Joint protection, as I said, is an integral part of pain management in human medicine. I love this. Ignore the dog's weight.
Turn a blind eye at the moment, but. Here we have a ramp in action. Imagine this dog's body weight going through those front legs if it was asked to jump out of this car.
Some patients may end up with faecal stennesus and possibly some flattened faeces, and this is due to the mass some of the enlarged sublumbar lymph nodes or potentially the primary mass causing an obstruction. They may end up with some hind limb weakness, they may end up PUPD due to hypercalcemia. They may also be lethargic, and there may also be some weight loss.
And in the early studies that have been done using stereotactic radiation therapy for nasal tumours, it does look like the vast majority of dogs improve clinically, about 70% of them will have meaningful tumour shrinkage, and you're looking at median survival times that are kind of in the same range as what's been reported with conventionally fractionated radiation therapy, so 12 to 18 month kind of survival time. So if I look at this eye here, this eye is definitely to be scheduled for surgery. We can see widespread iris melanoma.
We can see pigment on the interior lens capsule, which means there is already secondary UVITs, perhaps there is even secondary glaucoma. I would suspect cause I'm seeing a bit too much of the sclera conjunctaga here. This eye definitely has to come out.
But what about this eye? This is a real dilemma. So we're gonna talk about CPR review.
I'm, we're gonna talk about all things CPR, I'm a cardio pulmonary, resuscitation. And these are all under the recover guidelines. So I'm, I'm recover instructor trained, you can become recover rescuer trained.
And they do through that, through their website. And then as an instructor, I would then be able to come out and, get you fully rescuer trained. But basically, everything that I'm gonna talk about in this webinar, is based on their guidelines.
It's not necessarily their word for word, but, it's heavily based on like guidelines. So Recover stands for reassessment Campaign on Veterinary Resuscitation. And they banded together.
It's run by Dan Fletcher, along with a couple of other vets and, vet nurses. And they basically look at all the literature, and review all that literature and look into different ways of doing CPR, different drugs, and advanced life support that we might use for our patients, and how, how that affects the outcomes and the success of our CPR events. So the last guidelines actually were in 2012.
So these are based on these ones right now, but I will talk a little bit about that they are about to bring out some new guidelines. They were about to do that in 2019. That got delayed and then got delayed further by the pandemic, unfortunately.
So there are new, guidelines coming out. They're also really branching out into exotics, and large animal. They're looking at doing pet owner, resuscitation, resuscitation training and how that's gonna benefit us, within practise as well.
So firstly I want to talk a little bit about how to identify those at high risk of, cardiopulmonary arrest events. And the reason why I want to talk about this is because I think it's important to talk to owners, to talk to our clients about those that are at high risk, because then we can preempt and get a code early on rather than trying to bring them in the middle of CPR and trying to, you know, talk about the success rates, and the risks of CPR. Which are great, and again, the success rates are low, and obviously cost is also, tied into that as well.
So using previous assessments of our patients alongside things like our ASA grading and triage levels are all gonna help us to identify those that are at high risk of cardiopulmonary arrest. It's really important for those that we know that are going to be at high risk, that we talked to the owners early on about the risks of CPR, the success rates, and also to gain a code. So whether that's, do or sate, basic life support, advanced life support, whether you talk to the owner about how long you would continue the CPR, .
And what their limits were, and with some owners, they actually would leave that in the hands of the, of, of two veterinary surgeons to decide whether it was appropriate to continue CPR. So these are all things to consider with our patients, but those that are high risk, we identify their codes and if we identify that they want CPR, that we have the necessary equipment nearby, as well as the drugs calculated and potentially drawn up for ease if we know that these patients are gonna, crash imminently. This is actually just an example of what we do.
We have, we use Smart flow. So on our smart flow, there's an option to, to tick, to use a box for DNR, basic life support, etc. But we also put it on their kennel as well so that if anybody finds that I'm patient in a CPA event that they, I know exactly where to stop.
I'm doing the CPR and resuscitation. We also have this consent form. So this is in, all our consent forms, and we used to have tick boxes, and we would have them on like our space and castrates, but we found that that, sometimes it's a bit of a jarring conversation for something that's so healthy.
So, we have this, This little word in that talks about CPR I'm And basically they will begin CPR unless that owner specifies to us. So we no longer have a tick box. We just said that we're gonna do it.
And if they would prefer that we didn't let the event speak to us, and that kind of eliminated a few things, in terms of owner stress, and upset. So before we start talking about how to recognise a cardiopulmonary arrest, how to do our basic life support, how to implement our advanced life support, I just want to talk about what the perfect, and I say that in quotation marks, crash box or crash car is, because that is gonna be fundamentally is gonna help you with your, BLS and ALS. So basic life support and advanced life support.
So with our crash boxes, we want to standardise the contents of every box within the practise and how they're organised. And this is really important because if you have somebody that's never been to the practise before, they know exactly where to find things, in the crash box, they're well labelled. We use things like visual aids, to identify what should be where in the box, as well as, they're easy to restock, in which case anybody any member of staff can then restock if they're clear, clearly labelled, if they have.
A how to guide, so, with ours, we have a picture, of what is in each drawer, and therefore then, and how much of each, each, thing like syringes, how many syringes are in there, how many bottles of epinephrine are in there. And that just ensures that then when they come to restock it, that they know exactly what's missing, it can be, replaced, and they know exactly how it's organised. And if you went to a different crash box within the practise, that you know that those things are in the same place as well.
So it just means that it, creates a great ease of use, when in those, CPA events, it's high stress, and often. You need to find things quickly, and therefore, if you know where everything is, you're able to find those quickly. So readily accessible visual aids and a timing device, it should be near, so you can either have a clock on the wall, you can have a stopwatch attached to your crash box or in your crash box.
Digital clocks are really good, and you can actually get ones that you can start, a timer just like a stopwatch, but it's large and everyone can see it, so. It's a great visual aid for you to record how many minutes you've been doing the CPR when you last gave adrenaline or defibrillated, all those things need to be timed and recorded in order for us to be the most effective at our CPR as possible. The choice of box or cart is gonna depend on your practise types, so they may range from a toolbox.
So, for example, this is one of our crash boxes, so it's just a little tool toolbox that has two shelves and then, like a, a drawer underneath. But that is what best fits our practise and the size of our practise or where it sits in the, in the practise. You can get the stationary drawers and that they have the little plastic drawers, we have that in our surgical referral area.
And you can also get those custom resuscitation trolleys, or the large red toolboxes. So it it will be up to your practise, the size of your practise, the practise preference, the cost of them as well. The good thing, you know, they all have advantage disadvantages.
The small crash boxes are great for transporting them to the patient, if your patient isn't right next to the crash box when they go into cardio pulmonary arrest. By debriefing after every crash, we're really gonna hone down on what's important to have in that crash box. So you want something that is built for your practise and that works for your practise.
There are, minimum, minimal, items that you should have in there like, airway access. So like laryngoscope endotracheal tubes, potentially tracheal tubes, you may have . A guide wire or intubation.
You're gonna have ties, a cuff syringe, and then you are potentially gonna have an ambi bag. These are really useful for our, crash boxes. You don't have to then be set up next to an anaesthetic circuit, and you can ventilate using room air, just as effectively.
As well as that, you may have things like your advanced life support. So you as a bare minimum, you would have your adrenaline, maybe you would have atropine, you might have antiarrhythmics like lidocaine, so we'll talk about all the different drugs that we use in a couple of slides once we talked about our BLS. And like I said, we would also have our visual aids, timing devices.
We may have other things like, we'll talk about leadership and how we can identify leaders, syringes, needles, and then anything more than that is what is suited to your practise. And that might mean that sometimes you have things in there that wouldn't necessarily be used for a crash, . But it fits in your box and the the main items are very clear and easy to access, and then maybe you have those extra items in somewhere accessible, but I'm not taking the centre stage, essentially.
So what do we do when we, I'm recognise that a patient is in cardiopulmonary arrest. So first things first is that we would call for help every single time if we think that a patient is non-responsive, it doesn't look like they're breathing, you know, whether that be under anaesthetic, we go to their kennel, we find them unresponsive. A patient comes in with the owner and looks unresponsive and like they potentially are about to either crash or that they are already, that they're already in cardiopulmonary arrest.
So call for help, that's the first thing we're gonna do, whether we shout for help, we may shout and ask somebody else to do a call out on the phone system, whatever, is in your protocol for your practise. Make sure that it's effective in getting everybody's attention, because we want everyone to come to that event so that we can then have enough people for this cardiopulmonary arrest. Then, within a short amount of time we're gonna do a rapid assessment about airways, breathing and circulation.
This should take no more than 10 seconds. So we're gonna check there's nothing blocking the airways. And we do this by opening the mouth, and then we're gonna have a look down at this patient, see whether they're taking any breaths.
And finally circulation. So circulation is actually the least important out of these 2 out of these 3. So we would maybe feel for a quick pulse, but we're not gonna be, trying to listen with a a stethoscope and trying to feel the pulses for a long time.
If you, can't see, any breaths being taken by this patient and you do a quick femoral pulse feel and you can't feel anything, then we would initiate CPR immediately. And it's been shown, and this is in the recover 2012, that the quicker that you start that CPR, The better chance, the better success rate those patients have, because we want to limit that amount of time that that patient is in asystole or whatever rhythm it is in, and not sending blood to that brain and avoiding hypoxia. So we've identified that we have a CPA event.
And we now have, everybody is now coming. To this crash, we have all these people. What we really need now is a leader.
There's lots of different roles within our, CPR, so we would have somebody compressing, so somebody that found the patient is now starting those compressions right away. So talked a little bit about on that last slide. 0 30 compressions to 2 breasts, so this is our basic life support one rescuer.
So when we are just doing, when there's just one person, nobody's coming yet, we start compressions, and there's the 30 compressions at 100 to 120 beats per minute. We do 30 of those, we count them out, and then from that we would then do our two breaths. So we would close the mouth and snout.
Keeping the neck in line with the spine, and bringing, bringing our heads right down onto the floor and doing two breaths, into that sealed mouth. And then go back to doing our 30 compressions until and we continue that cycle 30 to 2, until somebody else is able to come along, intubate that patient, start ventilating, and then we would finish at 2 minutes. But we'll talk about that in a second.
So we have our compressor, and now we have somebody that's come along, we've got somebody doing airway our ventilation. And again, this is something that we're gonna talk about in basic life support. We potentially need somebody who is getting IV access in this patient, if it already has IV access and and once we've got IV access, we're gonna be looking at our advanced life support, so I'm looking at what drugs our patient needs, drawing those drugs up, giving those drugs.
Somebody's gonna be recording that, so they're gonna be recording when the compressor started compressions, when, when the 2 minutes is up, I'm the next compressor, what, what ECG trace was seen in between the compressors. And when the drugs were given, how many, you know, the, the ETCO2 of all patients are called up from our carnography. So our recorder's gonna record everything that's going on in that CPR event.
We potentially have a runner, if we've got enough stuff. So in an ideal world, we'd have somebody that's able to go and run and get extra items if we need them, go speak to owners. All these kinds of things.
Most importantly in these events, we need a code leader. And it's really important to identify that clear leader from the start, so that everybody knows that they are the leader, and that they are gonna, Make sure that everyone has their role, so it doesn't have to be a be. It should just be the person who's most experienced in CPR.
So for example, in my practise, if I was in the room with the at the crash event with some of our vets, I would potentially be that person that leads the code because I'm a recovery instructor, or those that are recover, rescuer certified, again, they potentially are more experienced in CPR than some vets. In other cases, a vet is potentially more experienced to run that CPR code. And with regards to, the drug dosing, I'm, there is actually, I'm one of the best, I'm Emily Gorman that I, teach and recover course with, and she's actually emailed the RCBS.
About, nurses leading codes, because obviously there is some element of prescribing drugs, and the RCVS agreed because it follows the algorithm, as long as they follow the algorithm, and that that's OK. I'm. Under, you know, that that those, those algorithms have been created under that direction.
And so, This is where, you know, it doesn't have to be a vet. It can be a nurse, it's just whoever's most experienced in CPR. So a good leader allows team members to question actions.
It doesn't mean that that leader is now necessarily, leading the code and saying this is this, you know, that this is a Sicily, and nobody else is allowed to speak up. A good leader asks, so, we'll talk about this when we come to our ACGs, but basically when You are checking your traces in between compressions, and we should be using closed loop communication, and that maybe is, OK, I see a system. Does everybody agree?
And then everybody in the team would agree. That's closed loop communication, that leadership, is clear that they are announcing. Things that need to be done or things that they're seeing, and they're asking people to relay back to them, is that correct?
And so there's many ways that you can, identify a leader whether you say I'm going to be the leader of the, I'm of this event. Sometimes you have hats, so this is just actually a picture of my daughter. And, she.
Obviously he's just wearing this nice fancy hat, you don't have to have a fancy hat like this, it could be a baseball cap. You could have a sash, you potentially could have a cake, whatever, whatever works in your practise, it can be as ridiculous or as sensible as you want. But often these visual aids are really good for identifying that leader and for all the team then to look to that leader for direction potentially.
I just mentioned closed loop communication. So in a most recent study, and it was shown that a blindfolded leader in the CPR drill encouraged participants to use closed loop communication more effectively. So this was a study done at Dick White referrals.
And they blindfolded the leader in, CPR drills, and they found that in comparison to those, where the leader wasn't blindfolded, That the closed loop communication was used much more effectively and therefore the CPR events ran more smoothly, and they were also would be potentially more successful in real in like in the real world. So, it minimises room for mistakes. By having close loop communication, so I use an example on that last slide about ECG traces.
Other things that we would do is, I'm the leader may say, OK, we're gonna give, I'm low dose epinephrine on when we finish, I'm. When we come to the end of these compressions, we're gonna check the trace. If it still is, we're gonna give a low dose epinephrine.
The person drawing up the drug says, OK, drawing up low low dose epinephrine. This close, this is closed loop communication, because they're basically repeating back what's been said, confirming that they've heard what's been said, and that they're doing what's been asked of them. And again, when that person then comes to give the atropine, but with the epinephrine.
And they would give the epinephrine, and as they're given the epinephrine, saying, I'm giving low dose epinephrine, however much it is, 0. 0.1 mLs, via the IV catheter.
So again, repeating back what's been done so that people can hear and acknowledge that that action has been taken. Again, this is really effective for the recorder to record that down. Then later on down the line, if people are a little bit confused, like, oh, did we give that epinephrine?
The recorder can go, actually, yes, I heard such a body saying that they gave that, that was given at that time. So it minimises that room for mistakes. And it also allows the whole team to participate.
So the example that I use the ECG again, this is an open, open question with, with the epinephrine as well, that, you know, we see asystole. We'll talk about the different rhythms. We see asyle and somebody, the leader says, OK, does everybody see asystole?
Everybody says, yes. OK, we're gonna give epinephrine low dose. And they'll say yes.
Potentially, if they, if somebody's leading and they, they weren't sure of a trace and they said, OK, I think this is pulseless Back, let's give low dose epinephrine. Somebody within that team would hear that instruction. And maybe go, oh, I don't think that low dose epinephrine is appropriate in this.
Should we be defibrillating in this patient. And that opens it up, allows the whole team to participate, allows the, leader again, to receive that feedback, to reassess and potentially implement new information. So here's the big thing, basic life support.
This is the thing that we want to be implementing straight away, this is the thing that is the most important. So basic life support is the attempt to sustain life by artificially maintaining blood flow and oxygenation of the blood. So the blood flow is created through chest compressions, while there's positive pressure ventilation from our ventilator that provides oxygen, removes carbon dioxide, from that pulmonary circulation.
So as I said, no longer than 10 to 15 seconds, 10 I would say is the appropriate, and then we should be implementing our basic life support. So I said about the research, the research showed that rescuers can be unreliable and accurately assessing the presence of pulses. There's no evidence that says initiating compressions, when an animal's not in arrest causes significant harms, whereas, commencing CPR where there's little delay, actually improves the outcome.
So. It's much better to start the CPR and then maybe stop than it is to, just to wait and see. So our main main things and our basic life support are our chest impressions and our ventilation of our patient.
So we talked about, that we want to initiate our chest compressions as soon as that cardiopulmonary arrest is diagnosed. And the real big thing with our chest compressions is that we want them to be good quality, so that we get that blood flow, to as high as possible. And we'll talk about the ways that we can assess, how our, how our, posture or technique or compression point are affecting.
Of of quality of compressions and how we can monitor that quality. So the goal of compressions, they're performed to create as much blood flow as possible to the pulmonary tissues for gas exchange, and they're there to deliver tissue, deliver oxygen to tissues, and to support metabolism, to restore function of the organs, and I, and then ideally, . Achieving this return of spontaneous circulation, so Rosk.
Even the most effective, administered compressions only provide 30% of normal cardiac output, and that makes the consistent application of best practises, of our CPR compressions critical. So just saying that 25 to 30% when we're doing really good quality compressions, it's still not very much for our patients. So we really want to aim to have those good quality compressions because the minute that we start deteriorating in quality, the less cardiac output that we're gonna have and the less chance for these patients that we're gonna get of Rosk.
So we want to maximise that organ blood flow. So these are some lovely pictures I took of me doing CPR on our I'm Teddy patient. So posture is really important.
It's really important that we lock those elbows. As you can see from the front picture and from the side picture that those elbows are locked, our shoulders are over our hands, . So that we are putting our weight through and using our core.
I'm. So it's not a shoulder workout, we're not pushing with our shoulders like we're doing push-ups. We're gonna be using our whole body, and so we're rocking from the waist essentially and using that core.
We want our hands, over the top of each other interlinked, with our, we're using our palm, the heel of our palm for those compressions over that compression point which we'll talk about. So all of these things are going to help us, achieve those good quality compressions. So thinking about with our patients, getting our shoulders over our hands, with our elbows locked, is that we need those patients at an appropriate height.
So this, we have a table that moves up and down, so maybe you have that, that you're able to do that. If you can't get good quality compressions either with a stool, and you're not getting that, alignment, put the patient on the floor. And then you can kneel and do that with the patient.
We'll talk about the difference with cats and small patients, but most of our patients we're gonna be using this posture with our hands interlocked. And we're gonna be using, we're not taking our hands fully off the chest. We will allow for recoil, so we're gonna lift that heel up and then allow that chest to recoil.
So the recommended rate is 100 to 120 minutes, and that's regardless of species, size, and again, this is under our, 2012, so this may be changing slightly for our exotics, and, obviously large animals. But definitely for our cats and dogs, 100 to 120 is our optimal rate. We want to compress the chest a half to 1/3 of the width.
So when we're pressing down, we're not pressing down too hard. So there's often the the myth that we aren't, if we don't break ribs, we're not doing chest compressions hard enough, and that isn't necessarily true. Unfortunately, rib fractures are often, they do often happen in CPR but that's not always the case, and that's not what we should be aiming for when we're, when we're compressing our chest.
So we're gonna go 1/2 to 13, and then we're gonna allow for full chest recoil, so we wanna be able to, allow that pressure to suck the blood back in, we'll talk about how those compressions work. So they should be performed in 2 minute cycles, without interruption, and this is because 60 seconds of consistent compressions is required to reach that myocardial perfusion pressure, and. 60 seconds reaches that maximum potential and then every second of interruption leads to significant decreases.
So once we get to 60, then we're gonna do 60 seconds at that maximal potential that myocardial perfusion pressure. So this is the, that 60 seconds there is that really important part. We'll talk about rescue fatigue on the next slide, but if we do feel like we are fatiguing within that 2 minutes, then it is appropriate to change rescuer and try and do that with as minimal disruption as possible.
So having the person stand right next to you, counting out, and again, close loop communication. OK, I'm gonna move off the chest, I'm gonna come in. And you start compressions at the same rate straight after so that you are continuing reaching that myocardial perfusion pressure maximal point.
When we are changing, I we'll talk about some basic life support, if we don't have our ECGs, we don't have our capnography. All those kind of things, we want to have that minimal swap over, so we're gonna have the compressors, swapping quickly while somebody just does a pulse palpation, maybe an osultation, but as quickly as possible. And again, once we have our ACG on, it's gonna be a very rapid assessment of our pulse and our ECG trace.
Before the next compressor comes on, because we want to try and prevent the complete loss of that accumulated myocardial perfusion pressure. It's really physically taxing. I, I think, people take it for granted, and especially when you're doing your technique, when you have the wrong posture, it's easy to think that it's not as hard as it is, but when you are using your whole body, you're using your core, by the time you get to that end of that 2 minutes, .
It's really tiring, so you must swap, the compressor every cycle. And if possible, if you have enough people, try and have a 33 compressor change so that you don't keep going from one compressor to the other cos by the time you've done 20 minutes of compressions, and both of those compressors are often very tired. So as I said, 2 minutes without checking the rhythm, we have those 30 compressions with the 2 breaths.
Once you're a patient, once you've got somebody else to swap with you doing compressor, you start the timer and do the 2 minutes from there. So there is an associated increased survival, compared to, with, uninterrupted CPR, in comparison to more frequent causes. So, we want to build that cerebral and coronary perfusion pressure.
And to avoid decrease. I just mentioned rescuer fatigue during compressions, so that can occur as early as a minute on in our. Compressions, especially when we're starting to get into like, say 1520 minutes, it can be really easy to start to fatigue, and often rescuers themselves fail to identify that they're fatigued.
So this again is part of our teamwork, as part of our closed loop. And we'll talk about our catnography. If we start to see that our catnography are ETCO2 isn't reaching the 15 that we want it to, that compresses, change positions, we change posture a little bit.
It's still not, it's still not, reaching that 15 millimetres of mercury that we want it to. Maybe we start to think that rescue is fatigued, they, they can no longer do compressions, we need somebody fresh to come in. So as I just said, swap out after 2 minutes because after 5 minutes, you can only be 18% effective at compressions.
So if you're only 18% effective at compressions, and at 100% we're only 25 to 30% effective at . Getting that cardiac output out, just think about how small that cardiac output is gonna be now. So it's gonna result in incomplete wall decompression, so often you can't do that half to 3, or we're gonna be leaning on the thorax.
So we're not gonna be permitting that full chest recoil, which is really important in our patients. So, chest compressions are a result of the blood being squeezed from the heart into arterial and pulmonary circulation. I'm And so there's two types of the cardiac compression and the thoracic pump theory.
And the cardiac compression theory, is that there's forward blood flow during chest compressions, and that presumes that the blood is squeezed into the heart from the arterial and pulmonary circulation. With closure of the mitral and tricuspid valves, and then as a result of that, they then prevent, retrograde blood flow, and then they open the aortic and pulmonary bowel valves in response to forward blood flows, then the blood flows out into the lungs around the body. And that is our cardiac compression theory, when we are doing our compression directly over the heart, we are basically squeezing the blood through the heart and out again.
The thoracic pump theory is slightly different, and it hypothesises that the blood flow, occurs when the intra intrathoracic pressure exceeds extra thoracic, vascular pressure. So basically the blood is squeezed out of the large vessels, the aorta and vena cava. And then together with one-way venous valves, it ensures a one way venous arterial direction blood flow.
So basically. It creates a vacuum that pulls the blood into the heart when the recoils allow. So this is why it's really important to allow that recoil.
So when we're doing our thoracic pump, we're gonna be doing it over the widest part of the chest rather than directly over the heart. And so we're creating that vacuum. We're gonna compress our chest at the widest point.
When we allow that to recoil, that sucks, that uses the vacuum and sucks all the blood into that thoracic area, . So slightly different between the two of them. In that the, cardiac compression theory when, when we relax the heart refills and the air passively returns to the heart, and that's just because we relax that heart.
Whereas a thoracic pump is used as kind of the, the actual vacuum of moving the blood into the heart is how we're creating the cardiac output. So with having many different breeds of our patients, that means that we will need a different compression point. So round chested dogs, and they have a width and the depth that are roughly equal.
So think about things like our Potential beagles, Labradors, they're kind of round, and they have the same depth chest. So we would use, our widest part of our chest in these patients because, because of that kind of barrel shape. We, using cardiac, the cardiac compression theory, the cardiac pump theory is gonna be too difficult to get, the compression on that heart.
So we would use the thoracic pumps over the widest part of the chest in these patients, keel chested, so things like our Dobermans, whippets, greyhounds, where the depth is greater than the width, then we would do direct compressions over the heart. That's not necessarily to say that those breeds fit in, fit in a box. And so if you're doing your compressions and you notice that your ETCO2 isn't changing, you're not getting a good, you're not getting a good output.
In those patients that then potentially would change your compression point and see if that makes a difference. So some patients are difficult to tell. So, there, you know, there's some, there's somewhat kind of, cross breeds that sometimes fit into both of them, or once you start doing compressions, you realise that actually doing like cardiac compression is gonna be the most effective in these patients.
But when we start, compressions, if we have a general idea of these patients. And again when we're thinking about those patients that we are looking at in advance that we know that they, that they, that they want CPR performing and that they're high risk, that we identify potentially and put, put on their kennel, but a note somewhere, what compression point that we want people to start with. And the people I'm Begin that compression point where and and try and make it the most effective that it could be.
So flat-chested. Are shaped more like people, so I'm, they have, I'm. These are our bulldogs or French bulldogs.
Anything that's that has basically a wider chest and it has deep so we want to do sternal compressions and dorsal recumbency. In these patients right directly over their heart. Again, however, if these patients start rolling when we're putting them in in dorsal recumbency, then potentially these patients aren't flat-chested, and we could actually switch and do.
a thoracic pump theory over the widest part of the chest. And again we're, we're gonna be looking at our, ETCO2 to see whether these compressions are effective. Other things that we might do whilst if we have enough compressors, are potential interposed abdominal compressions, and they have been shown to have some effort, so it increases blood flow.
I'm As well as blood pressure, venous return, cerebral blood flow, cardiac output, and they are unlikely to cause any harm. There isn't any evidence in cats, and I will say that it's only worth doing if your staff are well trained or that you are all confident in CPR. So basically, As the person is doing a compression on the chest, we would lift up the abdomen and vice versa.
So as they, as they recoil on the chest, we would compress on the abdomen, and that's to help with that blood flow back to back to the heart. So cats and very small dogs, we can use one-handed one-handed techniques. So almost always they're always keel chested, so they have a deeper chest than they have wide, so we can use one hand.
And we can use our normal, . Interlocked hands, for CPR as well, but just remembering that, that we're gonna be much lighter than we would do with a dog. So again, we are still keeping our elbows locked.
This picture doesn't actually look like the elbows are locked. But our elbows are still gonna be locked, we're still gonna be maintaining that good posture, but we are, gonna be. Very conscious of that half to 3 recoil, so the best way to do it in these small patients is to put your thumb up against your fingers in a flat V shape to promote ventricular e ejection.
Instead of a C, so it's very easy to get into a C, around the chest, and you fatigue a lot, a lot less quickly if you have your, thumb in a, in a C, but to get that ventricular ejection, we really need that flat V shape. So this actually really like out of all of them, I would say this causes the biggest fatigue, like that muscle there in your thumb. Becomes really sore, but this is actually the easiest that if you do get rescue or fatigue in one hand, you can immediately swap onto the other hand to do your V-shaped compression, so again 100 to 120 with these.
So ventilation should be started as soon as possible once compression's initiated. We talked about that single rescuer, so 30 compressions to 2, breaths and that's mounted snout. So we want to keep that airway as clear as possible, so we don't want to be lifting their neck up, and doing it near us.
We want to get it down to their level, stretch their airway out so that that's all, one clear airway seal around the mouth and snout to create, to create one airway and do one, a one second, inspiration. So a quick. 2 breaths and then about 2 compressions.
. Once we have more than one person, endotracheal intubation should be again performed with the patient in lateral recumbency. So, I think a top tip that I would have is that if you have a patient, if you are doing normal intubation in your healthy patients is that you start to practise doing lateral recumbency intubation so that you are more comfortable with that when you come to that in a CPA event. So we don't want to interrupt, compressions.
That's why we're gonna do it in lateral recumbency. Once we've got that tube in place, we're gonna cast that tube to create, that positive pressure ventilation, so it's directed into the lungs instead of, into the stomach or out of the mouth. We then are then gonna provide 10 breaths per minute.
So that's 1 breath every 6 seconds and again that's a 1 2nd inspiration time. So quick, and again if you've got the ambi bags, making sure that we're not compressing them too much thinking about our tidal volume. We might use a reservoir of our anaesthetic machine, or again ambi bag.
So manual resuscitate these ambi bags actually help with the inthoracic pressure, so they help to suck blood back. So keep the breath size and the frequency consistent, and that helps to eliminate too much carbon dioxide, which may cause hypocapnia, through hyperventilation, which can again cause cerebral vaso constriction and impaired blood flow to the brain. So we are aiming for more than 150 millimetres of mercury ETCO2.
So that doesn't seem like very much, but when you're actually doing your compression, you'll notice that how hard it is to get to that 15 and how hard it is to maintain 15 or slightly more. So if we have anything less than 15, we're gonna start talking to our team, we're gonna be looking at our compressor. Do they have the correct posture?
Do they have good quality compressions? Are they going at the correct rate? Again, with ventilation, are they going at the correct rate?
Are they giving a 1 2nd inspiration time or is it longer? We're gonna start thinking about how we can change our CPR to maximise that ATCO2. So this is the .
Recover CPR algorithms, so again this may change slightly in luck for the 2022. Up to date that they're gonna do shortly. But basically, once we've started our basic basic life support, we're gonna start our advanced life support.
So we're gonna initiate monitoring so we're gonna look at our capnography and ECG. Anything else is I'm a bit defunct, so blood pressure, we wouldn't particularly use or find useful in our advanced life support. Patnography and ECG is king essentially.
We're gonna obtain that vascular access, so, if we can't obtain vascular access, potentially, intra-osseous access, and if not, maybe we're gonna be giving our, reversals and our our drugs. Our CPR drugs in in our endotracheal tube. And then, next is, with our advanced life support is to administer reversal.
So if you've given anything or you know that that patient has anything, that could be reversed, we reverse that. So opiates, we're gonna use naloxone. benzodiazepines we're gonna use, themanazo and, any sedation so like a deer meatomidine, meatomidine are gonna be reversed with, Atipan.
And that just helps us because these potentially are causes for our cardiopulmonary arrest. And so we want to try and reverse those, get rid of those, so that we're stand the best chance, for this patient. And then we're going to talk now about drugs and defibrillation once we've talked about, our monitoring tools, and we'll talk about the ECG traces and what they mean, for our patients.
So as I said with Capnography and we want to aim above 15 millimetres mercury. These are a great indicator for the quality of compressions for our patients. If we have a sudden leap in our antidal carbon dioxide, this is gonna potentially indicate return of spontaneous compressions, circulation.
So we want to check for a pulse before we discontinue those compressions. We don't just see that jump from 15 to 50, and stop. We want to continue the 2 minutes, unless that patient.
Is moving or we can feel a pulse while the person is doing congressional you can feel a very strong pulse. And if we're not sure then we've finished the 2 minutes before we check. I'm As I said, we're aiming for our 15 millimetres mercury.
I'm Increases in our end tidal carb carbon dioxide are potentially from impending rust, but we do need to be careful if we have given adrenaline. Sodium bicarbonate potentially sometimes we get increases because adrenaline affects the coronary perfusion pressure correlation, and so if there's a small increase, I would tread carefully and with caution. And so usually, when we get our return of spontaneous, circulation, we get an overshoot, and that is because of the pool of carbon dioxide that's been suddenly returned to the lungs from the body.
So once we get that return of circulation, all the carbon dioxide that's been sat in those tissues in the whole body now gets dumped in the lungs. So often when we get ross, we get an increased, And tidal carbon dioxide, so we do want to try and monitor that when we're talking about Ross, which we'll talk about. But then again, if we have a decrease, this is associated with poor prognosis.
So this might be from displacement of our tube, so we're gonna check our tube, we might be checking our obstruction of our endotropeal tube. Again, remember we want to cast them, we wanna tie them in. Equipment failure or I would say again, compressor failure or ventilating failure, and then other things as well that might cause a decreased, capnography while we're doing our CPRs and pneumothorax.
So now we come to our ECG, our other monitoring tool that's really helpful, especially when we are changing compressors. To see what's going on with our patients. So we'll just go back to This algorithm, so we can see here that we have evaluate patient check ECG so we have ventricular fibrillation, pulseless Vac or asystole or pulseless electrical activity.
And so in the, in both the ventricular rhythms, we would charge the defibrillator. Home and give a shock as soon as we've noticed that rhythm. So we can, so we would notice Vfib or pulseless VA and start our compressions again until that defibrillators charged and ready to go.
Everybody clears the table, make sure nobody's touching the patient or the table that the patient's on. We shock that patient and we continue to do 2 minutes of compressions. And that's because when we use that defibrillator, we're shocking that heart into having no rhythm.
Basically we're making it go back to asystole so that then when we're compressing it, then hopefully we're either gonna get a rhythm. Or we convert it into asyle which then we can then give our epinephrine or vasopressin. So we'll talk about, our drugs in a minute.
But, so early electrical defibrillation in our patients with ventricular fibrillation, has actually been, associated with increased risk, and survival to discharge, in a lot of studies. And so it's much superior to antiarrhythmic medications that we would give. And as I said, it's the aim is to stop those ventricular myocardial cells from contracting and then then drive them into a simultaneously into a refractory period.
And then hopefully those pacemakers can take over, . So I'm These are our 4 rhythms that we just talked about. So pulseless electrical activity sometimes can look like a normal trace.
And they, but they will be without a pulse and often they're, below a rate of 80 beats per minute. And so along with that and asystole, so Asus is none and no beat, these are gonna be the ones that we're gonna be administering, our, epinephrine or potential vasopressin and maybe our atropine every every 4 minutes. Shockable rhythms are gonna be a pulse is ventricular tachycardia, VA, or ventricular fibrillation.
So these are choices that potentially you're gonna see. Pulse suspension for BTA again is one that is without pulses, . If you don't have a defibrillator in your practise, you may be doing a precordial thump, so it's basically just a a really large and heavy thump on that chest.
And again, we would use that the same as we would, with our defibrillations which restart our 2 minute cycle. So the aim of our drugs and CPR for our advanced life support is gonna be to treat the arrhythmia by modifying the heart rate or the character. It's potentially gonna be to enhance the perfusion to myocardium, and, it's also gonna be potentially to treat the disease caused when the arrest.
So these are the many drugs that are used in CPR. I'm so I'm the most important that are on that algorithm are adrenaline, the epinephrine and vasopressors. And then atropine is mentioned and so is lidocaine, and so atropine is .
Oh Sorry, atropine is, Are parasympathetic, that's used at like 0.04 makes the cake, on every other compression cycle. There's no real clear studies, to show benefits within CPR, but there's also again no evidence of harm of that.
So it's thought to be beneficial for those in asystoy, pulses electrical activity, or those that potentially have experienced high vagal tones, if they've had vomiting, ileus, they have gastrointestinal disease, or if they have respiratory disease as well. I'm As I said, phase depressant adrenaline, these are gonna be the most commonly used in CPR, and we'll talk about those on the next slide. So other things are reversal agents.
As I said, we want to reverse those as quickly as possible, so amazole, slumenazole, naloxone, they're all readily available and reversal agents for our alpha 2 agonists, benzodiapines, and opiates. We may have antiarrhythmic agents, we might use them, but there's not really any evidence to show the use of them, within CPR as a routine use. Amiodarone, if you're lucky enough to have it in your practise, it's very expensive and also has very high, risks associated with it.
And it can be good for patients with ventricular fibrillation that's a refractory to electrical defibrillation. Lidocaine can be administers those patients with, refractory ventricular fibrillation. And again, if we have a patient that we are suspicious that they're about to run into a crash that has ventriculal fibrillation, maybe we, we will be administering, lidocaine.
Other things that you might have are alkalizing agents, so things like our sodium bicarbonate, and that works as a buffer for metabolic acidosis. It's not really recommended, but they can be considered in those with prolonged cardiopulmonary arrest and because we get that severe asidedemia. Again, it has a lot of, Side effects, and risks associated with it, and it can lead to an extreme alkalemia that causes paradoxic cerebral and metabolic acidosis.
So, I'm again, used with caution and the same for like calcium, magnesium as well. Epinephrine is the most commonly used vasopressor during CPR, and it causes, vasoconstriction for its action in alpha 1, beta1 and beta2 receptors, . So beta 1 acts on the heart, beta 2 acts on our lungs, so B2, we just remember 22 lungs, and that acts to redirect blood flow from the periphery of the body to the vital core organs.
There's two doses suggested by recover, there's low dose, which is 0.0 1 mg per kg, and that is associated with a higher rate of survival to discharge, while there's a higher dose, which is 0.1 mg per kg, and that is associated with a higher rate of rust, but actually once you get that rusk.
It predisposes to arrhythmias, and, and actually survival to discharge is much lower, and that's possibly related to, the perfusion in the vital organs because of that severe vasoconstriction. So, I would, Advise, I'm having, been on the recovery course low dose epinephrine is recommended for at least 2020 minutes. So we would dose this every 3 to 5 minutes, so it makes, every other compression cycle an ideal time to do this.
So you can, administer it in the intra route as well, and you just double the dose for the IV and you use a long like urinary catheter, and make sure your drug is diluted 1 to 1 with saline or sterile water. And then you lower that into your airway through the endotracheal tube. Vasopressin, acts on vascular smooth muscles, through V1 receptor, and that again causes vaso constriction.
And that can be used in or in conjunction with epinephrine with the same effects. So again, this isn't, necessarily backed by evidence that vasopressin is better than epinephrine. So we just talked about that adrenaline high doses, so it does actually result in more patient harm.
It doesn't improve hospital discharge rate, 24 hour survival and neurological recovery, and, the recover guidelines strongly advise not to use, high dosing, unless, basically, unless you're kind of giving up. You have a patient back, you've done really well, you've achieved return of spontaneous circulation in this patient. We're now gonna talk about this algorithm and the kind of things that we're gonna look for that we're gonna be monitoring our patients and the things that we are gonna be potentially administering to our patients to help.
With that return of spontaneous circulation and also, with that survival to discharge, which is really hard to achieve. In humans, there's 60 to 70% of those cardiopulmonary arrest victims that achieve Ross and will not survive to discharge. That's quite a high percentage of humans and you think, you know, potentially we're looking at, we'll look into that evidence for us.
In veterinary, only 35 to 45% of those in cardiopulmonary arrest achieve Ross, but only 2 to 10% survived to go home following postc cardiac arrest care. So it's not very many, so again this is another reason why we want to talk to our owners about. And whether they want to go ahead with cardiopulmonary, arrest care, and whether they want to go ahead with CPR with resuscitation.
So this algorithm, again, I think this is another thing that's gonna be changing and coming up, but basically what we wanna achieve with these patients is we wanna kind of be in a Goldilocks situation and we wanna not have too much of something, not have too little, but we wanna just right, we want to keep it within those normal parameters, because these patients are gonna be very sick and they really need a respiratory support, and cardiovascular system support and, neuroprotective therapy. I'm So it's a really intensive process, it's similar to the care of like a septic patient, and that we really must keep an eye on all of these things and keep them balanced, because otherwise it can send those patients very easily back into another cardiopulmonary arrest. And it's really, likely that those patients will re-arrest during that period.
We have a lot of abnormalities that happen in this post resuscitation phase, and that's a combination of anoxic brain injury, post-ischemic, myocardial dysfunction, as well as the systemic response to ischemia and reperfusion. And the persistent precipitating, path, pathology of what's happened, what, you know, the underlying disease process. So we've got a lot of things going on in these patients.
As I said earlier, potentially now have rib fractures that we now have to deal with. We may have pneumothorax. As a result of those rib fractures.
So the care and the clinical abnormalities in these can be really variable and and basically our therapy is gonna be to alleviate those resulting clinical signs. So we really want to achieve early hemodynamic optimisation in these patients. So similar to severe sepsis and septic shock, it has been shown in human CPA survivors that That if we are quick at getting that hemodynamic optimisation that we have good success rates.
So we should consider any animal that has had a cardiac arrest and that they don't have that hemodynamic, optimisation that they're unstable. So central venous oxygen saturation of at least 70%, on normal lactate levels and should be used as global fusion metrics, and end points for our resuscitation. So I'm.
Central, venous pressure, central venous oxygen saturation, with our, you know, with our central lines, are kind of fallen out of favour and again whether this will be changed in the 2020 2022. Guidelines, but they say in this, in the current one that we have up on the screen, that central venous pressure monitoring is also a useful guide because this monitors, When the when we have hemodynamic optimisation, but often these are clunky, they're hard to use, they are, they require a skill level, and this is all something that we can do actually by monitoring our blood pressure, and we can do non-invasive invasive, but non-invasive is perfectly fine. So long as we're aiming for our normal intensive patients, so we're aiming for mean not a blood pressure of.
80 to 120 millimetres mercury, and a systolic arterial pressure of 100 to 200. So, we may aim slightly more because basically we want to get that blood, We want to achieve that that good circulation that's gonna help you know, provide oxygen to those tissues that have been hypoxic return that carbon dioxide, that lactate. And clear those, so we may aim on the higher end of our mean arterial blood pressure and again our systolic arterial pressure.
I'm When we don't achieve, when we have hypertension in our patients, this may be because we are giving presses to our patients, we give them vasopressin or epinephrine as a, CRI, to maintain blood pressure. We may have been given too much and maybe we need to scale that back a little bit. As well as that, we need to consider pain in these patients.
These patients have gone through a cardiopulmonary arrest event, you know, they've had their chest compressed half to 3, there may be rib fractures which are extremely painful for these patients. The underlying pathology of these patients may cause some pain and therefore it may become hypertensive. So we want to make sure that we all have a good multimodal analgesia plan.
In place, and that we're constantly monitoring that blood pressure. And if we continue to be, Hypertensive, maybe we start to consider administering an anti-hypertensive. Conversely, and more likely with these patients we would have hypertension, and this might be because of hyperbulimia, so we would, fluid challenge these patients, and see, if they have a response to these fluids using the blood pressure, heart rate, pulse quality.
Capill full time. All these things are gonna help us to assess whether this patient is hypovolemic and whether they're responsive to the fluid therapy that we're giving. Are they vasodilated, so make sure that they're, you know, that then they don't have a vasodilation potential.
These again, these patients are actually high risk for things like sepsis and septic shock, distributive shock because of the event that they've just gone undergone. And so this might be that we have a decrease in capillary refill time, so very rapid, refill time that these patients have injected brick red mucus membranes, and in which case we might be looking to vasopressors for these, we again might be looking for fluid therapy, we might start looking down, our sepsis, . Goals and, and treatment.
And then we're gonna, if we have decreased con contractility, so, you know, if we have a decreased heart rate, and the patient's not responding in the way that we think it should, maybe we will start thinking about positive onotropes. So, those that are gonna help to the heart to contract, and get that blood pressure up. I'm Again, when we think about fluid therapy, we want to replace light for light.
So if these patients have a drop in PCV if they have a less than 25%. If we know that they lost blood, and that was part of the underlying pathology of these patients, that maybe they had a he abdomen, that we would replace like for like so do blood transfusion, potentially we do, our, fresh frozen plasma transfusions for clotting factors, if we know that that's an issue. So we wanna transfusion, you want to make sure that we have a normal PCV and normal touch solids, that we're not dehydrated, we've not got blood loss.
And that we have lactate clearance. So looking at our lactate, is it less than 2.5 milli per litre.
Often these patients have, they will be spontaneously breathing. But if they aren't, then short-term mechanical ventilation is gonna, assure, it's gonna, make sure that we have optimal arterial oxygen tension. And our CO2 levels are normal as well, so 35 to 40 millimetres mercury.
And it's also gonna help us to prevent, respiratory arrests in the comatose postcardiac arrest patients. So we just wanna make sure these patients are ventilating sufficiently. If we think about these, we don't want them to now get an increase in, carbon dioxide levels because that's gonna cause, vasoconstriction in our brain.
It's gonna cause hypoxia again, may cause our patients to crash. We don't want them to be, have low levels of carbon dioxide, so again, that's gonna have detrimental effects on our brain. Phase ablation is gonna cause a patient to crash again, .
It's not too much, not too little, just right for these patients. Does that mean that we need to give our patients, oxygen as well? Most likely yes, so we think about the ways that we might give oxygen.
So we'll talk about neuroprotection on the next slide, but these patients seemingly sort of have some sort of head trauma, from the pathology, we're not gonna be placing, nasal cannulas because that's gonna increase our intracranial pressure. Maybe putting them in oxygen tents, oxygen cages instead. Or ventilating short term these patients, which we can do all, you know, we don't necessarily need to refer them out if we are going to have them on, short-term ventilation under 24 hours.
So once we get to 24 hours and that patient's been on 100% oxygen, if you don't have a ventilator that has the ability to turn down the, the percentage that the fraction of inspired oxygen, then we start looking at things like oxygen toxicity. I'm We are going to be potentially monitoring, venous or arterial blood gases. So arterial blood gas is gold standard, and, there's, lots of evidence that, looks at the detrimental effects of oxidative injury after ischemia reperfusion, and particularly when reperfusion happens under hypoxic hyperoxic conditions, so.
We want to titrate the oxygen to a non-oxic level. So I'm, I, there's no time to go through it now because it's a whole other bit, but look, if you are interested, look up, the oxygen oxygen haemoglobin disassociation curve, and that talks about the relation of SPO2 to our PAO2 our arterial oxygen. Content.
And so because of that, we want to target an SPO2 of about 94 to 96% because that's gonna, achieve our normal, levels of, partial arterial oxygen of, 80 millimetres of mercury. To 100. Anything more than that we get this hypoxemic condition, and we get this detrimental effect of this oxidative injury.
So we want to make sure that we've not got too much. So when we start seeing 98 to 100, because of the sigmoid shape of the this association curve. Now, anything past 100, we don't actually, 100%, we don't actually know what the partial arterial oxygen is.
So unless you have the ability to do, arterial blood gases, if you're just relying on your SPO2, then paying for 94 to 98%. I'm so we're gonna be supplementing oxygen to these patients, potentially ventilating these patients if they're unable to keep the ETCO2 at a normal level. And we're gonna be monitoring our respiratory effort rates, because another thing that, that is, a side effect or part of our post, arrest patients is that often because of that hypoxic event that that cardio pulmonary arrest, we get a thing called non cardiogenic pulmonary edoema and so because of that, .
And then we now get infiltrates and er fluid starts to fill those alveolis. And Dimazon doesn't, isn't effective in these patients. I'm just oxygenating and potentially be these patients are the most effective.
And so that's why we're going to be monitoring our patients. Again, pulmonary contusions potentially are possible because of that, because of those compression. So monitoring that patient's, respiratory rate and effort potentially doing, .
Focus our point of care ultrasound in these patients as well. And, and finally, part of the algorithm is neuroprotection, and this is really important, so. I'm There's a mild therapeutic hypothermia, .
For 12 to 24 hours after Ross and has been shown to improve neurological outcome in in humans that have cardiopulmonary arrest and also in some, Other species like dogs, when they remain comatose 1 to 2 hours after, resuscitation. So in humans, they pack ice on the patient, they really drop that they actively drop that temperature. It's not necessarily feasible in veterinary patients, there isn't enough evidence to support.
I'm packing them with ice and actively I'm. Making them hypothermic, but often these patients after cardiopulmonary arrest and after cardiopulmonary resuscitation are gonna have some Often I'm mild or I'm, you know, extreme hypothermia. And so, we don't want to rapidly active rewarm these patients because that's gonna be detrimental.
And then hypothermia is a risk of that and also harmful, but what we want to do is kind of monitor that body temperature. And maybe just do passive rewarming and time limit, an increase of 0.5 degrees per hour.
So we kind of have that mild therapeutic hypothermia in those comatose patients that we're rewarming them very, very slowly, and, and we achieve that hypothermia just through doing that. I'm So 32 to 34 degrees for 24 hours, 24 to 48 hours while ventilated. This is what was done in humans.
And so again, not enough evidence and maybe that will change in the 2022 guidelines, to support, doing that in our in our veterinary patients, but whether we just consider. Allowing them to rewarm very slowly so that they have the hypothermia. I'm.
I'm Manitol and hypertonic saline are appropriate if our patients demonstrate neurological signs. So, we can use the modified coma Glasgow the Glasgow and modified coma score, but it does have its limitations with these patients, and that often, we're not able to use some of those boxes. And again, this is something I think that is also being reworked, and potentially will be more applicable to our, cardiopulmonary arrest patients.
Our patients who are, who have gone through our cardiopulmonary resuscitation and achieved Ros should also really be carefully monitored for seizures and treated aggressively if they do have seizures or if they are at risk of seizures, with diazepam, if they occur, so. Putting these patients on seizure watch, making sure that we have all the equipment again ready for these patients, acting like these patients almost have head trauma. So, again, making sure that we are, potentially tilting them at 1520 degrees with their head and neck, up to allow drainage.
We're not gonna use jugular sticks to avoid increased intracranial pressure, . Again, when we're doing physiotherapy, not lead walking, and again, all things that we might consider in these patients. Making sure that we are emptying their bladder of their comatose.
So, general, comatose cares we're gonna use like maybe you use urinary catheters, potential faecal catheters if we have diarrhoea, making sure that we're trying to be as aseptic as possible with these patients when we're dealing with them, to avoid any nosocomial infections and potential sepsis for these patients. Catheter care, urinary catheter care, maybe we would, either be using, total or partial parental nutrition, if they're not able to eat, maybe we'll be placing feeding tubes again, making sure if we have any suspicions of neurological deficits that we're avoiding, like na nasogastric tubes, naso esophageal tubes. I'm, so there's been lots of complications seen with I'm With all I'm With Ross, so Pistatona, so where we have our rigid and front limbs and neck and soft back limbs.
Often these are like neurological signs that we're gonna see, so are neurosis, so often they'll have some degree of blindness, which often resolves within 24 hours, of achieving Ross, but some are, slightly longer, so we have to make sure that we make allowances to these patients if they're comatomes, and making sure that we're lubricating all mucous membranes, you know, mouth, tongues, vulvas, precuses, but also making sure that we are putting our lubrication on eyes. Vestibular cerebral disease as well, so they often get things like head tilts, nystagmus, and seizures is another one as well. So all of these things kind of, pin into that neurological, status.
So in human studies, where they've been performing CPR, . They sometimes talk about having the head elevated and may help help post neurological function and reduces intracranial pressure and increases the cerebral perfusion pressure. So this, I think this is something that is likely to affect the recovery guidelines that come in 2020.
I'm in 2022, sorry, that we might start to look at doing optimal head up CPR, so with the head and thorax elevation. But there's been no, angle that's kind of been, Determined that's been optimal. So just going slightly back to our compressions, if we do have a patient that's has a lot of Endotracheal, fluids, that's coming out, the advice is not to tip those patients over the over the table.
A, because they're gonna stop the, we're gonna interrupt those CPR CPR compressions, and B, we're affecting the airway. And as as I've just talked about, we're gonna change the intracranial pressure, we're gonna decrease that cerebral perfusion pressure. So, using suction, I'm using either syringes with catheters or using active suction to suction away all of that kind of goop and fluids is gonna be the most effective in these patients and maybe that's something that you consider having near or in your crash kits.
I'm Other things that we might have as complications would be shock. So again, as I said, often distributive shock is I'm a major player in these patients, and so we wanna make sure that we're monitoring very closely their heart rate, . Pulse quality, both femoral and metatarsal.
That we're monitoring the capillary refill time, use membranes, blood pressure is really important in these patients and that we're just doing, you know, that we're really getting a feel for these patients and monitor them very closely for any changes that may suggest a deterioration. And often they have drug interactions as well. So, because of that CPR and often, drugs are kind of left in the peripheral circulation and now come back and often we can get overdose.
We potentially, you know, have that buildup of drug that's gonna cause different drug interactions in these patients. So just being cautious of any additional medications that we give to our patients and how they might interact with those I'm already given. And just quickly, I just want to mention that debrief is really important in all our CPR events and, whether that's a hot debrief, so whether you do it there and then, after you've either achieved Ross or your patient, has, died and you're no longer doing CPR.
Or a call debrief, when maybe later, later on after the event, you all get together and you discuss what went wrong, what went right. And so it's really important again, that the leader leads us, that that there's no negative, culture, and that you are creating a culture where people feel like they can, discuss, what went right, what went wrong, what could change next time, and that nobody feels like anybody's being blamed. And this is something that's really, crucial and, For you to work on as a team.
And the more you do it, the more the the better it will become for your team. There are debrief sheets out there that you can use. I think Recover actually have some, and you can create your own.
Whatever works for you, but the, the use of debrief is to maximise, your efforts in the next CPR event. So knowing, what went wrong. So as an example for our practise, we did a CPR event recently and our crash kit, and the area that it was in.
Was not ideal. And from that debrief, we've now changed our crash box, we've changed the area, and we've we've cleared out a lot of the things that is less chaotic, in the hopes that next time when we have a CPR event that we will be able to effectively put in motion our BLS and ALS. Thank you very much for listening.
If you have any questions, you can either email me on my work email, which is the bottom one, Chloe at new priority.com or on my other email, which is Chloefay [email protected].
And again, if you. In the future, done your recover rescuer online and would like to complete that and become an official recover rescuer. And then please do feel free to drop me an email and I can, train your team, to become rescuer certified.