So tonight we're going to be talking about cardiopulmonary resuscitation or CPR. Now, you'll see an alternative term used for this in CPCR, and that's more widely used in the human field. And the CPCR represents cardiopulmonary cerebral resuscitation.
And the reason that the terminology has changed slightly in the human field is that they wanted to move away from emphasising that we're trying to resuscitate the heart and the lungs, i.e., cardiopulmonary, and to emphasise that really the ultimate goal is to have a full neurological recovery from a cardiopulmonary arrest.
So therefore, they've inserted the extra C for cerebral resuscitation as well. But generally the two terms are interchangeable really CPR, CPCR, but largely in the veterinary field we tend to stick to CPR as being the preferred term. Now, there are guidelines produced for human resuscitation, and these are produced by the International Liaison Committee on resuscitation.
And they generally update these every five years. So in 2010, for instance, sorry about that. In 10, for instance, there was a major change to the human guidelines.
And then in 2015, they updated those guidelines from 2010, but they actually made very, very minor changes from what had happened in the 2010 guidelines. Excuse me. And we're due another update for the human guidelines next year in 2020.
But I just put this link up on the screen, because actually, if any of you want to look at the human guidelines, it's actually quite a nice, quite a nice, area to look at. It's quite easy to read and it's not as dry as you might think. Now, we have actually got guidelines now for resuscitation in the veterinary field as well, and these were produced, sorry, my computer's frozen for some reason.
And these were produced by what we call the Recover Initiative, and Recover stands for the reassessment campaign on veterinary resuscitation. And the only guidelines that have been produced as part of this were sent out in 2012. And this was a consensus document from a group of experts looking at various experimental and clinical work on resuscitation on animals and humans, and also looking at the human guidelines and taking the important parts out of them.
Now, the initial aim of the recovery initiative was also that they would update the guidelines every 5 years, but unfortunately, there hasn't been an update since 2012. There was one that they tried to get out for 2019, but unfortunately, they've missed that deadline as well. But having spoken to them recently, I've been told that they're aiming to get an update in the veterinary guidelines out for 2020.
So what I'm going to talk about in this presentation is largely based around the recover guidelines from 2012, and I'll also be talking about some of the changes that have occurred in the human resuscitation guidelines over that time as well. So when we talk about cardiopulmonary arrest or CPA we're talking about the sudden cessation of functional ventilation and effective circulation. And this definition is actually quite interesting, I think, because we're not necessarily talking about a heart that has completely stopped.
The use of this word, effective circulation means that we can have situations where the heart is still got electrical activity going on, but has very minimal mechanical activity and therefore has inadequate cardiac output, and therefore does not gene. And effective circulation. And that therefore, would still classify as a cardiopulmonary arrest, even although there is significant electrical activity going on in the heart.
And I'll talk about that a bit later when I talk about the arrhythmias that we get with cardiopulmonary arrest. So we classify cardiopulmonary arrest as a 3 minute emergency, because generally within 3 minutes of the circulation stopping, we start to get ischemic damage to the brain. Now that 3 minutes of grace period can be extended, and there are 2 major things that can prolong this 3 minute period before we start to get ischemic and hypoxic damage to the brain.
And two of the major things that provide protection are barbiturates and hypothermia. Now, obviously, these days, we don't really use barbiturates like thiopental for anaesthesia, but in fact, they are still used in the human field for brain protection. So particularly in cases of traumatic brain injury, barbiturates are often used to induce a coma.
And the reason that they're used is because they actually reduce the cebral metabolic requirements for oxygen. So essentially they protect the brains, the brain cells against hypoxic damage. They reduce blood flow to the brain because of the reduced metabolic demand and therefore they reduce intracranial pressure.
The second thing that will protect the brain for longer than this 3 minutes during a cardiopulmonary arrest is the presence of hypothermia. So if you have a patient who's slightly cold at the time of arrest, you've probably got slightly longer than 3 minutes before you'll necessarily get brain damage. Where this becomes more important is one of the things that's been introduced into the human medicine, guidelines for postcarddiopulmonary arrest, post resuscitation, is mild therapeutic hypothermia or deliberately inducing hypothermia to protect the brain in those cases where people have had an arrest, we have the return of spontaneous circulation during resuscitation, but the patient remains neurologically unresponsive or comatose.
In these situations, humans will often be cooled down to a core body temperature of about 32 to 34 degrees, and that will be maintained for 24 to 48 hours to allow the brain time to recover. And again, I'll mention that a bit later at the end of the talk. Now this is a, a really busy slide, and this is really just to emphasise the causes of cardiopulmonary arrest are generally multifactorial.
There's usually several different things acting together to trigger a cardiopulmonary arrest. And on this list that you're seeing here, the one thing that stands out that can be a sole cause of cardiac arrest is the vagal reflexes thing. I'm sure you're all aware that when you remove eyes, for instance, traction on the optic nerve can trigger a vagal response and you can get severe bradycardia or sometimes complete cardiac asystole.
But in most other situations that we see with cardiopulmonary arrest, again, it's usually multifactorial, several things acting together to trigger the arrest. Now, when we look at signs of cardiopulmonary arrest, there are two critical things. One is that the patient will be non-responsive because they won't have adequate cerebral blood flow.
And the second thing is they will be apnea. Now, patients may not become apneic immediately the heart stops. It can take about 3 minutes again for the respiratory centre in the brain to become hypoxic.
So we can see a patient carry on breathing for maybe a couple of minutes after the heart has actually stopped. But in general, all patients with cardiopulmonary arrest will be non-responsive and they will generally become apne very quickly. They will also tend to have an absence of heart sounds and an absence of palpable pulses.
Now, we can see this in other situations, aside from cardiopulmonary arrest. So for instance, in patients who are very profoundly shocked, very severe hypovolemic shock, for instance, we may not be able to hear heart sounds because they're so quiet, and we may not be able to palpate pulses. Similarly, if we have a cardiac tampona, a severe pericardial effusion, heart sounds may be muffled, we may not be able to hear them, and we may not be able to palpate pulses very easily if there's a very poor cardiac output.
And in fact, there's a lot of debate now around whether we should be trying to palpate pulses at all in patients that we suspect of cardiopulmonary arrest. And there's a couple of reasons for that. Studies have shown that even with experienced rescuers, i.e., people who are trained to resuscitate human patients, less than 2% of them can detect whether a pulse is present within 10 seconds of trying to palpate it.
And what we'll talk about throughout this presentation is any delay to starting resuscitation significantly worsens the outcome for that patient. So that 12th period when somebody's trying to find a pulse and not sure whether they have one or not, can have a significant detrimental effect on how that patient recovers or otherwise. The second thing is the specificity of pulse palpation for cardiopulmonary arrest is about 65%.
And what that actually means is that about 35% of patients who try and feel a pulse in an arrested situation will think there is a pulse there when there isn't actually one present at all. And again, that's going to delay the start of resuscitation. So, generally now the advice is, if you come across a non-responsive apneic animal, if you have a very quick feel of a pulse, if you're not sure whether there's a pulse there or not, you immediately start chest compressions.
Because again, studies in humans have shown that where resuscitation has started, where we start chest compressions in humans who haven't actually arrested at all, the instance of serious damage to that patient is only about 2%, whereas we know that any delay to starting resuscitation will have a significant adverse effect. So the take home message is, if there's any doubt at all that that patient may be suffering from cardio pulmonary arrest, you immediately start resuscitation. So other signs that we see with cardiopulmonary arrest, there used to be a lot of emphasis placed on fixed dilated pupils as being a poor prognostic indicator.
Now, in fact, we know that the pupils will tend to become fixed and dilated within about 45 seconds of the circulation ceasing. And you'll certainly see people during resuscitation using pen torches to see what the pupils are doing, etc. In fact, we have evidence from experimental studies in monkeys that were arrested and then resuscitated, that show that the pupils can remain fixed and dilated for several hours after the return of spontaneous circulation.
And in these studies, the monkeys went on to make a full neurological recovery. So if the pupils are fixed and dilated during resuscitation, it really doesn't mean very much at all. If you start off with the pupils in that situation, fixed and dilated, and you start resuscitation, you start chest compressions, etc.
And the pupils start to constrict, then that's probably quite a good prognostic sign. It probably means that you're generating adequate cerebral blood flow. But as I say, if the pupils remain fixed and dilated, it tells you nothing at all.
It should have no bearing on whether or not you continue resuscitation. And then we have a various other signs associated with the cardiovascular system. So the mucous membranes may be pale or cyanotic during cardiopulmonary arrest, depending on the underlying cause of the arrest.
The patient, as I say, will be apne very soon after the circulation stops, or they may be demonstrating agonal gasping. And this is something that I've, I've seen people think, certainly during anaesthesia, when they see this type of breathing, they actually assume the patient is getting light because they take these very sharp, deep breaths, and it almost appears as if the patient's moving under anaesthesia. And the first thing they do is turn up the vaporizer.
And in fact, what's happening is that patient is actually arrested and it's an agonal situation. If the animal's undergoing some sort of surgical procedure, there'll be lack of bleeding at the wound sites generally. The capillary refill time during an arrest situation can be normal, prolonged, or shortened, again, depending on whether the patient's visodilated, viso constricted, or whatever.
And then if we're using an ECG, it will indicate one of the 4 cardiopulmonary arrest arrhythmias, and I'll talk about those 4 very shortly during the presentation. So when we think about management of cardiopulmonary arrest, again, the most important thing is to be ready, be prepared for it, because we have this very short period of time before the brain potentially starts to become hypoxic and ischemic. So by being ready, we should have an area in the practise where we know if we take that patient, we have facilities for establishing an airway quickly and also we have drugs that we will tend to use during an arrest situation.
It doesn't have to be anything fancy, it just has to be a dedicated area that you know you're going to have everything you need in that arrest situation. So the next stage is recognising the arrest, and again, I'll emphasise yet again, the important thing here is if there's any doubt at all, any doubt whatsoever, you start chest compressions in that patient. And if it hasn't actually arrested, you're very unlikely to do any harm.
And once we recognise or suspect an arrest, we carry out what's called basic life support. And then following on for that, or sometimes simultaneously, we perform what's called advanced life support. Now, that sounds really fancy, and in actual fact, I'll show you in a second that it's not particularly, sort of extravagant at all.
And then if we successfully resuscitate the patient, we then have to move into a period of post-resuscitative care. So with basic life support, essentially all we are trying to do is act as an artificial heart and lungs for that patient. So in other words, we're trying to make sure we drive blood around the body by compressing the chest, and we're also trying to make sure that that blood moving around the body has adequate oxygen in it to satisfy the tissue's needs.
With advanced life support, as I say, we always start with basic life support, but we then quickly run into advanced life support. In this situation, we're actually trying to ascertain the specific arrhythmia that that patient is suffering from. And as I say, there are 4 arrest arrhythmias that I'll talk about, talk about shortly.
So there's nothing fancy here. We're really talking about choosing the specific drug in most cases for that individual arrhythmia that patient's suffering from, and that's all advanced life support really involves. So basic life support begins with the ABC algorithm that you'll all be aware of.
A for airway, B for breathing, and C for chest compressions or for circulation. But in actual fact, the 2010 guidelines for humans threw that out of the water, and they completely reversed this. So now they recommend a CAB protocol.
So the first thing that's recommended if you find a collapsed non-responsive human is to shut, is to start chest compressions rather than worrying about the airway. Now, the argument for that is that when you perform chest compressions, as you compress the chest, you're also compressing the lungs, so you're automatically pushing gas in and out of the lungs anyway as you compress the chest. Now, there's a couple of reasons that they, they changed the order in humans.
The first one is that humans, it's relatively difficult to intubate the trachea in comparison to animals where it's fairly easy. And so they found that in situations where the air where people try to establish an airway in a collapsed person, that increased the time before chest compressions were started and it worsened the outcome for that patient. The second reason is that the majority of cardiopulmonary arrests in adult humans are related to primary cardiac events, so for instance, myocardial infarctions.
And therefore, it makes sense to target the heart as the primary thing to start working on rather than the airway. Whereas in animals, a significant proportion of cardiopulmonary arrests are associated with airway obstruction, rather than primary cardiac disease. So it makes sense in animals that we still establish apa in airway as quickly as possible.
So, it's a bit confusing just now in the veterinary field. In general, again, the take home message is, if you find a collapsed patient who you think may have arrested, you immediately start chest compressions, but you try and establish a patient airway as quickly as possible after that point. So usually in our patients, as I say, we're establishing an airway by endotracheal intubation, preferably.
Now, if you have a patient who's already intubated or you think is intubated under anaesthesia, for instance, and they've arrested, it's really important that you check the position of that endotracheal tube. Because particularly with shorter tubes, as the animals moved about on the operating table, for instance, the tube can pop out of the larynx and the trachea and end up in the pharynx or the oesophagus. So even if you think an endotracheal tube is in place in the trachea, it's important you have a quick visual check and make sure it is still there.
The second phase of basic life support is to start breathing for the patient. And at the moment, it's recommended that we try and use 100% oxygen for that. Now, there is a school of thought, actually, the air, using room air to ventilate, may have some benefit over 100% oxygen.
And again, I'll talk about the reason for that at the end, why that might be the case. But in general, at the moment, most people would still recommend we use 100% oxygen if possible. We use a standard rate of 10 breaths per minute, regardless of the size of the patient.
So whether it's a cat, right up to whether it's a great Dane, it's 10 breaths per minute. And we supply this either by squeezing the reservoir bag on a breathing system, which would be the most common situation in veterinary practise, or by using an automatic ventilator if you have one available. The recovery guidelines also suggest a tidal volume of 10 mL per kilo.
Now, the difficulty with this is if you're manually ventilating a patient by squeezing a bag, it's absolutely impossible to judge what volume you're actually given to that patient. So in general, all we can really say is you squeeze the bag so that you get a noticeable chest rise in the patient. That's probably about the best we can see, the best guide we can give for that.
But as I say, it's always 10 breaths per minute and approximately 10 mL per kilo or just a decent chest rise. Now, if you're on your own when you're resuscitating a patient, it's likely the most important thing is carrying out the chest compressions. And so you can just carry out chest compressions by themselves and hope that you're getting passive ventilation by squeezing the lungs.
Or some people will recommend that you do chest compressions followed by mouth to mouth to snout ventilation. Again, this is only if you're single-handed. So if you're doing mouth to snout ventilation, you do 30 chest compressions.
You then cup your hand around the animal's mouth to hold it closed. You put your mouth over the animal's nose and you give them two deep breaths, and then you stop and you do the 30 chest compressions again before repeating it. Now there is actually very limited evidence that this has any beneficial effects at all.
And in general, it's not something I would recommend people do. I would tend to suggest you just stick to performing chest compressions if you're single-handed when you're doing a resuscitation. Now when we do chest compressions in resuscitation, we produce forward blood flow through the body through two potential mechanisms.
One is called the cardiac pump and one is called the thoracic pump mechanism. Now, with the cardiac pump mechanism, the theory is that as we press down on the ribs, essentially we just squeeze the heart between the two sides of the rib cage, and that pushes blood forward out into the aorta. We will also get some retrograde flow of blood because all the valves become incompetent as we perform external chest compression.
But we hope that most of the blood will go forward into the aorta. And then as we release pressure from on top of the heart, blood will flow back into the heart. It won't flow back in from the aorta because the aortic valve will close, but we'll get passive refilling of the heart as we release the pressure on it.
So that's the cardiac pump mechanism. The second mechanism is the thoracic pump, and what happens here is, when we press down on the chest wall, we're actually generating an increase in intrathoracic pressure. And that increase in intrathoracic pressure causes indirect pressure on the aorta to cause it to contract and push blood forward, but it also creates pressure on the outside of the veins.
And because the veins are thin walled, this causes them to collapse where they enter the thoracic cavity. So the thoracic pump mechanism means that we tend to generate forward blood flow because of this indirect compression on the heart and the aorta, and retrograde flow is prevented because the veins collapse under this pressure. Now, why is this important?
Why am I bothering to distinguish between these two mechanisms? Well, it's likely that in all patients where we compress the chest, we get some effects from both of these two things. But we know that the cardiac pump is the dominant mechanism of forward blood flow in smaller patients, patients less than about 15 kg, whereas the thoracic pump is dominant in larger patients, again above about 15 kg.
That still doesn't really explain why it's important. The reason it's important is We vary where we put our hands on the chest as to whether we're trying to generate the cardiac pump or whether we're trying to generate the thoracic pump. So let me explain, in patients less than 15 kg, where we know it's the cardiac pump that's responsible for most forward blood flow, we place our hands directly over the heart itself.
So where we would traditionally think we're putting our hands. So, in some patients, that'll be one hand on top of the other if they're a reasonable size, compressing down on the heart itself. In smaller patients such as cats and smaller dogs, that might be a circumferential placement of the hands, so the thumb on one side of the chest and the fingers on the other side of the chest, again, compressed directly over the heart.
However, to generate the thoracic pump mechanism in larger dogs, dogs above 15 kg, we don't put our hands directly over the heart itself. We place them at the widest point of the thorax. And by placing them over the widest point of the thorax to compress, this means we generate a greater increase in intrathoracic pressure.
So again, you can see from this picture, we don't have our hands over the dog's heart at all. We have it further back and higher up on the chest wall at the widest point of the for. Now there are a couple of exceptions to this.
The major one is in dogs with what we describe as keel-shaped chests. So these are dogs with very deep, very narrow chests, and the classical example of the sighthound breeds. So in these we know actually that the cardiac pump is the main mechanism for generating forward blood flow.
So here, we do compress directly over the heart itself, even though these patients are over 15 kg. Now, when we do chest compressions, we perform them generally in lateral recumbency. I will mention an exception in a second, and it doesn't really matter whether we place the animal in right or left a recumbency, either side's fine.
We're aiming for a compression rate of 100 to 120 compressions per minute, so roughly 2 compressions per second. And we're also aiming for an inward compression of about 30 to 50% of the depth of that chest. Now if you think about the depth of a dog's chest, you're trying to compress that by up to about 5.
So that takes a lot of effort. And these two areas are where most people probably fail with chest compressions. A, they don't compress fast enough.
We're looking again at a minimum of about 2 per second. And in fact, there's some evidence that going faster, up to about 150 compressions per minute, may be even better, but at least 2 compressions per second, and we're pushing that chest in by about 50% of its of its width. So that takes a lot of effort.
It's very exhausting if you're doing it properly. And we're looking for a 1 to 1 compression to relaxation ratio. So in other words, the amount of time we spend pushing the chest in the way should be equal to the amount we're allowing it to recoil back.
And one thing that's been noticed in a lot of experimental studies looking at this is that when people are doing these chest compressions, as they allow the chest to recoil, they don't allow full elastic recoil of the chest. In other words, they maintain some pressure, they lean on the chest, and that's detrimental because it doesn't allow blood flow to fill the heart again. So you have to make sure that as you allow the chest to reflex, to relax back the way to recoil up the way, you remove all the pressure from it and you don't maintain any on it at all.
Now, as I say, you know, this is absolutely exhausting. If you do this properly, you will be sweating and you'll be shattered within the space of about 1 minute unless you're very fit. And again, studies have shown that it's impossible to maintain adequate chest compressions for more than 2 minutes, even under the best circumstances.
Once you get to 2 minutes, you start to lean on the chest, you don't allow it to recoil, and your compressions are not as effective. You don't compress as deeply or as rapidly as you should be doing. So it's important during resuscitation that the compressor is changed every 2 minutes, so that the person who's been compressing has a rest for at least 2 minutes before they start compressing again.
Now, having said that we perform resuscit, sorry, compressions in lateral recumbency, the exception to that is in dogs with barrel-shaped chests, and the classical example is given as of English bulldogs. Perhaps some staffies as well would fall into this category. And in these cases, it is more effective to do sternal compressions with the dog on its back.
And again, we're trying to compress directly over the heart, so it's a cardiac pump type of mechanism in this situation here. So, just to summarise, in general, patients less than 15 kg were compressing directly over the heart itself for the cardiac pump. Patients above 15 kgs were compressing at the widest point of the thorax, unless those are dogs with keel-shaped chests like the sighthounds, in which case we compressed directly over the heart.
And the other exception is in dogs with barrel-shaped chests, where it's probably better to do sternal dorsal compressions with the dog on its back. But the rates 120 per minute go through all these different positions and the compression depth of 30 to 50% stands regardless of what position you have the patient in. So we've got somebody compressing the chest, we've got somebody breathing for the patient at 10 breaths per minute.
And over the years, there's been lots of recommendations as to how these two people coordinate. The current recommendations are that you try and coordinate it so that the person breathing for the patient delivers the breath as the other person compresses the chest inwards, because that generates the maximum increase in intrathoracic pressure. However, I have to say when you do this practically, if you're standing there waiting to squeeze a bag to give a patient a breath, and you're looking at somebody compressing the chest at 22 compressions per second.
Excuse me, it's actually very difficult to coordinate it. Excuse me a second, I'm just going to have a drink. And hopefully my voice will come back.
So I don't really worry too much about coordinating these two things. We just have somebody breathing at 10 per minute and somebody else compressing 120 compressions per minute. Excuse me.
No, internal cardiac massage is a whole different ball game really in this situation. We know that in dogs, in larger dogs, external massage becomes less effective. So some American authorities would recommend doing internal cardiac massage in any dog above 20 kg.
I think that's probably a bit extreme, to be honest. Certainly, if we have no response to external massage within about 15 minutes of starting it, it may be time to think about doing the internal massage. Or if we have any situation where it's not going to be possible for external massage to generate an adequate increase in intrathoracic pressure.
So for instance, if we have fractured ribs, a diaphragmatic rupture, pleural effusion, for instance, then we should probably immediately open the chest if we want to do resuscitation. However, I do think it's something that needs to be considered very carefully before you undertake this. Excuse me again, sorry.
Because if you do get these patients back, there's a lot of intensive care and nursing involved in keeping them stable postoperatively. So it's something that you really have to think about before you get into that situation, whether you actually even want to attend internal cardiac massage or not. So while we're going through our basic life support or airway breathing circulation or circulation airway breathing, we really want somebody trying to establish IV access in the patient and somebody else trying to attach an ECG if we have one available to determine what type of arrhythmia we're dealing with.
And here, this is us now moving on to advanced life support. And advanced life support, again, nothing particularly fancy. We're just looking at which of the four arrest arrhythmias we have and choosing the appropriate treatment for that particular arrhythmia.
So, to know which arrhythmia you're dealing with, you have to have an ECG ideally, and that determines which drug you're going to use. And as I say, we have 44 arrest arrhythmias. So we have ventricular asystole, we have pulseless electrical activity, which used to be called electromechanical dissociation.
We have pulseless ventricular tachycardia, and we have ventricular fibrillation. Now I'm going to just briefly go through each of these 4 because again, as I say, for a patient to have a cardiopulmonary arrest, they must have one of these 4 arrhythmias. So I'm sure you're all aware of ventricular asystole, much loved of medical dramas, but essentially we have electrical activity, and then suddenly we just have a flat line, we have no electrical activity going on in the heart at all.
Now note that although we classically think of this as a flat line, we can occasionally still have atrial activity going on, so you may still see some P waves on that ECG, but there are no QRS complexes at all, and that's particular asystoy. With pulseless electrical activity, we tend to have what we see in this lower ECG here. We tend to have these wide sort of triangular shaped complexes.
Now, you can see, obviously, this patient is not asystolic, because we have some electrical activity going on here. We have movement around the baseline, but you can see it's obviously not coordinated, it's not recognisable as any normal ECG activity. Now with pulseless electrical activity, we can also have a relatively normal ECG as indicated by the top diagram here, but for reasons that we don't understand, the electrical activity is not coupled with mechanical activity.
This is one of the reasons that we never use an ECG as our sole monitor you in anaesthesia, because you can have what looks like a relatively normal ECG, but the animal may actually have no output at all from its heart. Now we tend to see pulseless electrical activity as a fairly late change, during an arrest situation. We often see it following on from asystole, or we sometimes see it in animals that are profoundly shocked or in the setting of a tension pneumothorax.
And sometimes if we relieve the tension pneumothorax, we can generate normal electrical activity again. And then the third arrhythmia is ventricular fibrillation. So up in the top left-hand corner here of the slide, you can see a normal beating heart, nice coordinated activity.
Whereas on the right, this quivering heart that you can see is actually in ventricular fibrillation, and you can see that there's unlikely to be any output from that heart because there's no coordinated activity going on there at all. And at the bottom of this trace, sorry, at the bottom of this slide, we have two ECG traces of ventricular fibrillation. The trace on the left is called coarse ventricular fibrillation, because we have quite a lot of movement up and down against the baseline, whereas the trace on the right is called fine ventricular fibrillation, because there's much less movement along the ECG baseline.
Now, the main difference between these two is that fine ventricular fibrillation tends to occur later on following an arrest, and it tends to suggest prognosis is much worse. So it's more difficult to get patients back with fine ventricular fibrillation on the ECG than it is with coarse ventricular fibrillation on the ECG. But they are treated exactly the same.
It's purely associated with prognosis, and that's the only reason I mention it here. And then the final, the 4th of the arrhythmias is pulseless ventricular tachycardia. Now, we see ventricular tachycardia a lot in our critically ill patients, but that's not pulseless.
With pulseless BT, essentially, we have one abnormal complex run straight into the other, and it's occurring at a very fast rate. So you can see here the rate is 212, and it's just so fast that it's not capable of producing any cardiac output at all. So that's what makes it pulseless and that's what makes it an arrest arrhythmia.
Again, we have normal or not normal, but we have certainly have coordinated electrical activity here on this ECG, but it's fast and it's not quite normal, and that's what makes it an arrest arrhythmia. Now, the, of the 4 arrhythmias that we get in animals, the two commoner ones are asystole and pulseless electrical activity, whereas in humans, the commonest arrest arrhythmia is ventricular fibrillation. And this immediately causes problems for us because of the 4 arrest arrhythmias, ventricular fibrillation is the one that probably carries the best of the prognoses, because essentially, it's just very uncoordinated electrical activity going on throughout the myocardium.
And if we deliver an electrical shock to that myocardium and put all those myocardial cells into the refractory period at the same time, we hope that what will then happen is the patient will then go back into a sinus rhythm because the sinoatrial node has kicked back in as the pacemaker because we've suppressed all the other electrical activity, or the patient may then progress into asystole. However, asystole and pulseless electrical activity, which again are the more common ones in animals, carry a much poorer prognosis. So regardless of how good we actually are at CPR, we're also going to, well, sorry, we're always going to have a worse outcome than what they have.
Now, I just want to mention defibrillation fairly briefly because I recognise that defibrillators are, are very uncommon in veterinary practise. They're actually very cheap to pick up secondhand. You can pick them up for a few 100 pounds, but you really have to be aware of what you're doing with them.
Now, in the setting of ventricular fibrillation and pulseless ventricular tachycardia, defibrillation is the treatment of choice. It's the one that's going to have the most success. So it is useful to have a defibrillator in those situations.
If you do have a defibrillator, there's two different types. There's monophasic, and in monophasic defibrillators, what happens is the electric current just goes from one paddle to the next, sorry, to the other, and of course, the heart will be sitting in the centre here. So the current only goes one way.
With biphasic defibrillators, the current goes from one paddle through the heart to the other, and then bounces back again, it's sent back, so the current passes through the heart twice. The reason that this is important is that biphasic defibrillators, which most of the modern ones are these days, allow you to defibrillate with a lower current setting. And the lower current setting means that you cause less damage to the myocardium.
So biphasic defibrillators are much more effective and much safer for the patient than monophasic ones are. The second thing is, we know that if we have a patient who has arrested who's gone into ventricular fibrillation, for instance, if we can defibrillate that patient immediately, there's a reasonable chance that we're going to convert them back to a sinus rhythm. However, if we have a situation where there's a delay in defibrillation, so if it's more than 4 minutes since the patient has arrested, then we shouldn't defibrillate right away.
We should start a sorry, we should start a period of external cardiac massage, external chest compressions, and do a cycle of at least 2 minutes before we attempt defibrillation. And that's really just to restore some blood and some energy supply to the myocardium before we defibrillate. And finally, I think the most important thing with defibrillators is these can cause a lot of harm.
So again, if you're inadvertently touching a patient, for instance, while it's being defibrillated, it's going to put all the cells of your heart into the refractory period as well, and you may well become asystolic. So in other words, unless you know what you're doing, you could kill somebody with a defibrillator. Excuse me again.
So I'd like to move on now to talk about some of the drugs that we use during CPR and the first drug I want to talk about is actually intravenous fluid therapy. No, certainly when I qualified, we were taught that as soon as the patient arrested. We got widespread hypoxia at the tissue level and the blood vessels these are dilated.
So we had this great big vascular bed to fill and we were encouraged to pour fluids in aggressively to patients who were arrested. We now know actually that this is detrimental in evolemic patients. So the vast majority of patients who suffer a cardiac arrest should not be given any fluids at all.
They do not require fluids. And we know that giving fluids to these patients actually worsens the neurological outcome because it contributes to cerebral edoema. It also, for a variety of reasons, decreases the coronary perfusion pressure, so it decreases the blood supply to the myocardium.
So, fluid should only be given during an arrest situation in patients with confirmed or suspected hypovolemia at the time of arrest. So for instance, if we have a ruptured spleen that's arrested, then obviously fluids would be indicated in that situation. But for most patients, we withhold fluids.
By far the most important drug be used during resuscitation is adrenaline, which we're now supposed to call epinephrine to tie in with our American colleagues. Now, whenever I ask most people, you know, why do we use adrenaline in an arrest situation, I would say 99 times out of 100, I'm told, well, it's because it stimulates the heart, it increases the heart rate, it's a positive chronotrope, and it increases myocardial contractility. It's a positive stroke.
In fact, both of these things do occur with adrenaline, but they're actually detrimental in the setting of an arrest, because what both of those things do is the increased myocardial oxygen demands, and that's bad in a situation where we're maybe not perfusing the myocardium particularly well. So by far, the most important effect of adrenaline during an arrest situation is the fact that it's an intense vasoconstrictor. It helps deliver all the blood away from the non-essential organs to things like the brain and the heart.
What most people tend to forget, I think when they use adrenaline during resuscitation, is it has a very short duration. It only lasts about 3 to 5 minutes as an absolute maximum. So we really need to repeat it very frequently during resuscitation.
And bearing in mind that we tend to compress the chest for 2 minutes, and then we change the compressor again for 2 minutes and then change back again, we repeat the adrenaline every 4 minutes during resuscitation, and this ties in with every second compressor change. So in other words, if we give adrenaline and the first person's compressing, we then switch after 2 minutes, no adrenaline's giving, and then we switch again after another 2 minutes. That'll be 4 minutes since the first dose of adrenaline, and we repeat it again at that point.
And you'll see lots of things in the literature regarding whether we should use low dose adrenaline or high dose adrenaline. And low dose adrenaline is 10 mcg per kilo.01 milligrammes per kilogramme of adrenaline.
And this is now the standard recommended dose during resuscitation. So we use this low dose adrenaline of 10 mcg per kilo, and we repeat it every 4 minutes during the resuscitation. If we get to about 10 minutes of performing a life support in these patients, and we aren't seeing signs of return of spontaneous circulation, then it's suggested that at that point, you go to high dose adrenaline, you go to 10 times the dose, 100 mcg per kilo, and you start to give that every 4 minutes at that point.
So start off low after 10 minutes, if you've got no response, increase to the high dose adrenaline. Now, usually the strength of adrenaline that we have, the commonest strength we get is 1 in 1000 or 1 milligramme in a mil, and for many situations, that's too concentrated to use for a smaller patients. So I've just got details up here on the slide of how you can dilute that if you need to do that for smaller patients.
Essentially, you just dilute 1 mL of the adrenaline into 9 mLs of saline, and that gives you a concentration of 100 mcg per mL of adrenaline. Now, another drug that's kind of fallen in and out of favour, it's a kind of newish drug and that it's probably appeared in the last 15 years as a drug called vasopressin. And one of the problems with adrenaline is when it causes its vasoconstriction, it does that by stimulating alpha-1 adrenergic receptors.
And sometimes, as the, as the in aiddotic tissues in particular, as the circulation fails and lactic acid builds up. These alpha one receptors don't respond particularly well to adrenaline, so you get a blunted effect, from what you would expect from the adrenaline. Whereas this drug, vasopressin acts on what we call V1 receptors in the tissues, and these are not affected by acidotic changes nearby.
So in other words, vasopressin will tend to cause vasoconstriction, even if the tissue is very acidic, whereas adrenaline may not in some of these situations. The other thing is that vasopressin only causes vasoconstriction, so it doesn't have what we now recognise as these two detrimental effects of adrenaline on the heart, i.e., the positive ionotropic effects and the positive trootropic effect.
However, it's relatively expensive, certainly much more expensive than adrenaline, and the jury has kind of gone in and out. So there's been a whole variety of trials, some of which showed it was superior to adrenaline, some of which showed no benefit, some showed poorer outcomes from it. And certainly, in the 2010 human guidelines for resuscitation, it was put in there as you can use this either alongside adrenaline or use it as an alternative to adrenaline.
However, in the 2015 human guidelines, the most recent ones that we have available, they've actually removed these repressing from the guidelines because they can't show any beneficial effects of it. So you will still come across it in a lot of textbooks and a lot of articles, but in general, no, we're not using these repressing at all. The other drug that we sometimes use during resuscitation is atropine, which is a vagolytic drug, so it removes the effects of the vagus nerve on the heart.
It's precise role in resuscitation is, is fairly unclear, and certainly what they now see in the human guidelines is, is unlikely to be detrimental, but whether it actually has any be beneficial effect remains to be seen. I tend to use it in situations where the animal has either been significantly bradycardic just before it's arrested, or we start to get a return of spontaneous electrical activity in the heart, but it's bradycardic at that point, and I'll give adrenaline. If you do want to use it, a lot of people use it routinely during resuscitation.
Again, like adrenaline, it's given every second compression change. So every 4 minutes, you give your adrenaline, you can, so you give your atropine, you can either give that at the same time as the adrenaline, or you can alternate it so that you give adrenaline at one cycle and you give atropine at the next. Sodium bicarbonate, we know that a lot of patients, as they arrest, the tissues will become acidotic as lactic acid builds up in it, and use of sodium bicarbonate will counteract the effects of that lactic acid will help maintain the pH.
The current recommendations from the recovery guidelines are that if we've been resuscitating a patient for longer than 15 minutes, then we should consider giving them a sodium bicarbonate to counteract any metabolic acidosis. And the dose is usually just 1 millimole per kilo, slowly intravenously over about 5 to 10 minutes. There are various concentrations of bicarbonate available commercially.
So the commonest one that we use is the 8.4% solution, because in that strength, 1 mil, there's 1 millimole of bicarbonate per mL of solution. If you get bicarbonate too early though, it's been shown to have a detrimental effect on outcome during resuscitation.
So it's definitely not something to be going right away. It's something to be considering later on in resuscitation. So as I say, at least 15 minutes in before you would consider giving sodium bicarbonate.
So how do we get these drugs during resuscitation during cardiopulmonary arrest? Well there's a whole variety of different routes that we can use that I'm just going to go through. We know that by far the most effective route to administer drugs is by the central intravenous route, so through a jugular catheter.
However, you know, it's not often that we have a patient who arrests who already has a jugular catheter in, and certainly during resuscitation, it's probably not the time to try and start giving drugs into the jugular vein because the animals moving about, not a route we use particularly commonly. So in most situations, we'll use what is certainly a second, a second base route, and that's the peripheral IV again because we're used to placing lines in the cephalic veins and the sophenous veins, for instance. So with the peripheral route, as I say, we know it's not as good as the central IV, but it's probably the one that we're most used to using.
We give our drug, we flush it in with a bolus of normal saline, and then you're supposed to elevate the leg for about 20 seconds, and that's really just to allow the blood to drain into the central circulation and deliver the the drug in there. And while you've got that leg elevated, you're still continuing chest compressions. And you want to do that for at least 2 minutes after giving the drug before you assess any effect on the ECG.
Again, the intracardiac route is one again, you'll see in lots of medical dramas because it's very dramatic, for instance. But in fact, the only time we ever inject drugs directly into the heart itself is if we can visualise it. So we only do it during situations of open chest cardiopulmonary resuscitation.
And the reason for that is if we give our resuscitation drugs through a closed chest wall, we can cause several quite severe problems. So we can damage the coronary blood vessels, and obviously that's bad news for, for myocardial blood flow. If we inject something like adrenaline directly into the heart muscle itself rather than into the chamber of the heart, we can set up a very resistant ventricular fibrillation, which may not even respond to defibrillation.
Obviously that's a bad thing. And finally, obviously, anytime we go through a closed chest wall, we can create a pneumothorax. So that's bad news.
So we never ever, even if we can't achieve IV access, we never give drugs intracardiac through a closed chest wall. It's only if the chest is open and we can visualise that we're depositing those drugs into the left ventricle. Into the left ventricular chamber I should say.
Another route that we can use is the intratracheal route, and that's suitable for most of the drugs that we use. Certainly the two common drugs, atropine and adrenaline. However, it's not suitable for sodium bicarbonate because that will inactivate pulmonary reacting.
And here what we do is we place a long urinary catheter down our endotracheal tube, as far as it will go essentially until it lodges within the lung itself, and we then administer our drugs. Now, it's quite difficult to know the exact drug dose to use. We don't have good guidelines on this, unfortunately.
And in general, the recommendation is that you use anywhere from 2 to 10 times the normal IV dose of the drugs. Administer that through the urinary catheter and then flush that in again with a bolus of sterile saline. Most people will tend to recommend that if you're given an adrenaline by this route, you immediately go for high dose adrenaline, so the 100 mcg per kilo dose that we talked about earlier.
Another route that's very commonly used now during resuscitation in humans is the intra-osseous route. And for reasons that we don't completely understand, when the circulation collapses during a cardiac pulmonary arrest, the bone kind of holds open the blood vessels in the medullary cavity. They don't tend to collapse.
And so any drugs that we give into the medullary cavity will be absorbed into the systemic circulation very rapidly. And it's essentially just the same as giving these drugs intravenously. And in in very small children and in babies now, if they're taken to hospital collapse in a collapsed state, in most cases, they won't even bother trying to establish IV access.
They'll go immediately for the intra-osseous route, and only once they have the patient suitably stable, will they then start to think about IV access. Now, it's obviously not a route that we use particularly commonly in veterinary patients, maybe unless you're used to doing exotic work, for instance. So if you're not used to doing intra-osseous infusion of drugs or fluids, this is probably not the time to start practising it, unfortunately.
It is actually relatively easy to do. You can get devices that do it. So this device shown at the bottom of this slide is called an EZIO gun, and essentially it's just a battery powered gun.
That drives a needle into the the bone and therefore you and then you can deliver drugs or IV fluids through that needle once. Now, however you administer your drugs, it's important to remember that ventilation is still continuing at 10 breaths per minute throughout this, and chest compressions are continuing at 120 compressions per minute. So maybe let's get a bit more practical now.
So what's the situation if you don't have an ECG and you come across a patient with a presumed arrest? Well, essentially, you would follow basic life support as before the ABC or the CAB, whichever way you want to do it. And if you're going to use drugs, you're going to use adrenaline because we want vaso constriction anyway, again, every 4 minutes, plus or minus atropine, if you're a fan of atropine, if you want to use that during your resuscitation, plus or minus sodium bicarbonate, if you have that available, but again, only later on in resuscitation if you've been going more than about 15 minutes.
But it's unlikely unless you've got a asystole, it's very unlikely, excuse me, that you're going to have any success with doing this. So, what about if you have an ECG and you know that the patient's got ventricular fibrillation or pulseless ventricular tachycardia, but you've got no defibrillator available. Again, defibrillation is obviously the treatment of choice for both of these.
It's the one that's going to give you the greatest success. Well, there are case reports of ventricular fibrillation spontaneously converting to sinus rhythm in very small patients, so cats and Chihuahuas, for instance. That's going to be very rare, so you certainly can't rely on that.
If you don't have a defibrillator, ventricular fibrillation may respond to a precordial thump. So essentially, you're just clenching your fist, you're raising it about 20 to 30 centimetres above the thoracic cavity, and then you're going to thump down directly over the heart in this situation, regardless of the size of the patient. And that may very occasionally, there are certainly case reports that we very occasionally convert the patient into a sinus rhythm are probably more likely it will do nothing or convert them into east.
Pulseless ventricular tachycardia may also respond to a precordial thump, but equally you may drive those patients from PVT into ventricular fibrillation. Pulseless ventricular tachycardia may respond to a bolus of lidocaine, so 2 to 4 milligrammes per kilogramme IV in the dog, probably about 0.25 to 0.5 milligrammes per kilogramme in the car.
You have to be careful with lidocaine in the cat because it's a cardiovascular depression, and it can also cause seizure in constipation. And again, ventricular fibrillation may respond to lidocaine, but it's very unlikely. The other drug that you might consider using is the Class 3 antiarrhythmic amiodarone at 5 mg per kg.
Again, this tends to be reserved for cases that are resistant to defibrillation, but if you don't have a defibrillator, it may be worth thinking about giving Abiodarone, although it can cause allergic reactions in dogs and it can cause quite marked hypotension. So again this is something that I would only consider as a last ditch effort unfortunately. So how do we know if we're actually successful with the resuscitation that we're getting somewhere?
Well, in the short term, again, if you look at some of the older textbooks in particular, it will say you should be able to palpate a peripheral pulse with each chest compression. Now, the problem with this is, if somebody's compressing the chest as effectively as I say, it should be, you know, that really fast rate of 120 per minute, that really deep compression of 30 to 50% compression depth, then the animal moves a lot and it's quite difficult, well, it's very difficult to feel peripheral pulses, even if you're getting a good, forward blood flow. The other thing that can happen is that during chest compressions, you also get retrograde blood flow.
And so if you're trying to feel a femoral artery, for instance, and you feel a pulse, you may actually be feeling retrograde blood flow in the femoral vein, and you may still not be getting a good forward blood flow. So in actual fact, the only time we bother palpating pulses during resuscitation, is during the pause and chest compressions when the two compressors change over. So after that 2-minute interval, when you're about to switch, you can have a quick feel at a pulse, but there's absolutely no point in trying to feel a pulse while chest compressions are actually going on.
The most important thing is in in telling us whether we're getting adequate blood flow is generation of end tidal carbon dioxide through carography, and I'll talk a bit more about that on the next slide as to why that's important. In the intermediate term, if we're getting successful resuscitation, we may start to see a return of a more normal cardiac rhythms we may start to see some normal QRS complexes, for instance. The patient may start to try and take spontaneous breaths, and we'll tend to see increased levels of consciousness.
So for instance, the eye will tend to start off central and non-responsive. As we get forward blood flow and adequate blood flow to the brain, the eye will tend to rotate downwards and we'll start to see a palpiro reflex returning as well. And then in the longer term, obviously what we're looking for is a return of consciousness and a full neurological recovery.
And unfortunately, we sometimes get the first two steps completely right. So we get a return of spontaneous circulation, good blood flow in the body, but some patients will never make a full neurological recovery, unfortunately. So when we use capnography in any, any patient, it's telling us a few things.
It's telling us, first of all, to get that trace on our capnograph. We have to have cells producing carbon dioxide through metabolism. We then have to have blood flowing past those cells, past those tissues, picking up the carbon dioxide and carrying it to the lungs.
And then we must have that carbon dioxide leaving the lungs to be picked up by the sensors. So in other words, we have to have blood flowing around the body and we have to have gas leaving the lungs. So, there's a correlation between how good our chest compressions actually are at creating a forward blood flow and what our end tidal carbon dioxide value is on our carnograph.
So studies would suggest that if we've got an end tidal carbon dioxide value of less than 15 millimetres in the dog, or less than 20 millimetres of mercury in cats, we're not getting good forward blood flow and that's associated with a poor prognosis. However, there is something to bear in mind here in that if you have a capnograph, that's a side stream capnograph, so these are the ones that have got the sort of 6 ft long, clear plastic tubing going from the connector to the endotracheal tube to your actual monitor, that these will tend to underread what the end tidal carbon dioxide value is in small dogs. And that's because they take a sample at a rate of about 200, 200 mL per minute from the breeding system.
So if you've got a patient with a very low tidal volume, not only are they going to sample that patient's tidal volume, but they also pull out some fresh gas from the breathing system, and that leads to an artificially low value displayed by the monitor. So in other words, I guess what I'm saying here is, I don't think the actual numbers are particularly important during resuscitation if you're using a kno graph. I think what is important is that you're getting a reasonable trace, you can actually see an obvious carbon dioxide trace on your knogram.
And if you're not seeing that, then you need to change how you're doing your chest compressions. You either need to be more forceful with them, or you might need to consider changing the patient's position or where your hands are positioned in that particular patient. How long should CPR be continued for?
Well, the general consensus is, if you start resuscitation in any patient, you shouldn't stop for at least 20 minutes before deciding there's no hope of carrying on. And certainly a lot of the times we'll continue CPR for over an hour in those patients we would get the return of spontaneous circulation, and then the rest again, and then it comes back again. So it's difficult to know, but 20 minutes should be the absolute minimum.
If we do manage to get a return of spontaneous circulation, we need to think about post resuscitative care. The most important thing I think to take away from this slide is that the vast majority of patients who suffer one cardiopulmonary arrest will re-arrest again in the short term. And so we should be prepared for that.
So any situation where resuscitate a patient once, we should be aiming to keep a, keep an eye on their cardiac output and their blood pressure. So we may need to use things like positive ionotropes or vasopressors to maintain their blood pressure. Make sure they're ventilating adequately and they're adequately oxygenating with a pulse oximeter and support the neurological functions.
So for instance, what I'm talking about here are really those patients who arrest and don't immediately recover consciousness. These are the ones that we really need to focus on here with all this support. And for the neurological side of things, we may be thinking about giving manitol or hypertonic saline to try and reduce cerebral edoema.
But just be prepared for a rearrest in most patients who've had one primary cardiopulmonary arrest. So as I say, the human guidelines are updated every 5 years. The 2015 guidelines didn't really change that much at all from 2010, apart from removing vasopressin.
But between 2005 and the 2010 guidelines were fairly major changes, so I just want to mention what these are. So, they moved away from establishing the airway as being the most, pivotal point, and they start chest compressions now in any collapsed humans. And I discussed the reasons why, yes, that's appropriate in animals, but it's also important to establish the airway as quickly as possible.
They recognised that aggressive fluid therapy was detrimental to the patient, especially if they were if they were normal volemic, if they were evolemic, and introduced fluid restriction in those patients. The tracheal route of drug administration was removed in the 2010 human guidelines, so you may wonder why I'm still, still talking about it and still teaching it. Well, the reason is that they've shown in humans that absorption of drugs from the lung is very variable.
Some patients will absorb them very well. Some patients will get zero uptake of drugs when you give them by the tracheal route. The reason I've left it in is because in situations where it's not possible to establish IV access in our animals during resuscitation, if you can't do intra-osseous administration, then you're left with no other alternative, essentially, apart from the tracheal route.
And that's why I still do it. The reason I've taken out the human guidelines is because they have the alternatives of either IV administration of these drugs or intra-OC administration. The human guidelines in 2010 also removed atropine, from the guidelines, and the reason for that was not because they could show any detrimental effects from it, but simply because they couldn't show any obvious benefit.
One other thing that they recognised and well, that we recognising with increasing frequency is that oxygen can be a relatively toxic molecule. It can generate lots of free radicals. And so it's been shown that if you have hyperoxia, or high levels of oxygen in the blood in the recovery period following cardiopulmonary arrest, it actually worsens neurological outcome.
And you may remember I mentioned earlier about when we're ventilating patients during resuscitation, we tend to use 100% oxygen, but some people are now recommending we just use room air, and that's on the basis of this potential oxygen toxicity in the recovery period. So it's still sort of Judy's still out about what we should use during the resuscitation, but there's overall consensus now that we want norm oxia in the recovery period. What that means is we're aiming to keep the pulse oximeter reading between 94 to 98%.
If the animal can't maintain its saturation above 94%, then we need to supplement oxygen to get it into that range of 94% to 98%. But ideally, we don't want the saturation greater than 98% if we can avoid it, because that may cause increased neurological damage during recovery. They've also introduced in the human guidelines the use of mild therapeutic hypothermia, and that's in people who don't immediately recover consciousness following successful resuscitation.
So they'll chill them down to 32 to 34 core body temperature cent. Now, it is something that we do as well in patients who don't make an immediate neurological recovery, but when you start this, you're really looking to do it for up to about 48 hours. They have to be mechanically ventilated, and you need really intensive critical care facilities to be able to do this.
So I think the important thing for people in practise is simply that if the patient has become cold during resuscitation, You shouldn't make vigorous attempts to try and rewarm it in the recovery period. You should let it gradually rewarm itself. If you are going to rewarm it, you want to do it at a maximum of 0.5 °C per hour, and certainly no more than that, probably slightly less.
But we recognise that a period of hypothermia is probably beneficial for the patient. But the major emphasis throughout both the 2010 human guidelines and the 2015 ones are the continuous uninterrupted chest compressions. So in other words, we no longer stop to look and see what's happening with the ECG or to feel a pulse.
We carry on compressing the chest with a changeover every 2 minutes, and it's only during that changeover we look at the ECG and we carry on compressing the chest until there's obvious signs of spontaneous recovery the circulation. Now to end on a depressing note, there's a few studies that have looked at the outcome from cardiopulmonary arrest in animals. And the first one a while back now, from University of California Davis vet school from Cass and Haskins, and they reported a one-week survival rate of less than 4% in dogs and cats that had undergone resuscitation.
In the same year, from, I think this is it's either the North Carolina, Colorado vet school, similar figures for dogs, but this report had up to almost 10% of cats surviving to discharge, so much better outcome. And then probably the biggest, most recent one is from the University of Georgia in 2009 by Eric Hoffmeister, who's Professor of anaesthesia there. And they showed they had much better success rates.
35% of dogs and 44% of cats had successful resuscitation, and that was defined as return of spontaneous circulation. So circulation moving itself, animal breathing. However, again, they showed that only 6% of animals actually survived to discharge.
So the prognosis for patients who suffer a cardiopulmonary arrest is appallingly poor, unfortunately. And in fact, what all the studies have shown is that animals who tend to have the best survival rates are animals who arrest either during anaesthesia, or secondly to some drug administration error or allergic reaction. And probably during anaesthesia, that's because the animal's been relatively closely monitored, so it's picked up fairly quickly.
They've probably already got established IV access. They'll have high levels of oxygen in their blood, probably because they'll be getting supplemental oxygen, and they'll have a patent air weight already established. So I think the important thing is I see a lot of patients where resuscitation is attempted, and in my mind it's inappropriate.
So those animals that have severe underlying pathology that's not correctable, I see very little point in attempting resuscitation laws. And the ones that you're certainly going to have the best outcome on are the ones that are during anaesthesia or secondary to drug administration. So that's it, I'm sorry my voice kept going.
I knew that was going to happen. I'm surprised I didn't cough more than that, but I'm happy to take any questions if anybody has any. Derek, that was absolutely fascinating and for a recovering man flu, patient, I, I think you did incredibly well and, and all the men on with us tonight will will understand.
Sorry ladies, you just couldn't possibly understand. No jokes aside. That, that was absolutely fabulous.
It really was and hugely insightful. I know some of my preconceived ideas that I was taught many, many decades ago have been changed tonight. So thank you for that.
It's good. I think Ian falls into the same age category as I do. I'm not gonna read his whole message about wheelbarrows and confusion, but he asks, could you please explain why, CO2 is measured in millimetres of mercury and not in percentages?
Well, it can't, there's 3 units that can be used for measuring carbon dioxide. There's millimetres of mercury, which is the oldest one. Excuse me, there's kilopascals, and pascals are actually the SI unit.
So they're, they're the units that we should actually be using. And there's also percentages. And essentially, the differences between them are percentages and kilopascals are almost essentially equivalent.
So 5 kilopascals of CO2 is equivalent to about 5%. And 1 kg particle or 1% is equivalent to 7.5 millimetres of mercury.
So, sorry, excuse me, I was about to choke again there. So if we see, for instance, people tend to see the normal CO2 levels in the dog are between about 35 to 45 millimetres of mercury, that's the equivalent to about 4.5 to 6 kilopascals, or 4.5 to 6%.
So they're all, it's all just different units, but it's all just telling us exactly the same thing. Millimetre of mercury, I think, is very, very common in the States. That's by far the commonest units used in the states.
In the UK, most anestheists will tend to use kilopascals, although some of us older ones will still tend to use millimetres of mercury as well. But equally, you could use percentage. It really doesn't matter which one you use as long as you know what the conversion factor is between them.
And am I correct in saying, Derek, as well, that it's the shape of the Kapnograph, that's important together with the readings? In terms of resuscitation or in terms of cartography generally, both. The shape of the shape of the capital graph here is very important because that can give you a lot of information as to what's going on.
In general, during resuscitation, you will have a standard, what we call single breath, a normal shape catnograph essentially during resuscitation. Excuse me, sorry, I've just gone again. The time that we tend to get an abnormal shape one and I don't, I don't actually have any reason this presentation that I can show you.
Pardon me, is if again, we go back to that side stream carnograph, which I was, which I mentioned in the presentation, and that's the commonest type that tends to be used in veterinary practise. The other type is mainstream, where the carbon dioxide is actually measured directly in the probe, which connects between your endotraum tube and your breathing system. But with the side stream carpnographs, the commoner ones, if again, if we have a patient with a small tidal volume, so generally our smaller patient.
As it takes that sample, we get a big dilution effect because of the size of the sample it takes. And rather than giving us our normal, normal shape catnogram, which I can't demonstrate because I don't have any pictures with me, it gives us one that goes up and down very quickly, so we don't get an alveolar plateau. So we get an abnormal shape of carnogram in that situation, and we also get an artificially low end tidal carbon dioxide value because of this dilution effect.
I, folks, I, I've really, my heart is going out to Derek and his voice, he's held it together very, very well for us. Derek, I'm not going to ask you any more questions. You have presented us with a, a huge, huge array of information which I know I have found very beneficial and I'm sure our members have as well.
So thank you for your time and Thank you for hanging in there, with the loss of the voice. Well, thank you for putting up with it, everyone. I know it's quite irritating, but it's probably more, even more irritating for me, I have to say when I keep coughing.
Oh bless it. Well, thank you and to Dawn, my controller in the background. Thank you very much for everything that you made happen tonight and to all of you for attending.
Thank you so much. And from my side, it's good night.
