible identical waveforms, just kind of looks like a squiggly line. So you might assume that you have a disconnection from your, patient or problem with the machine.
So check your patient before you check your machine, so it's just a nice little video. Of how it looks, you can see this atria still kind of trying to do the thing, but nothing's getting through to those ventricles. So if we see that ventricular fibrillation as following the recovery guidelines, that is a shockable rhythm.
And we are gonna be defib in that patient. If we're not able to do that, we can do a precordial thump, so it sounds quite harsh, but does the same kind of thing as the defib and in that it stops all activity in the heart, . Thank you very much for listening.
If you have any questions, feel free to email me. I'm I'm happy to answer them. Thank you, Chloe.
And bye-bye. Have a nice evening. You too.