Hello, everyone. Today we're going to talk about cardiopulmonary resuscitation. My name is Gerardo Poli, and I am a certified recover CPR instructor as well as certifier.
And CPR is something that we do numerous times on a weekend, on a busy weekend shift at our hospitals. I work in a busy emergency hospital. In the south side of Brisbane, and we might do CPR sometimes up to a dozen times on a, on a busy Sunday shift.
So, our team has gotten fairly good with CPR and today I'm going to share with you the fundamentals of CPR based on the recover guidelines. So, Going through first, the recover guidelines was a consensus statement that was Basically, the, the, the, the goal was to review human and veterinary literature and to see what evidence was out there to support different practises that were, going on in different hospitals around the world. There were different consensus statements from different journals, so it was good to, their goal was to get one consensus statement based on the available literature and, In the end, what they found was that there was no or very little concrete evidence for any of the recommendations, because it was very difficult to actually perform prospective studies in CPR so, What they did though, is they used, a combination of anatomy, physiology, and extrapolated from human data as well as some veterinary literature, and they brought together and, or at least combined it all into the recovery guidelines, which is what we're going to go through today.
Overall though, the 6, the overall survival rate for patients that have actually undergone CPR is quite low. Unfortunately, only somewhere between 4. To up to 10% depending on, on, on the source.
And it somewhat depends upon the, the nature of the patient when they've arrived. If, if they have multiple injuries, then that also affects the, the prognosis of the patient as well. So if a patient Gets hit by a car, presents, dead on arrival, and it has pulmonary contusions, fractured pelvis, and, obvious kind of internal bleeding, then, then beginning CPR, or if you start CPR on that patient, the likelihood of that patient actually continuing on and surviving is quite slim.
So it is somewhat affected by the presentation of the patient, but overall, the survivor rates are somewhat, maybe 25% to 50% of what happens in actually human hospitals. But where it becomes more important, or most important is patients who are anaesthetized. And the prognosis there is significantly better, 4 times better if not.
And the reason being is because we have a patient that has an airway that is secured, and there is also an IV catheter in place. There are monitoring devices already attached, so entitled CO2, ECG, SPO2, so, and sometimes, in general. Actually, what happens is that the reason why they've actually undergone and, actually resulted in, in cardiopulmonary arrest was because of medications that were administered or potentially, the mistakes that occurred on behalf of the veterinary teams, whether or not the, pop-off valve, closed over, whether or not the ISO, the anaesthetic agent was left too high, or, or possibly there was an overdose of a particular agent.
So, Those things could be addressed and reversed, and those patients then had all the access that was required, intubated, IV catheter placed, and interventions could be started immediately, and generally because of the patients being monitored closely, cardiopulmonary arrest was picked up almost immediately. So, So this is where it's important to understand the fundamentals of the recovery guidelines and implement them because we can have a dramatic impact on those patients. To start off with, though, there was a couple of things that the, the papers went through, and, and the first one was maximising preparedness.
And what they found was things that would actually make things or increase the, the success rate of, of, of CPR on a patient that presents an arrest, was having a crash cart that was actually dedicated towards performing CPR. At our hospital, we have a trolley that, has all the drugs, has the tubes, has a dedicated laryngoscope, dedicated tube set, It has medications such as adrenaline and atropine drawn up already. There is also charts, dose charts and algorithms, and at the crash bench we have a multiparameter that is designated purely for arrest patients, and we have a Captain McGraph and also we have Andy bags and so forth.
So. We have everything that we need for, a patient who presents in cardiopulmonary arrest right there when it, when we need it. So a crash cart.
And also, the contents and the location of the cart is audited. So for us, that's audited every 6 hours. So the contents of the cart is opened and a checklist is all ticked off, and also at the end of an arrest or at the end of resuscitation event.
The, the contents are, are replaced, because we do them so frequently. So one thing to consider in your practise is having a crash cart that is in a specific area where everyone knows where it is, and also the contents are audited at the end of the day, if or after each time a particular arrest event occurs. The problems that they identified were that crash carts, well, the fact that the items within the crash carts were often not used for, were often used for non-CPR events.
So this happens at hospital as well, the laryngoscope that's in the crash carts, some crash cart sometimes goes walkabout. And then we have to walk around our hospital, which is quite large, and track down the laryngoscope. So it's one thing that is a big no no in a hospital, and that's raiding the crash cart for things such as laryngoscopes and, and, and, ET tubes and so forth.
And what we have to do is obviously then, put some checks and balances in place, and that is checking at the end of each shift, and also making sure that the crash cart was restocked at the end of every shift, so every 6 hours. The other thing that they obviously they identified as well was that. Closed loop communication was really important.
So if there is only 2 of you doing CPR, then this still applies. We have potentially up to 10 people on shift, and, and if the arrest event, has, requires it, we can pull on all those 10 people to be there. And this is even more important when this, the, the concept of closed loop communication becomes even more important when you have numerous team members.
So closed loop communication essentially is when you are communicating to someone directly and they are acknowledging and communicating back to you directly. So this is not like, Could you please give adrenaline 3 mLs IV. Someone, could someone just do that, right?
And if you have multiple people there, no one really knows who you're talking to and, and who should do it. So there is a phase or a lag, let's say, before, between when you've initiated the order and when the actual order gets carried out because there's confusion. Solo wood can be canish is directed towards someone.
So it's clear and it's specific to a person, so you could point at, let's say Jenny and go, Jenny, can you give 3 mLs of adrenaline IV? Jenny knows that her job is to give adrenaline and 3 mLs of it IV. So then Jenny, being the receiver, acknowledges and repeats and confirms this.
So I will give 3 mLs of adrenaline IV and as she's done it, she, I have given 3 mLs of adrenaline IV once she's done that. And the reason why it's important that she acknowledges it verbally is because Jenny may have actually heard give 30 mLs of adrenaline IV, right? So, and if she didn't communicate that back to you being the sender, then all of a sudden she couldn't give it a 10 times dose overdose of adrenaline.
So when she acknowledges it, it, it, it tells you that, that she has heard it, and she also confirms that she's heard it correctly, and also when she tells it back to you, she knows, so you know that it's been given. So this saves time and reduces error and improves overall CPR team performance because people know what they're supposed to do and when because they have clear directed communication. One of the most confusing aspects of cardiopulmonary arrest is actually when has it occurred?
And you can see here that the indications of clinical signs of cardio pulmonary arrest are quite simple, loss of consciousness, absence of spontaneous ventilation, so no breathing, absence of heart sounds on auscultation, and absence of palpable pulses. You actually don't need all four of these to start CPR you just need one of them. And, You might be, you might be thinking that oh well what happens if the patient was still has a heartbeat, or what if the patient just lost consciousness, you know, maybe we could cause trauma to that patient if we do CPR and the thing to understand is that, The best thing to do is to start CPR because there are way more benefits associated with increased chances of survival with, with early initiated CPR and this outweighs the actual pros or the potential complications associated with CPR.
And provided that the CPR is done in an appropriate manner, the risks are actually quite low. If the patient was sleeping and you're starting CPR you'll soon know because the patient will wake up and tell you stop doing CPR. One thing to note is the absence of palpable pulses.
Is actually not, it, it can be actually quite a difficult clinical sign to identify, because 35% of rescue is actually documented a pulse when there was no pulse present. So this is one that I actually don't really like, essentially, if I can't hear a heart sounds and the patient's lost consciousness, we start CPR until proven otherwise. So, and I give out, I give our team 10 seconds to decide.
I give myself 10 seconds as well. So 123 is, is, is, is Bobby waking up, Bobby's not waking up. OK, 456, gonna hear heart and no, OK, start CPR.
So within 10 seconds you start CPR. And the most important thing to begin with is chest compressions. And the sad thing is somewhat, is that even with our best chest compressions, we're only getting somewhere between 25 to 30% of the cardiac output that the heart generates on its own.
And this is dependent on great technique. So, A fair chunk of this, discussion today would be about chest compressions and the technique there. It's all, awesome and cool to give adrenaline IV and defibrillate a patient, but if you don't focus on basic life support and actually focus on amazing chest compressions, there's no use in defibrillating a patient or imagery an IV, adrenaline or something if you're actually not achieving any cardiac output.
So, recapping when to start, you start immediately, there's a low risk of injury and there's a benefit of early chest compressions and they outweighs the risk of injury. And one thing to understand is it can take 60 seconds to reach maximum coronary perfusion pressure. So coronary perfusion is the perfusion pressure or the coronary perfusion is actually the, Amount of blood flow to the heart itself.
It's one of the key things with CPR is actually trying to deliver oxygen to the heart, not just to the brain, but actually to the heart. So if we look at this, diagram here, so chest compressions during the cardiac arrest and the magnitude of the of fusion resulting from chest compressions. So what we have here is this is our best possible perfusion pressure, OK?
So this is our 25 to 30%, normally it would be up here, normal coronary perfusion pressure. Then what this graph graph shows is that it can take up to 60 seconds for, The pressures to build to its best possible pressures, and then all of a sudden if you stop, there's a dramatic drop, and where there's no profusion, and then you've got to start again, and it takes 60 seconds. So the, the critical point here to understand is that, It takes 60 seconds, which means that if you are doing chest compressions and you decide halfway through a minute, look, I want to just listen and have a little listen and see potentially the patients come back and you stop and then get your stethoscope out and put your stethoscope under the chest to listen, you actually just lost all the pressure you generated.
So, this is the reason why the two-minute, cycle comes into play. So, when it comes to chest compressions, We want 100 to 120 compressions per minute, that's. 2 compressions a second.
There've been numerous recommendations, from in different consensus statements, and they range from 80 to 180 compressions per minute. And the best thing to do is to actually, download a CPR app and have that nearby the crash bench because it's surprising what, or how much variation there can be. Even if you try to sing a song in your head like, ah, ah, Staying Alive, you can actually sing that pretty quick, staying alive, and that's 180, or you can do it really slow, staying alive.
So, and that could be 80. So it's really important to actually get a metronome or something like that and use it to time your compressions. We want a third to half the depth of the chest, and this is a pretty deep compression, it's not just pushing and maybe potentially compressing the, the, the chest, we want deep chest compressions, and we want full recoil.
Full recoil is so important. You don't want to lean on the patient because that inter interferes with the actual blood flow returning to the heart. So you must allow the chest to actually recoil completely, that allows venous return to return to the heart, and then compress it down deep.
There's two, pump models. There's the cardiac pump model and thoracic pump model. The cardiac pump model is when we actually compress the chest over the heart and actually mimic the the action of the heart itself by compressing the ventricles.
That results in blood squeezing out of the ventricles out to the great vessels the aorta and so forth. The thoracic pump. Model, which is primarily utilised for larger breed dogs, is, is, or dogs where you actually can't compress over the chest itself.
This is where we actually use pressures in the chest to actually, create forward flow. So when we compress the chest cavity, we, we, we aim at the widest part of the chest. What happens is we're increasing intrathoracic pressure, that then actually collapses the cord of in the calf and the the aorta and somewhat the heart itself.
This then creates forward flow, and then when we allow recoil, the negative interthoracic pressure due to elastic recoil then sucks blood back in. So thoracic pump model is when we actually generate pressures in the chest cavity and cardiac pump model is when we actually gen compress the heart itself. And 2 minute cycles were out without interruption, so going back to that graph I showed before, so there is, it takes 60 seconds to actually reach the maximum coronary perfusion that you're possibly going to generate.
If we stop anywhere before that 60 seconds, 30 seconds, 45 seconds, even at 60 seconds, You can see now that actually what happens is we're probably not even generating any forward flow to the heart itself. So when we do a 2-minute cycle, it takes us a minute to get maximum confusion pressure, and then what happens is we have a minute of forward flow hopefully into the heart. So we have a minute of coronary perfusion.
And bearing in mind that it's only 25 to 30% of potentially what the heart does itself, provided that you actually do compress properly. So if you're not doing chest compressions properly and you're interrupting the flow and not doing 2 minutes, you might actually not even generate any, coronary perfusion at all. So you may as well not even do anything.
The other thing is that they recommended rotate compressors every 2 minutes, and the reason being here is that you might be able to do chest compressions for 10 minutes on a small dog, like a little caddy or something like that. But what happens is you lose concentration after 2 minutes, you might actually start to lean on the patient. When you lean on the patient, you have persistent intrathoracic pressure, positive intrathoracic pressure, and that then opposes venous return back to the heart.
The other thing is that When you do swap out every 2 minutes, it allows you to reassess the patient. I'm gonna show you a video, and, what I'll do after is go back through and then recap some, some major points and then we'll move on. But this is a video of us doing CPR and there's a couple of things we've done well and a couple of things we didn't, didn't, didn't do so well, and I'll demonstrate and we'll talk through those.
A big thing that's. Yeah. Yeah.
It's good. Yeah So going back to the start, there's a couple of things here. One is I was standing on the wrong side of the dock.
So I was standing on this side of the dog, and the reason why this is the wrong side of the dog is because, When I'm compressing, I'm essentially pushing the dog off the table. That means that one of the other nurses, one of your team members then has to stand there and then hold the dog. So essentially now you need two people to compress as opposed to 1.
The second thing is I wasn't able to actually perform proper CPR technique. I was, I had bent elbows and I wasn't, I didn't have enough height to generate effective CPR or to deliver effective chest compressions. So, what happened was that I then tapped out, but when I did tap out, one good thing we did is that this nurse here came through and continued chest compressions.
While I got up, walked around, then stood on a stool, which then gave me elevation to be able to do proper chest compressions. And then when I was up higher, I, I was compressing and the patient was then coming into my thighs, which means then that we didn't have to have another person holding the patient on the table. And then what you'll also notice is that these limbs here are then available for people to place IV catheters.
So it's very difficult to place an IV catheter for this particular patient because I'm standing right next to the patient and it'd be difficult for this nurse or even one of these nurses or vets to come through and place an IV catheter. So let's watch this again. Yeah It's like a big thing.
So. Oh. It's really good.
Yes So you can see there that I walked around, changed compressions, I was able to deliver deeper compressions because of the angle that I was standing, and also there was no interruption of of basic life support or chest compressions. So technique, straight arms locked. So have your arms straight and locked at the elbows, then pivot at the hip.
So it's not an actual compression power doesn't come from bending your arms. If you do that, you'll gas your try out and you won't last 2 minutes. Use a step to gain height.
Stand at the patient's back, so stand with the patient's back against your legs, interlock your fingers to focus the pressure on where you want it to be, to be delivered. So that if you're doing a cardiac pump model, then you would focus all your compression power over the actual heart itself. Otherwise, you would, if you're doing employing the thoracic pump model, then you would then deliver the chest compressions at the widest part.
One thing that's really helpful is actually grabbing a handful of skin. To stop you from sliding from sliding off. And I've been doing this for years, and I've never actually resulted, it's never resulted in, in hair being pulled out or severe bruising or subcutaneous emphysema.
It is really helpful and you can grab a handful of the patient's skin, and then that stabilises where your hand is on the chest. Otherwise, your hand will roll off and you'll continuously been trying to actually readjust where your hands are. So which pump model do we use for which, for which, which patients for large breed dogs, the thoracic pump model is over the widest part of the chest.
So we can see here, this is the heart. What we're doing is actually delivering over the widest part of the chest, straight arms, interlocked fingers. So this could be kind of mastiffs or even large Labradors, anything with a sort of a rounder, a round sort of body, but greater than kind of 25 30 kg.
For, for keel-chested dogs, we use, the cardiac pump model. So this could be greyhounds, it could be whippets, it could be great Danes, who have a real kind of keel chest. It could also be, Dobermans, some Dalmatians, Waimmoanas, etc.
So, so here, because of the fact that the heart of the chest comes down to a keel, we can compress directly over the chest, and it doesn't matter the size of the dog, it's all about the confirmation of the chest. In terms of barrel-chested dogs, so these ones actually surprisingly, feel weird doing chest compressions on, but actually, it's quite helpful because generally, these guys are sort of wider across the chest than they are deep. So, we do chest compressions like they do in humans, because our chest conformation is somewhat similar to these dogs.
And we compress over the sternum and, yeah, delivered direct compressions downwards. And generally what happens as well, these guys have skin rolls, that kind of form a saddle which helps keep them back on their, on their back. It is quite difficult to intubate these patients, you might need to intubate lateral and then roll them.
For small dogs and cats, then you can do cardiac pump model and you circumferentially place your hands around the chest and you can press down, you'll gas out your thumbs, in a couple of minutes. So it's the reason why you need to actually swap out, or maybe even swap hands, but generally swapping out is really useful. And otherwise, provided that the patient is big enough, then you can employ just standard chest compressions.
So the most important thing here is to remember that you want half to 1/3 to half the depth of the chest. So even in these small patients, if you focus on that depth range, you're not going to result in any significant trauma. If you do, and, and, and this has happened with me numerous times, if you are delivering chest compressions and you break ribs, then I always consider what is, I suppose, the outcome we're trying to achieve here, and that is bringing the patient back to life, because, if we don't deliver chest compressions and they have fractured ribs and so forth, then the patient almost certainly would be dead.
So, chest compressions, with fractured ribs is better than no chest compressions at all. Going on to ventilation. So there's two types.
There's non-intubated, so mouth to snout. What happens is you, close the dog's mouth or cat's mouth stuck, stick their tongue back in the mouth, close the mouth, then create a seal with the lips with your hands, and then put your mouth over the whole entire nose, create a seal over the nose with your mouth, and then deliver. And this is 30 chest compressions and then 2 breaths.
And then 30 chest compressions. So this is interposed. And then you have intubated, and this is the one I would definitely recommend.
Having done mouth the snout, it's not that exciting, nor is it quite nice on your mouth. But intubated is learn to intubate as soon as possible. Intubating lateral, learning to to intubate and lateral is useful.
Otherwise in the intercycle pores, roll the patient tube, and then put them back down. On lateral and simultaneous ventilation compressions. So, the patient, the, the, the person who was the ventilator actually delivers a breath, simultaneously as someone else is compressing.
And whether or not you time the, the breaths and the ventilations at the same time doesn't matter. But either way, you just, one person focuses on ventilation, the other person focuses on compressions. And the technique is, we want 10 breaths per minute.
So that's actually not very much. So I remember when before the recovery guidelines came out, I used to squeeze that Andy bag, like as if there was no tomorrow and try to get as much oxygen in there as much as possible. But when we think of 10 breaths per minute, it's 1 breath every 6 seconds.
So, breath, 1. 23456, OK? That ventilator person.
Unfortunately, he has a very boring job, but. The most important thing is count to 6. OK?
You don't have to do that for 10 to 20 minutes. So count to count to 6, deliver a breath. Count to 6, deliver a breath.
Tidal volume is 10 mL per kilo. So this is not squeezing the whole entire anti bag's worth of volume of air into the dog's chest. This can cause significant trauma if you don't have, a pressure valve or a release valve in your amy bag.
So, 10 mL per kilo, I guess, for a 5 kg dog is a 50 mil syringe. So if your em bag is huge, like a 2 million A bag, you could potentially be significantly overinflating small dog's lungs. So you gotta consider how much actual volume we deliver.
A 50 kg dog is 0.5 litre of air. So it's a quarter of a 2 litre am your bag.
So bear that in mind, 100% oxygen and 1 2nd inspiratory time. So that's deliver a breath for 1 2nd and then release. So it's not squeeze the bag, squeeze the bag, get the air in and let go 3 seconds of inspiratory time.
And the issue is that if we don't, if if our inspirator time is, is longer than 1 2nd, then potentially we have persistent positive intrathoracic pressure, which then impedes venous return to the heart, which then results in reduced cardiac output. So, 10 breaths per minute, 10 mL per kilo tile volume, 1 2nd period of time, this reduces the, excessive intrathoracic pressure and also reduces hyperventilation. Hyperventilation can actually cause, so this is when we breathe off too much CO2, that causes a reflex, vasoconstriction of the cerebral blood vessels, which reduces cerebral blood flow, which then negates the effort that we're trying to do, which, with, with CPR, which is trying to get oxygen to the brain.
Also, what happens is, One of our monitoring devices entitled CO2 is dependent on our standardised ventilation. If we're breathing off too much CO2, then we actually can't measure our, our CO2, which then is really important and I'll cover cover later what that why we do that. But just recapping, unresponsive apnea patient begin CPI immediately.
This is chest compressions, 100 to 10,020 compressions per minute. A third to half the depth of the chest in lateral recumbency, generally, unless they're a, a barrel-chested dog and then you do them on their back. Ventilation, so if you're doing mouth to snout, then 30 chest compressions and 2 breaths and have them interpose, so 30, and then then interpose them to 2, and then back to 30.
If they're intubated, 10 breaths a minute and simultaneously at the same time as as chest compressions. So this is basic life support. Basic life support must continue in the background continuously.
Before we even consider moving on to advanced life support. We don't even care about the ECG or an IV catheter unless we're able consistently to do this because it doesn't matter what we do here, we're not doing this, it doesn't matter, we're not gonna get that patient back. So, moving on to advanced life support, this is where we actually initiate monitoring, so it's actually not placed an IV catheter first, it's actually start monitoring, then place an IV catheter administer reversals.
So, ECG is our first monitoring device, and we should never use it as a tool for diagnosing CPR or sorry cardiac pulmonary arrest. And the reason why we, we, we don't want to use it to diagnose is because it can actually have pulseless rhythms. So pulseless electrical activity, but also, ventricular tachycardia and ventricular fibrillation, which don't regenerate pulses.
So we can't use it to diagnose because we actually may have a rhythm there. But it is our first monitoring device because it helps us identify whether or not a patient has a shockable or non-shockable rhythm. Not every patient requires adrenaline.
Or vasopressin or atropine. OK. Some, it actually can be contraindicated and and.
And it could actually make patients who have a shockable rhythm more difficult to actually convert. So If a shock or rhythm is present, then defibrillation is required. If a non-shock or rhythm is present, then adrenaline or vasopressin, plus plus plus minus atropine is required.
So looking at the algorithm here, so we have basic life support occurring in the background, we're coming down to advanced life support, we've placed our ECG and once we place our ECG, wham bam, go across and evaluate the ECG. We have ventricular tachycardia or pulseless ventricular tachyrrhythmia, then it's defibrillation. If we don't have a defibrillator, we do a preardial thumb.
Then 10 minutes later, we considered other things. Otherwise, if we have asystole or pulses electrical activity, and asystole being the most common rhythm or absence of rhythm that we see, then, then we, sorry, then what is indicated is low dose adrenaline or plus minus vasopressin, every other cycle, plus minus atropine. So If we give these drugs to a patient which has this rhythm, it actually could make it more difficult for us to stabilise that patient and convert that rhythm.
So we consider if the patient's shockable, if it's shockable, then we defibrilllate, if it's non-shockable, then we use low dose adrenaline and atropine. When do we evaluate the ECG? We only evaluate the ECG during the inter-cycle pause, and I'll show you a video soon.
And the reason being is because it actually creates artefacts which could be interpreted as a rhythm. And when we do evaluate the rhythm during the inter-cycle pause, we only want to do it for a short period of time, and if we can't determine what it is, still, we go straight back into chest compressions. Basic life support needs to occur continuously in the background, and anything above that, advanced life support's a bonus, right?
So, 2 minute cycle, we have 8 seconds in between the cycles to evaluate the rhythm, and if we're not too sure, we still go straight back in and then we start chest compressions. If we think it's a shockable rhythm, we still go back in and and, and start chest compressions while we charge a defibrillator. If the pace has just been defibrillated.
Then we actually don't evaluate the actual rhythm. We perform a full two-minute cycle of chest compressions before assessment. And this is because we may convert an arrhythmia back to a sinus rhythm, but the heart is in a hypoxic state, and it may not actually, you know, sorry, often that rhythm, the normal rhythm may not be sustained and may reconvert back to a malignant rhythm.
Because the heart is in a hypoxic hypoxic state. So when we deliver chest compressions for another 2 minutes after, we are assisting the heart in actually getting oxygen to the tissue, to the heart itself. So hopefully, then it is able to maintain its own rhythm, because we've addressed the cardiac hypoxemia or hypoxia.
So this is a video of ECG during chest compressions. So what we can see there is, it looks like as if it's a rhythm, and it looks like as if it's a shockable rhythm, wide, bizarre, fast. OK, so you could misinterpret that as actually a shockable rhythm.
So we don't even evaluate the ECG during chest compressions. Only during the inter-cycle pauses. Entitled CO2 is the second monitoring device, and the reason being is because it can indicate early return of spontaneous circulation.
So if the CO2, during chest compression sits around about 10 to 15 to 20, and all of a sudden it starts going 30, 40, 50, right, the only thing that's actually going to cause that is, Return of spontaneous circulation. The heart taking over and generating cardiac output itself. The other thing is, we can use it to monitor the efficacy of our CPR efforts, of our chest compressions.
We want to aim for 15 millimetres of mercury. So, why is CO2 useful? Well, CO2 increases with higher cardiac output and higher coronary perfusion pressures and are associated with fraternal spontaneous circulation, but it does require standardised ventilation rates and depth.
So we're blowing off too much CO2 because we're breathing. At a respiratory rate of 60 breaths per minute, so breath, breath, breath, breath, and off all that CO2, we can't actually measure or, or, or interpret the CO2. So when the heart starts to take over, producing cardiac output, what happens is we're getting much more venous return.
We're getting all that CO2 that's in the tissues and in the venous blood supply, and that's going to the right side of the heart. The heart, right side of the heart is pumping into the lungs, and then we are ventilating it out. So that's the reason why we can use CO2, because if we generate enough forward flow, then we should ideally be able to get CO2.
Around about 15 millimetres of mercury in the, breath out. So we monitor the CO2, in the breath out, and the entire CO2. Better.
Yeah, you going out to. OK. You could see there that the title suture was 9, and then the feedback we gave was pump better, and then the compressor, Tara, then adjusted her compressions and then you could see it went from 9 to 12 to 15.
So, real time, you can make adjustments to your CPR technique and then actually result in increased cardiac output. It's not the, the tallest, strongest person. That generates the best chest, that, that generates the best cardiac output.
Sometimes it could be the smallest person who's actually doing proper technique that results in the best, cardiac output. So, I followed after and I was only able to generate around about 10, CO2, and Tara jumped back in after my cycle and got 15 again. So, there was definite technique differences which resulted in increased CO2 from Tara from, from the chest compressions that Tara was delivering than to the chest compressions that I was delivering.
Other monitoring devices, I'm just gonna cap this at really the auscultation and and auscultation of heart sounds and palpation of peripheral pulses. And the reason being is, no other kind of monitoring device is actually useful. SPO2 is not useful.
Placing an ultrasound Doppler probe on the eye is not generally useful either. And then the reason being is that when you are doing chest compressions, you'll create movement and the, Doppler probe will pick that up and then result in sounds, so it's not accurate. So, but even during CPR, Having someone auscultating your chest while doing chest compressions is actually really difficult.
And palpation pulses, look, if you had a spare person to do that, they're great, but I wouldn't prioritise a person to palpate pulses. I would look at the CO2 to actually give us a better indication of cardiac output. And when do we check for pulses and heart rate, and, and, and listening to the heart only during the inter-cycle pauses, and we only give ourselves 8 seconds.
One, 2345678, and bam, straight back into the chest compressions. If we can't tell, then chest compressions. If we could tell, then we probably should be able to notice.
Effective, I suppose, cardiac output that's generated by the heart within 8 seconds. So, if in doubt, start again. So just recapping what we have here, we have an unresponsive apne patient, either that or that, begin chest compressions immediately and or continue, oh sorry.
Commence basic life support immediately and starting with chest compressions at 100 to 120 compressions per minute, at a depth of a third to half the depth of the chest, in lateral recumbency, unless the patient's a barrel-chested dog. Then the next thing is to intubate the patient, deliver 11, sorry, 10 breaths per minute, and simultaneously as someone is compressing, then this continues reliably in the background, and then if you have a spare person, then we Go straight into advanced life support. So we attach the entitled, the, we attach the ECG.
Next thing we do is attach the entitled CO2, then that person may move on to actually placing the IV catheter and administering reversals. I'm not going to cover reversals because we won't, be able to fit it in the time frame, but essentially, if you're given a drug that you can reverse, reverse the drug. OK.
And the most common ones are, Opiates that have been given or Alpha 2 agonists. So reverse them if you can. Then what happens is once we place the ECG we evaluate the ECG for a, Shockable rhythm or a non-shockable rhythm, if a shockable rhythm is present then defibrillation or precordial thumb, if we don't have a defibrillator.
Otherwise if it's a shockable rhythm, we have low dose adrenaline or atropine, and we'll go into that now. So, Drugs. I'm not going to cover two drugs, because the other one, and I'll explain the reason why I'm not going to cover the other ones, but adrenaline is the main one that comes to people's minds.
And when I ask people, why do we give adrenaline, the most common answer we get is because we want to increase the heart rate, which is a positive isotropic effect, and Increase, sorry, increase the heart rate which is the positive chronotropic effect, and increase the strength of contraction which is a positive ionotropic effect, but this actually results in increased myocardial oxygen demand, where it's like a horse that's running as fast as it can, And then you're trying to whip a horse faster, and it doesn't run any faster and it just collapses and dies. OK? If you have a heart that's only just holding on because it's, it's on the, in the cusps of running out of oxygen, then we give it adrenaline, and then we make it beat harder and faster, it's going to conk out quicker.
So, The main reason why we use it is for its alpha 2 adrenergic activity, which is the peripheral arteriola vasoconstriction. So, What does that mean and why? So when the, the blood vessels in the body are in a constant state of tone, and when you, when you go into a rest, the blood vessels dilate and there's literally not enough blood within the body to actually fill those dilated blood vessels.
So, we can start chest compressions, OK, and we can start generating cardiac output, but what definitely helps out is actually having something to compress against. So when we give adrenaline or vasopressin, what happens is we then cause vasoconstriction, those peripheral blood vessels, that then shunts the blood centrally, so we have more blood supply coming back to the heart, which we can then, which would then go to the core organs like the heart and the brain. But blood pressure is a function of cardiac output and systemic vascular resistance.
So our cardiac output is generated by chest compressions, but we need systemic vascular resistance, i.e., vasoconstrictional blood vessels to actually result in any blood pressure.
So this is where adrenaline and vasopression come into play. And there are 2 doses, there is the low dose and the high dose, and the low dose has been associated with both, OK, so the high dose actually has been associated with higher rates of return of spontaneous circulation, but overall, hasn't resulted in actually increase in the number of patients that survived discharge. And the potential reason being is that maybe it results in malignant arrhythmia is more likely, and results in increased consumption of oxygen in the actual heart itself.
When you do get a return of a normal heartbeat, it actually could then run out of oxygen quicker because it's got so much, betagenergic drive there generally consuming all the oxygen. So the recommendation is low dose, which is a 0.01 milligrammes per kilogramme, IV.
Every other cycle or every 4 minutes. You do pull out the high dose, and this is after 10 minutes. After you've been going along for 10 minutes and you haven't actually resulted in a return of spontaneous circulation, then literally at that stage you gotta try anything, and then you can use the high dose.
And again, every other cycle. The drug that I didn't cover was vasopressin. And it's a non-adrenergic vasopressor, and it works in an acidotic, environment, which is generally every patient that's actually gone on arrest, and it works in a hypoxic environment, which is also any patient that's undergone arrest.
But the reason why I haven't really covered it is because, one, it's expensive, and 2, it actually hasn't been proven to actually be more beneficial than adrenaline. Adrenaline is available everywhere, and, it's relatively cheap as well. So, my recommendation, based on the fact that, it hasn't been proven to be any, any better, I would just stick with adrenaline.
The next drug that is generally used is atropine and say parasymptolytic and indicated in patients which have asystole or pulseless electrical activity, PEA pulseless electrical activity, or conditions of high vagal tone. And, Conditions of high vagal tone. Include patients with high high intracranial pressure, high ocular pain, or ocular disease, respiratory conditions or respiratory disease and gastrointestinal disease, so potentially any patient that actually has resulted, In actually going into cardiopulmonary arrest, could have had high vagal tone before the patient but, you know, arrested, so, It has been proven to be, to be of no real benefit, but also at the same time, to have, no real detriment.
So we administer it at the same time as we do adrenaline. So, place the ECG and then we evaluate the ECG during the inter-cycle pause at the end of the two-minute cycle, and if there's a flat line or pulse electroactivity, then what happens then is we administer atropine and adrenaline. At the same time, so you don't have to deliver one in one cycle and the other in the next cycle, we just deliver at the same time.
The dose rate is 0.04 milligrammes per kilogramme every other cycle, or because there's such a long, Long half-life, with atropine, you can just deliver it once. To keep things simple, in our hospital, we deliver atropine at 1 mL per 10 kg, which is around about 0.07 milligrammes per kilogramme.
And that's because we dilute down our adrenaline, our, the small 1 mL of adrenaline diluted down in 10 mLs, and then we use 1 mL per 10 kg of the diluted down adrenaline. And 1 mL per 10 kg of atropine. So basically what happens, it's like 1 mil per 10 kg, adrenaline 1 mil per 1 kg of atropine, IV every other cycle keeps it simple, no math involved.
With regards to shockable non-shockable rhythms, the non-chockable rhythms are asystole, so. That's an absence of a rhythm, pulseless select activity, and struggle ones are ventricular tachycardia, pulseless ventricular tachycardia, and ventricular fibrillation. So asystole is essentially the absence of a rhythm, so it's flat line, this is the most common rhythm in dogs.
Pulses electroactivity is difficult because on ECG it can look completely normal. But there is little or no contraction. So, you can listen to the heart and not hear anything.
You can put an ultrasound on the heart and see it actually just twitch. But it can have a completely normal looking ECG. So the electrical conduction pathways are still firing normally, but the actual muscles aren't actually contracting.
So you'll have lack of heart sounds or lack of palpable pulses, and generally this rhythm is normal or slower than normal. Pulseless ventricular tachycardia. So this is organised electrical activity where the QRS complexes are wide and bizarre.
And it's, you can have ventricular tachycardias which actually result in cardiac output, but this is pulseless ventricular tachycardia. So, essentially, you can't hear the heart sounds, or you may hear heart sounds, but actually it may, the heart sounds may actually not result in any effective cardiac output when you might not even get any pulse, Femoral pulses or any pulse pressure. So pulseless, ventricular tachycardia, and then we have ventricular fibrillation, and ventricular fibrillation is just a squiggly line that goes all over the place with rhythm, with if you've got an ECG or you'll buzz to 180 to 200 to 300 and something, then back to 200 and so forth, so fire all over the place.
Ventricular fibrillation is a rare cause of cardiopulmonary arrest. It's common enough in humans. That's why there are defibrillators everywhere in every gym next to every pool, and so forth.
So, defibrillators are, are commonly used in humans, but not very commonly used in, in, in veterinary patients because of the fact that actually these, these shock rhythms are not very common. These algorithms are common though, or more common in larger dogs. And the reason being is, the larger the patient, the more likely or the, the, the higher the risk they have of actually developing and, maintaining a malignant rhythm because the heart is larger.
So, Great Danes and so forth can, can have ventricular tachyrrhythmias because their heart is big enough to start to actually result in the re-entry rhythms and so forth. So, of the patients that come through the door, chockable rhythms are more likely in your larger patients or boxes and things like that. So, a general rule, which is quite helpful, and we use this in our hospital, and that is the shockable rhythms such as ventricular fibrillation or pulseless ventricular tachycardia, have rapid rates.
So you can have a ventricular tachycardia, which is less than 180, but still generating cardiac output. But once it gets above 200 or so, it actually starts to then, have compromised cardiac output. So, if the rate's greater than 200, then, and The the rhythm is wide and bizarre, then defibrillation is the definitive treatment.
So shock or rhythms are rapid rates with wide bizarre and squeakly looking lines. If no defibrillator, then precordial thumb. And then after 10 minutes, then antiarrhythmic drugs.
So antiarrhythmics, amiodarone and Lidocaine are generally not indicated, If a defibrillator is, if you have a defibrillator in your hospital, because it actually could make them resistant to the effects of the, the defibrillator, and, also because most anti rhythmics actually result in, some kind of depressant effect on the heart and the heart is in a compromised state, and if we can convert the rhythm back to normal with a defibrillator without affecting the actual heart activity itself with anti-rhythmics, then that is better, that is more ideal. So defibrillation, biphasic defibrillators, the most common defibrillators out now, even probably the last decade, they're probably all biphasic. And that means that the current, when you press the paddles, the current goes from both paddles to each other.
So you, so the current goes, from one paddle to the other, but at the same time. Where monophasic actually is when it goes from one paddle to the other only. So it doesn't actually return the, the electrical current.
And by phasic, you generally need somewhere between 2 to 4 joules per kilo, but if you have a monophasic then you would double that, 4 to 8. No stack shocks, means, so in, in, in, Movies and TV shows in the past, you've probably seen arrest events or CPR being delivered on to patients or to humans. And they charge the defibrillator, they charge it, charge it, and then it's ready, clear, shock, and then they will look at the actual ECG and it's still bad.
Well, generally on, on, on those video, on, on those TV shows, it's a flat line, which is not a shockable rhythm, right? But anyway, if it was still a, a ventricular fibrillation or, or ventricular tachycardia, then they would charge it again, and then they would increase the dose by 50%, and they would clear shock and then re-evaluate, so they used to do 3 stack shocks. Essentially they've proven that that actually doesn't result in any increased, chances of survival or successful outcomes.
So no stack shocks. Deliver your chest, your, your defibrillation, and then commence 2 minute cycle immediately before before assessment. So deliver 2 minute cycle, wait for the next inter-cycle pause, and then assess.
So only assess you in the inter-cycle pause and have one person directing the actual defibrillation attempt. And essentially it's charge, clear. Fire away to discharge and then straight back into compressions.
All right, wait, wait, don't touch it. OK. So Charge, and then you hear the defibrillator, charge up and then it generally creates some kind of alarm, like, and then indicates that the charge is ready to deliver.
And then clear, so let go of the patient apart from the person who's actually holding the defibrillator paddles and then discharged and straight back into compressions. What you can see in the video here is, right, wait, wait, don't touch no middle table. Oh yeah.
So what I highlighted there was actually the dog's legs, but actually what you can see there is these little straps here, and that was actually sandbags, X-ray sandbags holding the patient down. If you don't have something like that, what happens is the dog will jump, literally, and, and then, maybe pull the ET tube out if he didn't tie it in, or, make a big mess, and then you've got to reattach it to all the leads and so forth. So it's good to hold the patient down.
What we have here is defibrillator, sticky pads. And they're quite useful, but in a big hairy dog like this, you actually have to clip the dog, then stick it on, then it falls off and so forth. So, I would, if in the, I would probably not recommend get getting these, I would recommend just using paddles, and you can have paddles where you have the standard paddles like in humans, where they, they look like handles, and then you have to rotate the dog onto their back, and then, put the paddles on either side of the chest, hold the, hold the dog still, and then deliver the, the, the discharge or the charge.
And then let the patient go back and lateral, then do, do chest compressions. But what you can also get, depending on your brand of defibrillator, you can get spatulas. So you have a spatula paddle, which goes underneath, and then you have the handle paddle which goes over the top, and then essentially you slide the paddle under, one on top, zap, and then straight back in.
So if you get, if you are able to get one of those ones, they are much better. Precordial thump is striking the patient with the heel of your hand directly over the heart, and the goal is to actually mechanically shock the, the, the heart back into refractory period and then hopefully the first, myocytes which come back into, to reach threshold potential are the SA node, and the way they actually, Found this out was they actually had a human, patient in the back of an ambulance who had a, a malignant arrhythmia, and they were driving through in the, the car park, in the hospital car park, screaming along. The ambulance goes over a speed bump.
The, the patient at the back and everything else goes up in the air, wham bam hits back down again. And the patient's rhythm converted. And hence, then they were like, what the hell happened?
And they then figured out that if you delivered a strong enough, mechanical kind of, interruption or a strong enough mechanical blow to the heart it could interrupt the, the rhythm and potentially convert the rhythm. But it actually has minimal efficacy compared to defibrillation. So if you have a defibrillator, then do that.
The most important thing if you're going to do a pre a precordial thump is to warn your team, and the reason being is that, It can appear quite shocking and quite aggressive if you start striking the patient with the heel of your hand. And I've personally done this. A nurse, the, it was a new nurse who, who came to the hospital, and, he was doing a pericardiocentesis.
The heart scraped the catheter tip, went into malignant ventricular ventricular fibrillation. I could actually ultrasound, you can see the heart spasming. And the patient went from pink to pale and lost consciousness.
We did CPR and every time we did CPR, the patient actually started to wake up. But we, the rhythm was, a ventricular fibrillation. We didn't have a defibrillator at that stage, so then I pre I proceeded to perform a precordial thump.
And then I did numerous, numerous, precordial thumps over this, over the, the resuscitation, event. And the result, the result was the nurse actually screaming at me to say, stop hitting the dog. So, Inform the team that you're gonna do that before you look like a crazy maniac, essentially that's the, the, the tip there.
In terms of anti rhythmics, only after 10 minutes of CPR. So only after 1010 minutes of CPR do we then consider using anti rhythmics, and that's Liocaine or amiodarone. And it's really important to have, algorithms and dose charts and you can get them off the web.
If you go to recover. Recover at www.recover initiative.org, you can actually download the papers and you can purchase, Yeah Algorithms and also dose charts which make things really useful and helpful and easy because the last thing you want to do during an arrest, a a CPR.
The event is to start thinking about math. But The crux of anti-rhythmics is only after 10 minutes, and it goes, if it's a cho rhythm, defibrillation, if not precordial thump, straight back into chest compressions, precordial thumb, straight back to chest compressions, if not, then amiodarone and Big McCain. The final thing we're gonna cover is one of the, the, the, the final things we're gonna cover is IV fluids, and the important thing with IV fluids is that not every patient actually needs IV fluids.
So The reason being is, if we can look at the anatomy here, when, when the heart delivers, when the heart com compresses and generates forward flow, the left ventricle contracts, pressures start to build up in the aortic arch, then they start to, the blood starts to flow out into the coronary arteries to the actual heart itself. When the heart contracts, it squeezes all the blood into the right atrium. If we have a patient who is normovolemic, then potentially what happens if we give massive doses of fluids like big, big fluid boluss, then we can increase this right atrial pressure, and that then can oppose the flow of heart through the, the flow of blood through the heart.
So, fluid bolus are only indicated if the patient's hypovolemic. But if you have, if you're only able to obtain a, catheter in the back leg, then you might have to use an enlarged dog, 50, 100 mL of flush to get that, adrenaline to where it needs to go. So, flushes are OK, but generally, big bs are not indicated for patients who have no prior documented history or evidence of, of poor profusion or hypovolemia.
Regarding intratracheal administration of drugs, generally, this is not very effective at all. And, we used to do it a lot, but then there's issues with safety, with regards to spraying adrenaline and atropine and so forth down the ET tube, and then it's spraying back into people's faces when chest compressions start to commence again. But if you are going to do it, you can use, you can do with any drug and it relies on absorption of the drug across, in, across into the lungs, into the bloodstream.
And if you're going to do it, then you have to put it down as far into the respiratory as possible. So they recommend using a catheter, a long catheter, and pushing that catheter all the way down through the tube right down until it doesn't go any further, then delivering a drug down there. But also then using a higher dose and also diluting it down as well.
So, maybe double the dose and then and then increase the dilution just to, to be able to get enough of that fluid down there so it absorbs across a large enough surface area. Essentially it's not very effective. So, if you decide to do it, then do it.
If you are going to do it, then probably tilting the dog up as well, putting the drugs down the, down as far down into the respiratory tract as possible, then, pulling out the catheter, putting the AA on, maybe delivering a couple good breaths, and then start chest compressions, but generally what happens is all just ops out of the mouth or pours out into the ETT tube. So in summary, We start Basic life support when whenever we consider that the patient is unresponsive, so unconscious. Not spontaneously ventilating, absence of heart sounds or palpable pulses, we begin basic life support, basic life support needs to occur continuously in the background.
Compressions 100 to 120 compressions per minute, 3rd to half the depth of the chest and lateral recumbency. Then the next thing we do is intubate the patient, deliver 10 breaths per minute, same time as chest compressions with a with a 100% oxygen, 1 2nd inspiratory time. Then if we have enough people, then we move on to advanced life support.
The first thing we do is place an ECG, determine if it is shockable or not shockable. Then place the entitled CO2 to give us a gauge of how our chest compressions are going. And remember that we need to have standardised ventilation rates to be able to interpret the ECG.
Place an I catheter, administering reversals if, if, if, we're able to. Then, in our next intercycle pause, we then assess whether or not our rhythm is shockable, and if it's shockable, we defibrillate. If you don't have a defibrillator, we record your thump.
If it's been greater than 10 minutes, then we then can consider anti-rhythmics, and also we can consider, pressor agents. If the rhythm is asystole, so flat line or pulse is electroactivity, so this is a normal looking rhythm that has no heart sounds, no pulses, and is generally normal, if not slower than the normal rate of the heart. Then consider either low dose adrenaline or vasopressin, and then atropine, so at our hospital, we just do low dose adrenaline atropine at the same time.
Then after 10 minutes, consider adrenaline a high dose of adrenaline, and even maybe consider bicarbonate therapy. And then this occurs in the background, sorry, this basic life sport occurs in the background and, and this is all a bonus. So, I hope that you found that useful and you implement this into your, in your hospital and you start saving lives.
There is more detail on the recovery Initiative.org website, and you can actually download all the papers and there's 6, I think, and it explains everything that I have in more detail. So good luck and I hope all goes well.