Good evening, everybody, and welcome to tonight's webinar. My name is Bruce Stevenson, and I have the honour and privilege of chairing tonight's webinar. Before I get started, I just want to say a big thanks to many pets, our sponsors tonight.
And, we really do appreciate having them on board and the fact that they are sponsoring, this nurse series for us. Little bit of housekeeping quickly. If you have any questions, move your mouse over the screen.
You'll see a Q&A bar or Q&A box on the black bar, normally at the bottom of your screen. Just click on that. Type in your questions there.
They'll come through to me and then we will hold those over to the end. Tonight's speaker has been on the webinar vet quite a few times, so she doesn't need much introduction. But Chloe qualified as a veterinary nurse in 2012.
She gained her vets now ECC certificate in 2016 and her VTS ECC in 2018. She has a strong background in ECC and referral nursing. Chloe is currently the clinical lead at New Priory Vets in Brighton.
Who also provide cardiorespiratory and internal medical referral services. And on top of that, she's a mom of two young children. So she's certainly got her hands full at this stage.
Kobe, welcome back to the webinar vet, and it's over to you. Thanks very much and thanks for joining me. And tonight we're going to talk about nursing the cardio respiratory patients.
So, This is a very wide spanning topic, so I'm gonna try and condense it as much as possible into this webinar, and what we're really gonna talk about is those patients with cardiorespiratory distress, and those emergency patients. So we're gonna talk about any treatment past that emergency stage, . Often these patients either have trauma or longer standing pathology, and regardless of the actual cause of cardiorespiratory distress, all patients are going to show very similar, out with the evident signs of labour respiratory effort and, and things like the inability to, ventilate, so physically moving the air in and out of the pulmonary system.
To respire, which is the ability to exchange oxygen and carbon dioxide in the lungs efficiently, so that BQ mismatch, which we'll talk a little bit about later on. We know our general signs are gonna include like increased respiratory rate, heart rate and rhythm, collapse, syncope, pulse deficits, and. I've grouped cardio respiratory together.
They both present very similar, and they both need urgent attention to avoid the risk of things like cardiogenic shock, acute renal injury due to this poor circulation that this heart's giving, respiratory failure. So, you know, we start to get things like acute lung injury, acute respiratory distress syndrome, as well as respiratory arrest and cardio respiratory arrest. So the key to a successful outcome is this rapid localization problem and also stabilising these patients.
So we'll talk about a little bit how we can do that. So I'm gonna sort of group respiratory emergencies together, there's a lots of different ones, there's thoracic trauma, there's obviously lung pathology like pulmonary contusions, pulmonary edoema, pleural effusion. Pneumothorax, they all come under this respiratory emergency umbrella.
So these patients are gonna be dyspneic, and these patients require immediate attention and this treatment is rapidly going to influence the outcome and reduce the morbidity and mortality in these patients. When we think about our patients with . Trauma and they're gonna have multiple organ systems affected affected as well, so we just have to be conscious, conscious of that in the background.
So these patients are gonna have this laboured respiratory effort, and they may have different types of efforts, so you'll get a different effort with pulmonary edoema versus pleural effusion because if you think about the pathology and pathophysiology of it, our pulmonary edoema is that wet lungs, so there's fluid in those alveoli. So it's really hard to inhale any oxygen and exhale any, you know, or to exchange that oxygen, carbon dioxide in the lungs. So you're gonna have a very increased effort in both .
Inspiratory and expiratory and our pleural effusion, think about the fact that that fluid is around the lungs. So if you think about trying to expand those lungs, trying to breathe in that oxygen, it's not possible for those patients. You're gonna have this really enhanced inspiratory effort, you know, you're gonna get that abdominal sucking paradoxical breathing, .
So these are the things that we're gonna start looking out for, and looking at whether this patient can ventilate, so whether it can physically move the air in and out of the pulmonary system like we just talked about, or whether they can respond. So when we talked about that, pulmonary edoema, they, they don't have that ability to exchange oxygen and carbon dioxide in the lungs efficiently. So we're gonna see that in ways of our cyanos, mucous membranes, obviously postures that they're doing, and things to do with our circulatory system are gonna start to be affected because that body, you know, that circulation isn't taking oxygen-rich blood to the muscles, to the other organs, we're gonna start to see other organ failure because of this inability to exchange oxygen.
So yeah, general signs are gonna include our increased respiratory rate, adapt in different postures, open mouth breathing, and alterations in respiratory patterns as well. So thinking again of pulmonary edoema, we might have this very shallow quick breathing because it's it's almost like drowning, they're just trying to get as much air in as possible and as quickly as possible. So urgent attention is needed to avoid the risk of respiratory failure, cardiac arrest and hypoxic damage to the tissues.
So we just talked about the fact that these tissues aren't getting the oxygen, and we're gonna start to get hypoxic damage, and we're gonna start to have cell death, apoptosis, and necrosis as well. And therefore that leads to things like acute kidney injury and organ failure as well. And as I said, and I'm gonna keep saying, the key to a successful outcome, is rapid localization problem and stabilisation.
So we'll talk a little bit how we can do that, later on. What I'm gonna give you in this webinar is the tools to look at these patients and the things that we can look at. As nurses, to kind of localise, obviously, we're not diagnosing anything, but if we are a bit more aware of what we're looking for, and we can help in with the vets to help localise that problem, and, and start that stabilisation process.
The most useful tools are history and a thorough physical examination, so, you know, listening to that chest, auscultating and looking at that patient before you even touch it, how is that patient breathing, . You know, getting a thorough history of when it started, how long the patient's been like that, whether they are changing positions a lot or whether they've been in a certain position, and whether they've been, you know, whether they have been in a drowning incident, whether they've been. In a, in a trauma like a road traffic accident, all those kinds of things are gonna build a bigger picture to help us localise where that problem is in the lungs.
Often when we look at respiratory, that respiratory effort and the way that those patients are breathing are gonna. Help us. So cardio failure, cardiac failure, often is as a result, of lot of, of conditions.
And so heart failure is a clinical syndrome. It's not to be confused with the condition. And in heart failure, you have this impaired cardiac pump which leads to decreased ventricular output, and venous venous return and cardiac output as well.
So as a result, myocardial cells deteriorate and progressively worsen, so you get this inability to pump enough blood, enough to mean stroke volume, cardioramer, and this arterial blood pressure. So this is where you get this forward or systolic heart failure as they now call it. So you can get backwards as well, so you get this left and right, .
Heart failure or forward and backwards, . And As a result of this, you get things like this tachyne coughing because you get this wet lung because basically the, the fluid has, you know, the blood has nowhere to go, and you start to get pulmonary edoema as a result. You can also get pleural effusion with these patients as well.
So you get coughing as well because obviously they've got this fluid on their chest, exercise intolerance obviously goes without saying that these patients, if they can't breathe, they're not gonna want to do exercise, and then there's dyspnea. I'm so I'm. This is because of diastolic dysfunction, and this is an impairment for ventricular filling.
So, this backwards heart failure so the heart's unable to empty itself, and venous reservoirs, and it leads to this congestion, so pulmonary edoema pleural effusion, ascites, and this is why we refer to it as congestive heart failure. Most of these patients that you see for cardiac. Cardiorespiratory patients as an emergency, are gonna be in some element of congestive heart failure rather than it just being their primary condition causing them issues unless it's a an arrhythmia like a a serious arrhythmia.
So because this heart's unable to cope under this big stress and do a normal maintain normal homeostasis, we get this initial rise of blood pressure and cardiac output via this rash system, so our renal renin, angiotensin, our deerone system. And this is, I'm not gonna go into it too much because otherwise it's gonna be a very long webinar, but if you haven't heard of it, look it up because it is very, it works synergistically with the heart. And when your patient is struggling, this is the thing that kind of bolsters up, brings that blood pressure up by, retaining sodium so you get that osmosis, you get more fluid drawn in, that's why the patients are often dehydrated, .
There's other things like water retention, in the kidneys, and also causing. I'm That systolic blood pressure because of arterial contraction. So because of this, we then start to get this vicious cycle because, If we have this congestive heart failure and the heart's not able to pump out, it's essentially dumping out fluid elsewhere.
It's dumping fluid into the lungs, it's dumping fluid into the abdomen. So it, it doesn't have any more to give. You might be able to draw as much water out as you can and that patient's super dehydrated, but eventually that RAS system is pumping nothing, you know, it's like an you know, it's like an empty, water pump.
You know, you can pump it as much as you want, but water's not gonna come out. And in which case then your patient's gonna start to decompensate. So, you know, often we get our patients coming in on a scale of this decompensation or initial compensation in thisRAS system.
So they often present with this respiratory distress and collapse due to the physical changes that we've just talked about. And sort of worst case scenarios we can get this pitton edoema, so fluids then starts to just get dumped out in all the cells surrounding the body and we get pit and edoema. Pericardial fusion signs very similar, I'm gonna skip through these a little bit other than just talk about muffled heart sounds, and syncope, and this, so we get muffled heart because we have this fluid around the heart and this pericardial sac.
We get this poor pulse quality, quality, which is pulses paradoxus, and that's because, if you think about the heart's not able to really beat, especially when we start to get this, cardiac tamponade, which is when our left atria sort of, bellows in because there's so much fluid around the heart and that pericardium that it starts to put that pressure in on the left atrium. So you start to get a, a dangerous arrhythmia, and this is why we need to correct it by doing a pericardiocentesis. So we get hypertension because we have a poor pulse quality, because we're not getting efficient pulses out every single time, and often we'll get jugular distention because if you think about where the jugular is in comparison to the heart, we have this backup.
And again, we get electrolyte abnormalities, possibly because of vomiting. So our key treatment that we're gonna talk about and we're gonna concentrate on this one is oxygenation for these patients, . It's really imperative to minimise all stress in these patients and keep a calm environment.
They they are like so close to the edge that anything is gonna tip them out. These patients are like so close to having a CPR event that what we really need to do is try to back them off that ledge. So the way we're gonna do that is minimal handling.
We'll talk about different option therapies and how that's gonna affect our minimal handling, ethos, and and ziolytics are a big one in these patients and they work so well, . And so quickly as well, and it just gives us that chance to either give oxygen therapy to maybe do an ECG or . Ultrasound, which we can talk about in a minute, and just generally calm that patient down and because if you think about, you know, the, the pathophysiology that we've talked about, essentially are these patients feel like they're drowning or they just have nothing left to give and and when you get.
So that sort of decompensation, thing. I, you know, you have tonnes of cortisol running through your body, and so you have this high stress event and any other cortisol stress event that's gonna happen, it's just gonna be too much, you're gonna have a rush of adrenaline debt, . Again, think about your position and patient.
So, our poly traumas. I'm thinking about how these patients, are gonna sit, whether they're gonna be comfortable going circling back to angiolytics. So most of our cardiorespiratory patients, buorphenol is really effective in these patients.
You can give it I I am. I probably won't give it most of these patients we talked about that dehydration. We don't know when it's gonna get to them.
If you're able to get an IV in without stressing them out and killing them. Then you can put it might be, but iron, it's really nice, quick iron, pop it in oxygen, let it calm down. You can do whatever you want with it then, or if you've got poly trauma thinking about maybe you need to get something strong like a pure new like methadone.
And then obviously, our general treatment is gonna be oxygen therapy. These patients can't get oxygen into them for whatever reason, whether it's because they're not having efficient exchange because of the circulation that poor heart contraction from cardio, cardiac disease or because of a respiratory disease, I'm, you know, this is, I'm, that they're not ventilated properly, they're not getting, they're not physically respiring. So we have this cessation of the smear, and this is because of low oxygen blood levels.
So oxygen support is indicated in patients with low oxygen levels of less than partial arterial oxygen of less than 18 millimetres mercury or on your SPOT monitor less than 95. I'm not gonna go into it because again, it'll make this lecture. Very, very long, but look up if you haven't already seen it and you don't already understand it, is the oxygen disassociation curve.
And that relates to our PAO2 and our SPO2, and why we look at that 95% measure, ideally we want 100%, but, anything below 95% is a cause of concern, if you're able to do arterial samples, but in these patients, again, that's a high stress, activity, if you're getting less than 80 millimetres of mercury on your, On your readings, on your arterial blood gases, then panic can get them potentially get them ventilated, . So yeah, so the aim is to increase the percentage of inspired oxygen, which then increases the oxygen blood levels and therefore reduces our dyspnea. So therefore less struggling, hopefully.
So we want to be oxygening our patients from triage due to stabilisation procedures, treatment, anything that we're doing with these patients unless their respiratory rates come down, unless we've fixed or on the road to fixing whatever we've fixed, what needs fixing, then these patients should be oxygenated at all times. I, I am a big advocate of oxygen for all patients, emergency patients that come in, because whatever event that they're going through, often they are struggling to be because they, you know, pain is gonna cause these patients to, hyperventilate and therefore they need more oxygen or antics and things like that. So, so these patients, it's not non-negotiable, need oxygen, so we need to consider the route.
And whether it's gonna cause further stress to our patients, increase, resulting in an increased demand for oxygen and causing further deterioration. General anaesthetic, intubation and positive pressure ventilation are completely viable options in these patients. Don't discount it because it seems like too much.
It seems like, you know, that you should be doing. Less in these patients, especially those patients that are really have that high BQ mismatch, that ventilation perfusion mismatch that that have no way of ventilating themselves because of whatever path pathology that's going on, . You know, doing that ventilation for them is a viable option.
Obviously we're not going to be knocking them out and, and putting them, you know, putting them on this, or ventilating them ourselves. But this is something to bear in mind, sort of talk about your talk about with your vet sometimes when you're getting these really low partial arterial oxygen, and you're getting really high, you know, you get this hypercapnia that you can't get down no matter what you're doing with this patient. And that it's, you know, to talk to you about this being a viable option.
So these patients can have hypoxia or hypercapnia depending on the disease process. And I'm so supplemental oxygen is gonna help these patients. And hopefully you know that room air is 21%, of a fraction 21% fraction inspired oxygen.
And so there's a variety of methods which aim to increase this percentage. So if they're breathing room early they're getting 21%, if you think about a patient that's really struggling. And it's also affected by the size of patients.
So think about some of these patients like Labradors, you know, big dogs, that's a bigger surface area for that 21% to try and get across. So if we increase our fraction of inspired oxygen, that's gonna increase the ability of oxygen to get to all that area of that dog. Again, respiratory rate, if our patients are hyperventilating, it's really difficult to get a 21% in, all in one go, that's, you know, That that's not gonna be possible for them if they're breathing very quickly, they're not really getting that much air as they're sucking it in.
So if we increase the FRO2, then we increase the ability for that patient to get as much oxygen in within within each breath as possible. And again, oxygen flow rate, we'll talk about with the roots of administration and I think it's in your notes as well and how much we should be given for each roots administration because it's then gonna increase our ability to oxygenate these patients. So the big thing to think about with these types of administration is whether it's gonna stress the patient further and whether it's appropriate for the length of stay.
So often these patients aren't gonna be in for a night, they're gonna be in for a couple of days whilst we get on top of whatever's causing the cardiorespiratory emergency. We can use a variety of oxygen sources. And it will vary between practises, and dependent on facilities and economics and .
Finances, so you can do direct from the oxygen cylinder using tubing, you can do a breathing machine attached to an anaesthetic machine. You can use a piped oxygen source, you can use oxygen tubing, or you can use a breathing system, and you can get oxygen generators as well, so we actually have 3 or 4 of the oxygen generators in our practise, we often get, with being a cardio respiratory referral, we get quite a lot of in these cases, we need lots of extra oxygen sources as well as we have have lots of piped oxygen sources and piped oxygen sources in each of the wards. So routes of administration, there's lots of different routes, which ones are appropriate are probably I'm, you know, gonna be, I'm .
Oxygen tents, not oxygen cages, to be honest, so longer term, Longer term routes of administration are gonna include our nasal prongs, so as you can see on the, left with the Labrador, we have these that they're designed for human use, . And you can get them in two sizes, so adult and paediatric. So they advance about 1 centimetre into the nostril and they provide about an oxygen and FIO2 of about 40%.
So they're minimally invasive, but they can be easily displaced by an intolerant patient. So, mm, on a scale of 1 to 10 and stress level with 10 being the most stressed, these patients probably sit around a 4 or a 5. I'd probably say a 4 if you get them on and they're successful and they don't bother.
Often if the patient's too sick, then they're not, they're not looking at them. Obviously in cats, it's definitely gonna stress gonna be more like a 10 and trying to put anything on their face. But in dogs you can have success, but also think about how they're breathing.
So these patients are panting and putting a tube that's 1 centimetre into that, nasal cavity is, like throwing a glass of water on a bonfire. It's not really gonna get to the patient because they're they're panting and the, and the physiology of where the air's coming in and out is gonna be changed. So I'm just thinking about those, you can put proximca into the nostrils.
These, I guess if you've got your patient stabilised, you can put these patients on that if you don't have oxygen tents, and, you can take so you can proxmecaine before we put them in so they don't bother them as much, and then you can take them on and sometimes we also do a little loop of, . I suture material, but often the tape is fine. But you know, they will interfere with it, and often you'll find that sometimes you go into the kennel and and they've got the problems like.
Pointing up towards their eyes and then just oxygenating their eyes. I'm So Other things that we have are these buster colours, and these aren't really effective for long term, because, so basically you cover a bust colour with 75% of . Cling film or saran wrap or something like that, something plastic, and then you have this 15% up at the top where the air is allowed to exit and then you have your oxygen sourcing coming at the bottom.
So obviously with these ones, again, not good for long term because what we're going to see is a buildup of carbon dioxide in this area. So these patients already have this inability to exchange oxygen, and you're gonna start adding carbon dioxide rebreathing. So I've added this in just to sort of say that.
You can use it, I guess, if you really wanted to, if you have nothing else, but I'm not really appropriate in these patients. They are for. Sort of aggressive patients as well.
I'm And then on the right side with the cap, this is probably the preferred route of administration in our Disney cardiorespiratory patients because it's a very hands-off approach and these in particular these like oxygen cages are clear like PVC you can change this actually it's got a nebulizer on it, but you can change your oxygen concentration by it's like colour coded. So like white, yellow, red, and that'll change the fraction of inspired oxygen for you. So they do require, a large volume of oxygen to fill it.
So often what I do is if I think that there's a patient with the cardio respiratory emergency coming in, I'll get that blasted with some pipe oxygen, using a, you know, a breathing set. And just fill that pool of oxygen, close it up, and, and then just start our generator on it, just it's like keeping oxygen in it. And often what what we can mean is we're gonna get high, high percentage, but what that also means is a disadvantage is every time that we open this cage or if there's any leaks, and we change that practise of inspired oxygen, you can actually get.
Little monitors, I think. We get ours from Burton's, but you can pop them in there, they're quite small, they don't really affect, the size of the cage, and it'll tell you what your fraction inspired oxygen is, and you can also, get them with temperature monitors because these cages get quite hot, especially if you've got a very dyne like a dog, or a cat, but, especially like dogs, sometimes we put King Charles Cavaliers in these, and if they're panting and panting and panting, it gets really hot. Obviously, the windows fog up.
So we've got ice packs on the top, and you can get cool mats inside, and what we do is blast the air conditioning in that room as well to try and keep the, like the PVC as cold as possible as well. It's not ideal. So if you do have the ability to have like oxygen cages, they often will have, humidity and, temperature controls on those as well.
So, these are the most ideal, and like I say, very hands off. You can X-ray with them as well, so, you just take out all the bedding and you can pop the X-ray and play underneath them, and the radio. I'm aa So other supplementation routes, our mask that we can use.
So you can see these patients really just, they've got apnea and they had a big, actually I think they have paradoxical abdominal sucking in and this patient was so done with trying to save himself breathing that he was just like OK, you can just hold my hand, I'll put my head in here. And this obviously is an ideal situation because most of the time these mass supplementations are gonna cause stress these patients puts something on their face, especially in cats. So sometimes flow by, if you're doing initial treatments, at 2 to 10 litres.
Per minute, it's gonna get you up to about 40%, whereas if you're doing a mask, you can range from about 1 litre per minute for cats and small dogs through to 10 litres per minute for giant breeds. It's quite a lot. So don't be afraid to whack up the oxygen level in the bigger dogs, and you're gonna reach hopefully a percentage of about 8 to 90%, in a tightly fitted mask.
But obviously a lot of them are gonna not tolerate that tight fitting mask. So it's gonna be more like 35 to 55. So again, not great, but it, it may be better, and thinking again about that tight fitting mask, we're also gonna be introducing carbon dioxide, just because we've got no escape for that .
Although we have got the breathing system, but I'm just thinking about, you know, build up of carbon dioxide in that area as well. In some patients, we can gently hold a mask over a muzzle, . Which allows sort of free movement of patients, but often they're not gonna tolerate the mass or the muscle.
So yeah, don't do it if the patient's struggling, it's counterproductive, you know cause increased stress, increased muscular activity, and so only best on collapsed or very weak patients who have given up essentially, . And also remember these patients become hypothermic. So this patient had a tracheostomy tube, again it depends on what's going on.
So if you have like upper respiratory swelling, again, placing tracheostomy tube in these patients isn't . You know, it's a viable option for some of them, and, it's gonna give you the ability to give that patient 100% oxygen, potentially. So longer term for these patients, is nasal catheters and, and basically put these into the respiratory tract or the nasal nasal cannulas.
And cats and dogs you can use feeding tubes. So 5 French is appropriate or for cats and small dogs and 8 to 10 for bigger dogs. As with the nasal prongs, obviously think about your respiratory effort and mode, so if they're counting a lot, but what you can do is just push them, so you basically put them in and and head for the medial cancer of the opposite eye.
And you can sort of push it down a little bit further, towards the parents, because usually you would stop at that medial campus, and measure to there, but you can put it a little bit further in to get the oxygen. So just quickly talk about humidification, if you have a patient on more than one hour of oxygen administration, or if you have a patient with nasal or tracheal catheters, or if a patient's on chanical ventilation, like positive pressure, then you need to think about humidifying, your inhaled gas, and it's something that's overlooked. So think about that .
So the pathophysiology of the trachea, and your, respiratory system is that that's usually a nice moist, wet thing, and we're introducing that dry oxygen, and it's gonna cause desiccation to those tissues. I'm, so basically humidifying your air, I'm. Because otherwise we can get ancillary activity and mucus movement impaired, inflammatory changes in the course of this ciliated pulmonary epithelium, you get things like pneumonia.
You start to see this coughing up as mucus that you can see in this picture, so often with oxygen cages they are integrated, in like the fancy ones, so if you're lucky enough to have one of those, then great. Otherwise, you can do an oxygen bubble through water. So a lot of people will just have these on the outside of cages if you've got like a a kind of oxygen cage, often they'll just have these on the outside, and it's just an oxygen bubble through.
You can make them, yourself. They're pretty easy. You basically just need like a plastic container with a lid, and almost like a straw type thing, and the other thing you can do is like nebulization, so.
As you saw on the auction and cage, the oxygen like cage, the buster one that I had in the last picture, in there, I, you can see the nebulizer here, but you can buy ne nebulizers really cheaply for like tra tracheal intubated patients. And you can nebulize them or you can just nebulize patients that have got respiratory problems and have like nasal cannulas, you can run them through the bubblers and you can also do nebulization like in their sort of room air that they're sucking in through that through the rest of their nose. So another big thing that we're gonna talk about, especially in terms of our cardiac patient, is gonna be ECG interpretation.
So This is a big topic, and I'm gonna run through it a little bit, but I do think if it's something that you struggle with to go away and like look at a little bit more. But basically, this is like your manual ECG machine. You can get them on your multi parameters, and they're both fine to use, but I think if you have an arrhythmia on your multi parameter, often it's worthwhile doing a manual one, so.
The recommended settings suggests that, you know, the philtre turned off a paper speed set at 25 millimetres per second, and then the gain of sensitivity, which adjusts the size of the complexes to set to 10. So it's it like optimises your recording of them. So you can play around with it as well, and you can print your paper off if you change that sensitivity, and often it'll change the size.
And so if you can't really see the arrhythmia, change your sensitivity to a higher sensitivity and it'll increase that size of that complex. But obviously not so large that it overlaps on the other leads. If the heart rate's fast, you might increase your papacy to 50 millimetres per second, as it makes those complexes wider.
So, depending on your multi parameter or your, manual, so the manuals will often be this white right for limb, black left for limb, red left hind limb. And green Right hind limb. So the green is neutral, so it's still just reading off the three leads, but you just have a neutral one.
And then on some multi most of our multi parameters, apart from one, it's red right forelin, yellow left for ing, green left hind limb. So the way that I was taught was, traffic lights are red for right, yellow left, and then obviously you follow your traffic light round. And then sometimes these have black for the neutral as well.
So our critical patients, you are again, if you're lucky enough to have like defibrillators and and using conductive gels of alcohol, because you can avoid burning the patient. So what we're seeing on our our trace, . So we have bipolar triaxial lead system and basically what it does is look at the It looks at the at the electrical activity measured between a positive electrode and a negative electrode.
So as you can see on here, we have negative electrodes and then positive electrodes. So we're looking at that way from the negative to the positive, . And so we look at the orientation of a lead with respect to the heart and that's the lead axis.
So what we mainly look at and what you probably have set on your multi parameters or you know, when you're looking at your paper trays, we're gonna be looking at this lead too. And that, if we look at this direction of this, it. Sorry, well let's go back, so we look at this, diagram, this triangle.
Is that that goes down from negative to positive, and it goes through, through the atria, down into the same sinoatrial node, down into ventricles, and obviously then we get these negative deflections when, when we have diastolic actions, so. When we're refilling, we get this negative deflection back to our negative lead. So, obviously, with our ventricles, we have much bigger muscle, so this negative deflection, is gonna be more visible.
This is our T wave. We can sometimes get a a negative deflection or sometimes a positive. But basically this is because there's a bigger muscle, it takes more for that to take more electrical activity for that to refill.
So, other leads that I'm not gonna talk about, I just have them on this, presentation is our AVR ABF and ABL. So these are just different directions again at looking at the heart. So sometimes when you print off, on our, On our paper trace, you'll get the 123 ABR ABL ABF.
But what you're essentially looking for on that paper trace is that all those matchups, you can see on our AVR ABL and ABF is that our QRS is actually in the negative deflection. And if you look at this is going from positive to negative, so that's why. But it still has a QRS the same as the ADL, the same as the ABF, as well as the T wave deflection.
And a pee wave deflection as well. So basically we're just looking to make sure all the leads are the same. If they're not, then it might be because, there's something specifically wrong in one part of the heart, or it could be that your leads are off.
So just thinking about where our leads are as well. If for some reason you can't get to a limb or like let's say a patient has a poly trauma. You, I'm, you're gonna Look, at potentially moving those leads.
So if you're gonna do that, I'm obviously just looking at remembering where you're putting them and and thinking potentially you're gonna get a negative reflection rather than a positive. So we have our where our beats originate from our new ECG so we have our sinoatrial node, this is where all electrical activity starts, hopefully fingers crossed, in this little sort of button here, and then you have the electrical activity that moves across your atria. And this causes a contraction of your atrias, then blood, you get this systolic, mode and you get the blood flows into your.
Ventricles at this point. Your electrical activity now goes into your atrioventricular node, your AV node. Another little button again, hopefully it gets this one, otherwise it'll miss it and we'll talk a little bit why.
So if we get an AV node, we miss, often this is characteristic of a ventricular rhythm. So supraventricular rhythms are, problems with our atria and our sinoatrial node, and then problems with our ventricles, our ventricular rhythms are gonna be ventricles. Our kanji fibres and our AV.
So we get this initial depolarization of the intraventricular septum, and you get this negative scene in the queue where the cue dips down a little bit because we have this this depolarization of the septum, all these electrical bundles go boop boop. And set off one by one, and then, then we get our entry to the depolarization, oh, and, this is, . Sorry, I'm Yeah, so eventually the depolarization is I'm.
Is caused by the electrical impulses, travelling down the kanji fibres in the hispoundi system, and part of the heart that depolarizes the basilla portion, so you get this negative Sleion. And then we get this repolarization so ventricles then refill with blood, and we get a, a T wave which is negative or positive. So, so we talked a little bit about this, so we get this number one goes get this first electrical activity.
Our atria depolarized, all that blood flows down, so we get this little wave. Just think about the size of the atrium. In comparison to our ventricles, and so we get this little wave, and then we get a normal when it, when that, repolarizes when the blood flows back into the atria and they relax and dies all, we don't actually get a positive in this one just because they're so small.
So then we get, I'm QRS interval, again I say we get this small negative deflection in our Q and that's because of all those ventricular muscles depolarizing, and then we get these ventricles, boom, they depolarize, we get this huge positive inflexion, and we'll talk a little bit about our ventricular rhythms and why these are different. And then this Punji system fires up as well. We get a negative S.
And then we go back to 4, back to our be calls where they repolarize, again, diastole, and we look, what we're looking at here is our representation of normal conduction with this pattern that we've just discussed. So our normal trace, so 5 questions to ask for your ECG. So what is the heart rate?
Is it slow? Is it fast? Some machines are gonna provide your heart rate, especially on multi parameter.
We might need to double check it. Obviously we would double check it as a rule, but you can do, if you're doing a paper trace, and you can do an ECG ruler or a thick pen with the lid on, . So question two, I'm.
As we talked about, is there a P wave for every QRS complex. So thinking about how that heart works, we need that atria to pump that blood down to the ventricles. So we should have a P wave and it should be associated with that QRS.
We should be, that blood should be flowing from the atria down into the ventricles and the ventricles pushing it back up, so you get this P for QRS. So with this one, atrial fibrillation, we don't see a P wave with every QRS. We do get QRS's, but they're completely different, to what's happening in between them.
And so with we get atrial flutter and atrial fibrillation. Atrial flutter is like a saw tooth sort of pattern in between and then this fibrillation is sort of like basically these atria just firing randomly and so they're sort of wheeling around rather than actually depolarizing and and contracting and pushing that blood into the ventricles. But because the ventricles sort of work on their own as well, they're like, oh no, we need to get blood out, so they just randomly will depolarize and that's why we get this QRS.
Is there a QRS for every P wave? So again, it's not as simple as that P waves then equal QRSs. Sometimes you can have P wave, P wave, P wave, but you don't have an answer down the bottom.
But you sometimes, the ventricles again, like I said, they're like. You know, there's, there's a disconnect. There's nothing, there's no messages coming into the, the ventricles saying that there's blood coming to them.
So every now and again they go, oh, man, we should contract, yeah? So as you can see in this one, we get, this is when we get to get our, type 2 blocks, or type 3 blocks, and get type 1s as well. But the ones that we're most commonly going to see in cardiorespiratory are type 2 and type 3.
Type 3, we're gonna to get in lots of syncope. Because there's really a big disconnect. Whereas with our type 2, often we'll get a couple of P waves and then, but you can see there's no rhyme or reason.
The P waves are completely separate to that QRS. So even though sometimes it looks like, oh yeah, there's a P wave and then a QRS, you can see in each scenario, this P wave is a different, there's a different P to R interval, so it's not connected. And then are they consistently and reasonably related?
So as you can see, and I just talked about, you have these pee waves. Are they related to any of them? Are they?
You know, in this, you've got a P wave here, but it's right on top of a QRS, so that, that atria is still firing and all of a sudden as that atria is firing, the ventricles are, oh, we should fire too, right? . And then number 5, what is the QRS morphology?
So this is gonna give you a big answer about what is happening in your ventricles. So is it tall, upright or wide and bizarre? So tall and upright often suggests a problem with our atria, because basically, like I say, these ventricles, are, are still firing, but they're not getting a, they're not getting a joint message from the PE wave, they're just getting their own sort of message and doing it.
So they're just doing a quick sharp depolarization to be like, oh, OK, we're gonna go, we gotta go. Whereas ventricular rhythms are wide and bizarre, so you can see this is like ventricular. Fibrillation, or BTA, and there's no, there's no P waves, and your QRS is very wide and it's bizarre.
So supraventricular tachycardia, we have this atrial flutter I said about this sore tooth, thing. I like waves in between the QRS and then atrial fibrillation is, so often what you get is atrial flutter before atrial fibrillation. So the atria kind of contracts, but they're not actually doing what they're supposed to be doing, and, and then atrial fibrillation, that muscles so worn out but it's just kind of like.
Wobbling around. And it's often caused by, ectopic focis within the atria. So then like I said, these, complexes then very tall and narrow for our QRS.
So sometimes it is actually hard to tell the difference between a QRS and a P wave. The key features are gonna be our abnormal or absent P waves and then like a normal or tall and wide QRS, . You can do things like vagal manoeuvres, you can put pressure on the eyeballs, or we're gonna be giving calcium channel blockers to these patients, but as I said, oxygen is very important in these patients, and reduce stress.
So supraventricular tachycardia is above that AV no there's sinoatrial node sinoatrial node and atria. Ventricular premature contract, complexes are what you're gonna be most commonly seen in practise, and these are premature beats that originate from the foci with the ventricles. So, often we get multiple, sometimes we get multiple foci, and these lead to sort of BPCs with a different structure, or, they get multifocal, BPCs.
So they, they're, they can look different. They might, but what we're really looking for is this wide and bizarre. So as you can see in this one, you get multiform down the bottom, is that there's a wide and bizarre one here, a wide and bizarre one here, and a wide and bizarre one here.
The one in the middle doesn't look the same, but that's still a BPC. And actually, more commonly, you're gonna see this one as a BBC. But because this is the one that's gonna throw you, if we still look at it, that QRS morphology is wide, and bizarre.
So these can be caused by heart pathology, myocardial hypoxia, and myocardial trauma so often things like being hit by a car, so we have respiratory distress as well, with associated pain, and aidemic estates. So again, respiratory acidosis is gonna causeuncture complexes, and some drugs as well that they might be on. So often we treat these for lidocaine, but what we're gonna be looking at is whether they have, By Gemini or Trigemini, which is like, 1 every 2 beats or 1 every 3 beats, if they have more than 10 in a row, or if they have ventric the tachycardia with this as well.
So this is another example. And another example, so this is our bargemini and Trigeminiy. So we have the 2, and then 3.
So vent to the tachycardia, is designed, defined as ones of three or more VPCs in a row. So it's quite common in arrhythmiave patients. So often the patients are gonna have a rapid heart rate of about 150 to 300 beats per minute.
So think about your patient as well, whether it's a cat or a dog. Obviously, cats are gonna be higher up in that 300 range. Again, we're talking about that wide bizarre QRS complex and without an obvious P wave associated with that.
So because of these, we're gonna have this reduction in top cardiac output, and the quicker this gets, if you think about these ventricles are just pumping, what, what blood are they pumping if they're not given the chance to have a pee wave? Where's, where's the blood coming from? So eventually these patients are gonna start to decompensate and what you're gonna end up with is ventrial fibrillation.
So we talked about. I'm We talked about, the atrial fibrillation. It's very similar.
It's recognised by complete erratic rhythm and, so no discernible or identical identifiable waveforms often what you get before is a ventricular tachycardia, a pulseless one, and then they get Bfib and go to, a rest. So, I just wanna show this video because I think it's really cool. You can see that bottom of the heart is just jiggling around, and that's ventricular fibrillation.
So for these, with Vfib, we're gonna be shocking them or doing a cardiac stunt, there's more on the recover guidelines, or I feel like we're lucky enough to do defib. So cage side monitoring we just flip through this quickly, again, a whole other topic, but, focused assessment of sonography for trauma, also known as point of care ultrasonography provides a more focused and . It's a limited, rapid assessment of the patient's clinical outlook.
So it's really good for nurses, and especially in the ECC environment. I like to use it as part of my triage if I can. Obviously it will depend on your practise and whether they're happy for you to do that or whether they're happy to do that without initially charging, you know, just to build up your skills as well, I think, and obviously it's, it's less stress than a radio, a radiography.
A radiograph, so, you know, it's gonna show us whether this patient has got wet lungs or bee lines, where this patient has pleural effusion, whether this patient has pericardial effusion, whether this patient has cardiac tamponade. It's also, it's a good standard of care. It's great in those patients, especially pulmonary edoema, we can score those systems.
There's a really good betlo scoring system by Greg Lo Andrew. He's like the king of ultrasound, and he's over the years developed many different. I'm Papers and techniques of ultrasound assessment of the lungs and the abdomen as well.
But it's repeatable, it's portable, you can have that scoring system in your practise and as a nurse you can score that, you can take pictures again, we're not diagnosing, but if we do a CAT scan, we take pictures and videos of what we're looking at on our ultrasound machine. That's gonna provide a more rapid assessment for that vet to look at what's happening. Then they can also pop on the ultrasound scanner as well.
. A really good ultrasound and nursing, . Instagram page to follow is Jacky RVN, and he talks a lot about how nurses can be utilising this. So patient preparation, obviously in lateral recumbency is the best, but if our patients, you know, if we're assessing our lungs, we can do sternal, and if our patients are extremely distate, we're not gonna be like lying them down on their sides because we're gonna be causing a decreased ability to expand that lung on that side, so.
Often, when I think about these patients that are really dissonate like our cats, they're open mouth breathing and stuff, we give them an anzylitic, put them in the oxygen cage, wait a couple of minutes, and you don't need to click, it's, you know, if you can, great, but you don't need to, you just need to wet, wet the, . Chest, so you can do water first and then add your gel or you can do alcohol if you don't have a defibrillator, and it works really well. You can just part the hair wet where you need to and you still get a really good image.
So again, think about the trauma, if the patient's got any trauma, and also if you need any ECT in patients, particularly if they, if they've got per pericardial effusion and that patient is gonna be, having a pericardial centesis. So yeah, it's gonna, you can pop it in through the auction cage, often what I do is I sort of zip it up. Put my arm in, zip it back down again to, facilitate keeping the oxygen in.
And just, you know, it, it barely, it's barely touching them. Often they're not bothered by it, especially once you've had that anxiolytic, you can pop it on, and you basically just fan your, you have your drotic notches use like a little bump on your ultrasound machine on your probe, so get used to what how to use your ultrasound machine. And you can fan it up and down, side to side like rock it side to side, and you look at all the structures within that.
So often what there's 3 sides, there's 3 sites, but you can do more with the vet blue. I'm not gonna go into that because it's copyrighted, and, you can look, you know, like I say, it's a big, big topic. So often what we're looking at is chest tube site views, so between that 7 and 8th rib, or pericardial chest site view.
And our substyphoid are diaphragmatic to you, so we're gonna look at that diaphragm and whether it's intact, and often we get pockets of fluid in there as well. Again, huge topic. I think if you're not comfortable with it, I think it's a whole other topic, to look into, learning about.
I think it's really beneficial for nurses. So basically we have the ribs that are identified as hyperchoic, or white structures with, distal black for shadowing so our feet, we call it the backside, as you can see on this one, And so these are little ribs up here, and then that your ribs, yeah, your ribs create this black shadowing, and then in between is your lung tissue, or the GAA sign, which I prefer because it does actually look like a little, alligator, with its eyes popping up. So your eyes are ribs, and then in between is your, lung tissue.
So the glide sign, tends to this line above, your gate eyes, and basically this should move, and I, it's been described in a couple of ways. The best way that I like it is, like little ants moving across, and some people say a shooting star moving across, but basically they should be intact. This is your pleural against .
Your thoracic cavity I'm rubbing up against, so I'm. You know, we want to make sure this plural line moves to and fro, and, and that's the motion of the parietal and the visceral pleural sliding over each other. A lines then refer to the hori horizontal line of decrease in eogeneity and between underneath this glide sign, so essentially the glide sign went under.
I and so I'm they move, I'm And they decrease in ecogenicity, so you can see up here they're quite strong, but then you don't really see them down the bottom. Things move, I'm between the airlines, and the lines don't fade. I'm.
Sorry, so bee lines, they're known as long rockets, and these are vertical lines that go through. So, They move to and fro, with the inspiration and expiration moving, and they pass through these air lines without fading, so you get these bright white lines like lung rockets, let's see if we can see, . So yeah, these are all lung rockets.
As you can see, they're down, and they would span with the movement. So as a patient moves, it would move to the left, and exhales, move to the right, and they go through those A lines, that's all you can see. So they, they increase, with the amount of fluid that is in the lung.
I'm so I'm Often this is what we can be scoring, we can score this 1 to 4 in all different areas. And then we have free fluid in our thoracic cavity, and this pops up as these black, so these anechoic tri thoracic cavity triangles. So as you can see, we've got a diaphragm, and then we have our pocket of fluid here, you can see, .
Like a reflection of the heart is a . So we get pulsing, but often these triangles in pockets. We got a little amphibrous bits moving around as well.
I'm with . With a pericardial effusion. Obviously we'll see this around the heart, but it'll be it'll be in a circle rather than a triangle because it's the hyperchoic sac.
So you get this really bright white line around the heart with the anechoic lines so the black in in between the heart and this line, and that doesn't, that fluid doesn't move. So whereas you see with this one, it moves, and that doesn't move, even though the heart's beating so the heart beats, but it's beaten into that fluid and the outside line doesn't move. I'm assessing the covena cava, and you can do these in our patients, good for emergency patients.
It's just to measure our cove cava, aortic ratio. You can do this down by the liver by the diaphragmatic line, so on the diaphragm just underneath the liver, you'll see that, cornal vena cava pulsatum. And obviously, if it's large, then the patients over, you know, over infused with fluid and so often with our cardiac patients, we're gonna have a large called a vena cava because of that that heart failure, that congestive heart failure, .
If we have a very depleted one, a very narrow, like we, like a thready one, you know, you just see it, with a sharp beat, then obviously these patients are under perfused. I'm not going into too much, but our specific consideration for our patients is how we can utilise on ultrasound and congestive heart failure. So looking at our I'm Oh, I'm.
Bee lines, you can see there's quite a few in these. I'd say this is almost white out, so 3 out of 4, and then this one's got 1. This one actually has a glide sign, a shred sign, which just means that the glide sign up here that's moving backwards and forwards, you can see in a minute, has his pocket here that shouldn't be there.
So that's a a pneumothorax, . And then in the middle, we have our gallbladder. So when we look at our liver, often we have this anechoic black circle in the middle.
And this should just have a black, it just should just be a black circle and then like your, mottled liver appearance. But often with congestive heart failure, what we get is a back because of the backup of fluid, we get edoema in our gallbladder. So what we get is this gallbladder halo so we get this really bright, White line around the structure and then sometimes you get another little black line around this, you know, hyperchoic line so it looks like a little halo to the gallbladder.
And if you have that like maybe they'll be on it to you every time you see it. And then again in our congestive heart failure, we might look at our abdomen for, free abdominal fluid with ultrasound, but then we're also gonna look at free, free fluid in our chest, so, pleural effusion. So to review, emergency management of congestive heart failure and our cardiorespiratory patients are gonna be.
Oxygen, angiolytics, maybe an IV catheter if you're able to, and the aim is to remove excess fluid. These patients often with diuretics, think about our electrolytes, and our intake of our patients, and looking at our urination. If these patients aren't urinating, they're on the diretics, and we need to pull that up to our vets.
They're gonna be on this ACE inhibitor, so we talked about that, RAS system. This blocks that rest system from keep going and obviously like I said depleting the body. Again, minimal handling is key in all of these patients, not just in congestive car in all cardiorespiratory patients, avoiding radiographs as I talked about and that we can do bust cages, we can do a sternal X-ray, if you want to, but I think in these patients ultrasound is minimally invasive, less stress, repeatable.
And it's, you know, it's cheap as well, and instant results, . So yeah, you can do it before that and More stable to have a radiograph. And yeah, that's response to treatment with ultrasound, so we can loop diuretics, you would hope that that fluid, especially that pulmonary edoema, would start to dry up, and then maybe we might need, abdo abdominal centesis to get to reduce the amount of free abdominal fluid that ascites, that might be causing abdominal pain, thinking about the pressure that it puts on your diaphragm, that diaphragm can't expand.
When there's fluid in the abdomen, so just increasing the ways that that patient can breathe, and thoracentesis, obviously pleural effusion, we want to get rid of that pleural effusion and pericardal effusion as well. And so obviously we're not doing those, but setting up, having grab bags, is what we have for our emergency patients. So having all the equipment you need ready in a bag or in a box, if you have the room and then when that, you know, or if you see on your.
Ultrasound and you take a picture and then your vet says, yeah, OK, we're gonna do that. If it's already set up, great, you are minimising that time that that patient is having to deal with that path of physiology. ACG I'm probably a problem with fusion.
I'm I, we get this decrease R wave amplitude, we get tachycardia, and then we get these electrical alternans. So as you can see in this one, is that the waves are all different sizes, so it is quite hard to appreciate in this, but basically waves just start, your QRS waves, you know, dip and aren't always the same length. So if you have a paper trace, this is great because you can look at how many little squares they are.
And so your R wave, altitude varies markedly from beat to beat, and electrical alternans are often a sign of our cardiac tamponade, and so as I talked about that pushing in of that left atrium, and you might also see electrical complexes as well, in more severe cases. So just talking specifically about these patients, again, we're gonna look at the pericardial site when we're doing our, ultrasound, and they're gonna need a clipped, if they're gonna have a pericardial effusion and pericardiocentesis, so clipping from the 56 intercostal spaces bilaterally. I'm And we're gonna look at our ultrasound.
So as we talked about this is our atria sorry our right atrium, our left atria, and that gets pushed in, . And we get this fluid around this pericard infusion, so you can see this wouldn't this wouldn't this outer layer wouldn't move. This might move because of the heart beating but essentially have like a ball of fluid around your heart.
So again, emergency management is oxygen and xylosis, and these patients are clotting profiles really important before we start sticking needles in them, especially if we don't know the cause of pericardial effusion, so this can be a cause of, rat bait toxicity. So doing a clotting profile, is important. So getting an IV in these patients is, again, once you've got that, anzoolytic on board is really important.
And then pericardiocentesis again this is another grab bag that we have, you can get the kits and so then all we do is chuck in a bag like sterile gloves we do actually do ours now with . Buster drapes on them, you know, penetrated drape, and we have ECG pads ready to go, and as well as that we have like a cover on our ultrasound probe as well so you can use it sterilely. And then fluid analysis, lots of different tubes as well, and these patients don't need diuretics.
So that's a lot of information. I appreciate I've probably overloaded you, but if there are any questions, feel free to ask now or you can always email me as well. Chloe, thank you very much.
You certainly did provide a lot of food for thought and a lot of good information there to be considered in these cases. So, thank you for your time tonight. Also, a big thank you to our sponsors, many pets.
We really do appreciate your support on these. And, of course, to all of those of you that joined us and, and are watching the recording, thank you for your time. And I hope you got as much out of it as what I did.
Chloe, we have run a little bit over and we don't have any questions. So I think I'm going to wrap it up. And, just once again thanking you, for your time tonight and for sharing your knowledge with us.
All right. Thanks very much, guys. Thanks everybody, and to Dawn, my controller in the background, as always, thank you for making things run seamlessly.
And from myself, Bruce Stevenson, it's good night.
