Good evening everyone and welcome to one of the last sessions for the webinar vet of 2023. Tonight I'm going to be discussing ventilating the respiratory patients and also some arterial blood gas analysis towards the end. So it's quite a lot to get through, but I'm hoping to give you as much information as possible in order for you to feel more confident with some of these cases that you might be dealing with.
So the learning outcomes for this evening, we're gonna go through some basic physiology of the respiratory system, especially with regards to ventilation. Identify what parameters that might indicate the patient that needs ventilation and or how to perform this efficiently and effectively. Hopefully feel more confident in understanding different ventilatory needs for different respiratory patients.
And then at the very end, we're gonna go through some blood gas analysis measurements and basically hopefully get you to feel more confident in interpreting the values. So some of the definitions I'm gonna be talking about quite a lot this evening I just sort of go through them quickly before we start. So tidal volume is the volume of air inspired and also expired in one breath, and that's in mills.
The minute volume, which is also in mills, is the volume of it inspired over a minute, and this is tidal volume times the respiratory rate. Respiration is the process of oxygen supply and the use within the body, and also the elimination of carbon dioxide. Ventilation is the movement of gas in and out of the RVO line.
Enidal CO2 is the entidal carbon dioxide which is measured at the end of each breath, essentially, so the proportion of carbon dioxide, carbon dioxide that is expired. Hyperventilation, so often people think this is a low respiratory rate, but it's not, it's the, that the alveolar ventilation is low relative to the metabolic rate of that patient, and we'll look at that a bit further later on. And the opposite for hyperventilation.
And then the peak inspiratory pressure is the maximum pressure in the lungs at the peak of inhalation. So going through some physiology of the respiratory system, respiratory control is actually controlled in the hind brain by the medulla oblongata and the ponds. The medulla is the primary control centre and that sends signals to contract and relax the muscles, and the PONs controls the rate and the depth.
Pulmonary reflexes such as the heron brewer, so some of you may remember that from your VN training, that sends information back to the brain about the degree of expansion of the lungs. And what I wanted to focus on is the variety of receptors involved, so the Mecana receptors detect effort. But the chemoreceptors, so these are the ones that I wanted to discuss a little bit further, so they're located the central ones on the surface of the medulla, and they detect changes in pH levels.
So carbon dioxide is obviously a gas, but when we transport it around the body, it's transported as carbonic acid. So it's an acid and that obviously affects pH. When we get changes in pH that is detected on the surface of the medulla in the CSS.
And that essentially is what drives respiration in mammals. OK, so the opposite in reptiles, they're driven by oxygen in mammal in mammals. This is our primary control mechanism is to drive breathing through changes in pH levels and that is obviously altered by CO2 levels.
We do have peripheral, although they're not very peripheral because they sit in the carotid and aortic bodies, they do detect falls in oxygen. So if there's any problems, obviously with the receptors, and any drops in oxygen as well will also be detected by these receptors, and they will obviously drive respiration as well. Gas exchange, so the only place that gas exchange takes place is in the lungs.
Oxygen and carbon dioxide diffuse across a a blood alveolar barrier down a diffusion gradient. Carbon dioxide diffuses much faster than oxygen does, so twice as fast, in fact. And patients oxygen levels are therefore often affected first because of this, especially in the awake patient's breathing room air.
Carbon dioxide levels are usually only then affected in sort of moderate to severe disease. However, when we place these patients on 100% oxygen, like what we often do during anaesthesia, this can change slightly because we're obviously providing 5 times the inspired oxygen than on room air, and therefore, the oxygen levels not always can therefore improve and we often get CO2 changes that happen much quicker. Carbon dioxide clearance is actually directly proportional to minute volume.
So what we discussed before, minute volume is respiratory rate times the tidal volume. So if we increase our minute volume, whether we increase our respiratory rate or tidal volume or both, we will clear more CO2, and we will clear less CO2 if that minute volume decreases. Obviously disruption to any of these processes, especially with our respiratory patients, can lead to further problems.
The respiratory physics, so when we are breathing spontaneously, so not mechanically in any way, our intercostal muscles contract and the rib cage moves up and outwards. The diaphragm contracts downwards, and air is drawn in through a negative process into the lungs. So a little bit like you're pulling back on a 20 mil syringe, the air is drawn into that syringe through a negative process.
That negative pressure that is therefore created in the chest also encourages venous return to the heart. Whereas mechanical or manual, whether you do this manually through a manual IPPV, is using positive pressure ventilation. So this is doing the opposite of that 20 mil syringe.
We are now pushing air into a space, so into the chest, and that can massively disrupt that negative pressure that was therefore once there is now switched and it will essentially reduce our venous return. So this is something to factor in when we're ventilating patients that you will more often than not see a drop in blood pressure. So the end CO2 and PACO2 relationships, so they are intertwined with each other.
So the PACO2 is the partial pressure of carbon dioxide in arterial blood. The entitled CO2, like what we mentioned before, is the carbon dioxide that is released at the end of an exhaled breath. Both are almost identical with roughly a 1 to 5 millimetres of mercury difference, providing that we've got all of these factors stable.
So alveolar ventilation. Metabolism and circulation, so we need good alveolar ventilation, good metabolism and good circulation, therefore perfusion. Obviously, with our respiratory patients, some of this can be disrupted and this can alter the reliability of using that tidal CO2 as a surrogate marker.
And that's where our blood gas analysis would help us, so we'll talk about that a little bit more later on. Normal entitled C2 values. So in the healthy and awake patients, you've got, this will vary from book to book, but dogs are 35 to 45, cats are a little bit lower, some references even go down to 26, being the low normal for a cat, around 30 to 40 if you sort of to average, some of the references out.
Anything above this is termed usually hypoventilation. So like what we discussed earlier, it's the alveolar ventilation is low compared to the metabolic rate of the patient. So in this picture on the left here, I appreciate you can't see the respiratory rate.
Hopefully you can appreciate that it's, it's not in any way low. So it's around 24 to 28. But we've still got an entitled CO2 of 50, so this patient is still hypoventilating despite having a, a higher respiratory rate during GA.
So this patient is hyperventilating despite there being a source of normal to slightly higher respiratory rate. And all that, the reason why that is happening is because anaesthesia depresses the respiratory system centrally within the brain. So within the brain we're depressing the brain using anaesthetic drugs.
We're also causing profound muscle relaxation and then we are also often they are in some kind of recumbency, so lateral, dorsal, etc. So all of those factors often decrease tidal volume. It's only when your patient gets a little bit deep and potentially arguably too deep, that our respiratory rate drops as well.
So what drops first is our tidal volume, and as we discussed before. That is within our minute volume. So any changes in our minute volume will change our CO2.
So if we have a decrease in tidal volume that is affecting our minute volume, and we are then going to see an increased level of CO2 and that is then coming through on our end tidal CO2. There are other causes of increased levels of entitled CO2, so hyperthermia, whether that be malignant or . For some reason, pyrexia or obviously it's a hot day, etc.
It's a big hairy dog. All of that will increase entidal CO2, so CO2 production and also laparoscopic procedures as well. So there are other causes of hypercapnia, not just hypoventilation, but the majority of patients under anaesthesia are hypoventilating.
We have something called permissive hypercapnia, and some of you may have heard this. We expect during anaesthesia because we know these drugs suppress the respiratory system, we know they cause muscle relaxation, that we understand that there will be some level of hypercapnia. In sort of the healthy patients we can allow usually up to around 60 in a dog.
This will be anaesthetist dependent and around 50 to 55 in a cat before we consider sort of intervening. Unless there are other things going on which I will discuss shortly. When we start to get to this sort of 60 millimetres of mercury level, we're entering the moderate respiratory acidosis level, and this will cause a catecholamine release, so release noradrenaline and adrenaline, and this will or could potentially irritate the myocardium and predispose that patient to arrhythmias.
Hypercapnia patients are often mistaken as well, just as I mentioned for being a little bit too light. So if we look back at that picture before, we've got an entitled CO2 of 50. But we've got quite a high-ish respiratory rate of 24 to 28.
That is a normal response as well to be hypocapnia, so we've got that respiratory drive. It is blunted during anaesthesia in a dose dependent manner, but if this patient is light or in a moderate plane of anaesthesia, it still has the respiratory drive to get rid of that CO2, so we start to see an increased level. Of respiratory rate and also hypercapnia patients as well.
So conoxide is a vasodilator, so it will cause your mucous membranes to become pink, and also, as I say, because it can release catecholamines as well, you do get a slightly increased heart rate and blood pressure. So if you're looking at a patient that has a slightly increased heart rate, slightly increased blood pressure, slightly increased respiratory rates and pink because membranes. All of that might be considered as that patient being a little bit too light, when in fact it's just the the CO2 being a little bit high.
So we try and sort of get that down, it can often make some of these parameters a little bit sort of better. However, if you have a metabolically acidotic patient. This is the patient that we don't want to allow this permissive hypercapnia, and there are other circumstances as well.
But essentially, if they're already acidotic for a metabolic reason, we don't want them to add to that acidosis with the CO2 problem as well. This could obviously lead to some organ damage and dysfunction. The indications when you would choose to ventilate a patient, so I've gone through one of them concurrent aidemia.
The hyperventilation, so when they're reaching that source of 60 mark and over in the dog, 50 to 55 in the cat, that can be an indication that the patient needs supporting. Hypoxemia as well, so a PAO2, that's our partial pressure of oxygen within arterial blood, is less than 60, so that's where you would need a blood gas analyzer for that, or that does correspond with an SPO2 of 90. So SPO2 of 90 or less, that patient needs some intervention.
Also open chest surgery and also increased intracranial pressure patients. So again, if you've ever heard of that and you're not sure why, essentially carbon dioxide, as I said before, is a vasodilator. If we've already got an increased intracranial pressure within that cranial space, we then don't want to put more blood flow into that.
Brain, because that could be the tipping point of the herniation. So we want to keep that sometimes normal, sometimes if they're quite severe, even a little bit lower and cause a small amount of vasoconstriction. And then there's a few other things like if you're using neuromuscular blocking agents, for example, you would need to ventilate because that paralyses the muscles, including the intercostal muscles and things like myasthenia gravis, when they've got a muscular weakness there, phrenic nerve damage, tetanus, botulism.
There's a few other causes as well, but they're the main ones. So the basic aims of ventilation, whether this is manually or mechanically ventilated, is to deliver around 8 to 15 breaths per minute. Again, we can change that patient dependently, but this is sort of a rough starting figure.
Tidal volume is documented to be 10 to 15 mL per kilo. In the majority of patients. However, anything with a long and deep chest, and this even goes to the to the dachshunds, so they have a long and a deep chest relative to their sort of body weight because it's their legs that are the short bit.
German Shepherds, and even sort of Labradors and some spaniels have sort of a long and deep chest. So all of those sort of size patients often have a higher tidal volume and greyhounds have actually been And seem to have a total volume of up to 40 mL per kg. So I thought I'd just put 10 to 20 mL per kg.
I don't want you to think that you can't go over 15 mL per kg because actually a lot of these big deep chested, long breeds are often at the higher end of at least 20 mL per kg sometimes. So I just wanted to put that in there. But when we are worried about tidal volume, if you're not sure, we are usually looking at peak inspiratory pressure.
So this is on our ventilator. So we're looking to deliver between sort of 8 to 15 in a normal patient, but 10 to 20 is sort of the usual range that we, that we use. We don't want to go over 20, even though there are studies out there that alveolar rupture in the healthy patients.
Doesn't sort of rupture till you get to sort of 80 to 140 centimetres of water, I think it is. But we don't want to go over 20, and ideally we don't really want to have to use over 15 centimetres of water. The more pressure we put on the chest, the more decreased the venous return we're going to get.
So we don't want to affect our blood pressure too much if we don't have to, and definitely don't go over 15 in a cat, so we're starting really low. On a cat, we want to sort of aim between 8 and 12, and definitely not over 15 in a cat. Also puppies and kittens, we can cause some bar trauma, some trauma to the lungs there.
They have really compliant chests, so they've got like quite poor muscle development. So we don't really want to go over 15 centimetres of water with a puppy or kitten either. Entitled CO2, ideally keep it within the normal reference range, but again, I've, I've thought we can allow up to 55 millimetres mercury in that, so it's a healthy patient that doesn't have any concurrent asidedemia, for example.
Because if we are sort of sitting on a hypertensive patient whilst we can support that with blood pressure drugs, we can also allow the entitled CO2 to be slightly over the normal limit because we're not essentially going to intervene until it hits sort of 55 to 60 anyway. So if they are sort of sitting at 50/51, that's not necessarily a problem, but it will be very case dependent. And we're looking for normal chest excursions, so we're not looking to massively inflate these lungs and deflate.
So when you're delivering manual IPPV, it's really important to look at the chest excursions and to try and aim for normal. I think often people sort of overdo it a little bit and we're going to decrease our venous return when we're doing that. So the equipment that you're gonna need to ventilate the patient yourself, whether that be you with a mechanical ventilator, you need to be able to set that up correctly and be confident in using the ventilator.
Or manually selecting the correct circuit, and you can, you can use any circuit to deliver IPPV. It's just things like mini lacks and circle systems are meant to use those lower flow rates, so you just need to increase your flow rate slightly. But you can deliver IPPV with with any circuit, so you don't need to switch circuits in order to deliver IPPV.
It can sometimes be easier if you know you're going to deliver from the beginning to choose a circuit. That might be more suitable, but actually just changing your flow rate you can deliver IPPV with any circuit. You do need a leak-free ET tube in order to ventilate the patient appropriately.
So you should be doing your cough inflation after intubation anyway, but it's always best when you're going to ventilate the patient to just check that again because if there's any type of break in the seal, when you're delivering a breath, some of that is going to be escaping around the ET tube and you're not going to be able to have a true reason as well with the with that pressure. Within the chest, so you need a leak-free ET tube in order to sort of ventilate that patient properly and reliably. A pressure manometer, ideally, you need a pressure manometer.
You can get these for circle systems. So on the previous slides, if I just go back and quickly show you here. So that on the top of the circle system you can get those and just attach them to any of those circle systems.
You can also get them for non rebreathing circuits as well. That's the gauge that you're going to look at, and sort of, when you're doing manual. IPPV when I said about not going, ideally over 15 centimetres of water, peak inspiratory pressure.
So that's the pressure gauge that's gonna help you deliver the breath in order to not go over that pressure. And obviously if the if you're using a mechanical ventilator, this is all inbuilt within that so that will display the value on the screen. You need your capnography and SPO2 to help guide the ventilation, and in an ideal world, an arterial blood gas analyzer, would be really useful, especially in respiratory patients, which I will explain a little bit later.
So how to ventilate manually if you are, if you don't have access to a mechanical ventilator in practise. Ideally, one person should be used to solely ventilate, and I understand in first opinion that the person monitoring the GA is often opening kit, etc. But I think when the patient needs to be ventilated, I think that's when you do need that extra pair of hands to come in the theatre to do those.
Things for the surgeon and also to even you know sort of scribe the monitoring parameters down for you as well because you can't really be Ventilating the patients and then trying to monitor everything else at the same time. So ideally one person to solely ventilate. Choose that circuit with the pressure manometer if you haven't done already.
Reservoir bag needs to be appropriate for the patient. So if it's too large, you've, you've also got the chance of squeezing that bag a little bit too much and therefore going over that pressure within the chest. Check the full flow rate is not too high or too low.
If it's too high when you close the APL valve, the, the reservoir bag will fill up really quickly and therefore the pressure could go also down it then becomes a closed system, go down to the patients and into the chest. If it's too low when you close, if you're using low flow. For example, on your circle system, when you close the APL valve, actually, it will take forever for that reservoir bag to fill up.
So just check your flow rate, close the APL valve, press the reservoir bag, I never like to say squeeze because often people think squeezing needs to be quite firm and therefore that's when you can overinflate your lungs and then quickly reopen the APL valve. You're looking for 8 to 15 centimetres of water in a cat and 10 to 20 centimetres of water in a dog on your pressure gauge. Normal chest excursions as I said before.
And around 8 to 12 breaths per minute, even though a respiratory rate, especially in a smaller dog, is often sort of 16 to 20, for example, we still, despite the sort of . Saying we shouldn't over ventilate normal chest excursions, we still have a tendency to overinflate slightly, anyway, so we can drop down on that respiratory rate a little bit. And observe the SPO2 and the capnography to guide you.
So I'm just going to show you a little video. I just want you to watch the pressure manometer here. So the pressure manometer is delivering around 15 centimetres of water.
This is to a dog, and I want you to look at the chest excursions. They're really, really minimal. So this just shows that delivering 15 centimetres of water, pressure within that chest and the chest excursions are very, very minimal.
And the chest chest excursions are really, really minimal. So you don't need to overdo it with when we're delivering manual IPPV. The negative effects of positive pressure ventilation, as I said before, it will decrease venous return even in the healthy patients.
So patients with cardiac output problems, whether that be cardiac disease or it could be hypovolemia, dehydration, etc. Probably won't tolerate IPPV very well. Now that's not to say that they can't have IPPV.
There's obviously an indication for you to consider that. It's whether you weigh up, weighing up the risk obviously in with your veterinary surgeon. If the patient definitely needs to be ventilated, we then need to support this cardiac output problem, whether that be obviously restoring some fluid balance there or giving blood pressure supportive drugs.
The pulmonary stretch as well might induce a bradycardia. It's very, very rare, but, and especially if we're using those lower sort of peak inspiratory pressures, we're not sort of going to 20 over. But the, the inflation of the lungs sometimes can induce a bradycardia just through the vagal nerves.
So it's just something to watch out for. You can get lung damage, so again, this isn't risk free to place an animal on a ventilator or to deliver a manual IPPV cause we could be causing barrow trauma, which is excessive pressures in the lungs and it induces a lung injury. For your trauma as excessive tidal volumes and that again will do the same.
Probability, as I say, in healthier lungs is quite minimal because we know that the alveoli rupture is quite high, . Sort of the pressure to, to rupture those is quite high, but obviously with these respiratory patients, especially, we need to be really, really careful not to damage any, any alveoli at all. So that is why we say a maximum inspiratory pressure of about 15 in a cat, 20 in a dog.
You can also get an inflammatory response to ventilation. It's usually long-term ventilation and it happens a lot more in humans, but you can have a bit of an inflammatory response as well, and you can obviously, then get pulmonary edoema form after. So that is a risk factor again to consider, especially with fragile lungs.
If we're not ventilating adequately, whether we're overdoing it or underdoing it, we're gonna get blood gas disturbances as well. So if we're not ventilating adequately, this will lead to a decrease in pH and therefore respiratory acidosis. And if we overdo it, over ventilate the patients, it will result in a respiratory alkalosis.
It'll drop that sorry, increase that pH a little bit too much. Obviously an animal that already has pH changes, whether they're acidotic or alkalotic, this could actually be detrimental. So in patients with pH changes we're better to keep the entit CO2 within a normal reference range if we can.
Well, how to minimise these effects, so with all these risks. Monitor anaesthetic death really closely for two reasons for that. If we can get away with not ventilating a patient, so if they're hyperventilating, their entitled CO2 is over 60, if we can reduce the depth and help that patient to sort of blow off more CO2 by themselves, that is better than to put these risks to that patient.
The other reason I say mon monitor anaesthetic that closely is if you do decide to manually or mechanically ventilate the patient. The reason why you're doing that is often to exchange gas better for them, so get rid of CO2 and provide them with more oxygen. But obviously with that you are delivering an inhalational agent, so often your depth will increase when you start a manual or mechanical ventilation.
So I often already have this in my brain and I often decrease the iso level slightly before I switch on the ventilator because I know I'm gonna change that depth because I'm able to exchange gas a little bit better for that patient. We need to allow sufficient time for exhalation. Minimise resistance to flow of gas, making sure we're using the largest port ET tube that we can in the patients safely and any minimising any bends and connections that there are as well.
Correct. Any hypovolemia or dehydration, that should be done obviously in the pre-anesthetic period. There are times when this might happen during a procedure, hypovolemic, blood loss, etc.
Or it may be that there's an emergency anaesthesia warranted, but ideally we should be correcting acid-based balance and any dehydration or volume deficits. Ensure the patient is receiving fluid therapy throughout the anaesthetic anyway to compensate for losses and blood pressure supportive drugs might be indicated as well to ensure that the perfusion, and also those cardiac outputs or venous return problems aren't going to compromise that patient too much. If you're ever unsure whether you should ventilate the patient or not, given an occasional manual breath yourself, so sometimes called a sigh breath.
And observe and the entitled CO2 for any what we call mismatch, and I'll show you a video of this in a minute. It can mean when you are delivering that breath, if you see the entitled CO2 number of your breath much higher than the patient's own breath, that can often indicate that the patient for some reason isn't ventilating themselves very well. They often got really high respiratory rates, these patients, these are the ones that you're unsure about.
But they won't be adequately exchanging gas, so they won't be getting rid of CO2. They won't be taking in the oxygen and sort of absorbing the oxygen as well. And they won't be taken in that inhalational agent either.
So I'm just going to show you a video of what I mean. So this patient is essentially what we call, you might say hyperventilating, it's not, it's got a high respiratory rate and then there's my breath, so that normal catnograft trace. And as you can see, it's much, much higher than all of the other patients' breath.
So actually. This patient isn't hyperventilating in any way. It's got a high respiratory rate.
What it is doing is shifting a lot of its dead space rather than ventilating itself adequately. So this patient does require ventilation. Obviously to try and get to the bottom of why they're doing this, it could be it's got a temperature, increased hypothermia, etc.
It could be panting, it could be a pain response, for example, but these are the patients that need your support, because these patients will lead to potentially a respiratory crash, essentially they're not able to get rid of their CO2 properly absorb oxygen. So these are the patients that do need your intervention whilst you deal with why this is happening. There is something called a recruitment manoeuvre which you may Need to weigh up whether this would be indicated, there's a couple of conditions that it might be indicated in.
So if the patient's not doing well, in any way, whether that be it's desaturating, etc. And obviously arterial blood gas analysis would help in this instance as to how bad things are, or you suspect that this patient might not recover well, so maybe they've been a diaphragmatic hernia, it's been there for a few days. Well, despite you, well, the surgeon sort of removing the intestines and everything else out of the chest, the lungs are still quite collapsed down cause it's been quite a long period of time.
So essentially a recruitment manoeuvre reopens collapsed alveoli, a bit like blowing into a latex glove, or a marigold glove and popping the fingers out. So essentially that's what that does. Now it's not risk free.
But usually chronic cases, as I say, diaphragmatic hernia, pleural space diseases, and sometimes severe abdominal disease where it's been put in pressure on the diaphragm for a prolonged periods of time, could benefit from a recruitment manoeuvre. So we're basically reopening those collapsed alveoli and so better gas exchange can take place. Ensure the blood pressure is normal first, and again, this is all in discussion with your veterinary surgeon.
Because there are big risks. But essentially what it means is you close the appeal valve and you press the reservoir bag and hold it a pressure of around 1020 to 30 centimetres of water for around 5 to 10 seconds. Now it is reported up to 30 seconds in some literature.
Personally, I think I feel a bit uncomfortable with that because that pressure within the chest will massively reduce venous return for all that time. Observe the SPO2 for increase, and if you see an increase, you may, you know that there has been a positive response to that. So it might be that that needs then again repeating a few minutes later because they can collapse back down again pretty quick.
Often if you do have a mechanical ventilator once you've done a recruitment manoeuvre. You should put them on what we call peep, so positive end expiratory pressure, so you're just preventing the alveoli from collapsing completely back down again. Re-expansion pulmonary edoema and reperfusion injury is a massive risk with this.
So what you can essentially get is a reaction to that being popped open so you can get. Essentially, lots of toxins being, being released and that alveoli is now reperfused, and you can get a pulmonary edoema secondary to that. But if the patient really isn't doing well, it can be a little bit of an emergency intervention to help it through that recovery period.
So again, it is not risk free, but it can be very, very beneficial. Now, ventilator considerations specifically for respiratory disorders, I just wanted to go through a few individual ones, but as a general rule, most respiratory patients will have an increased work of breathing, so muscle fatigue is really common and obviously. Will get worse as that time goes on.
Excuse me. What we think of I've put in quotation marks as stable, respiratory patients will often decompensate at any point really, but especially with induction of anaesthesia. They've obviously got an increased respiratory rate and effort.
Their muscles are working really hard. We then go and induce anaesthesia, which not only depresses the brain itself centrally from a respiratory drive, but also profound muscle relaxation. So these patients can massively decompensate really, really quickly when we induce anaesthesia.
To really be prepared with these patients and have the equipment at hand to ventilate from the very beginning of anaesthesia. So Boas patients often live hypercapnia. So just also mention these because these are the ones that people are are unsure whether to ventilate or not, or sometimes they do have.
At complete apnea. So chemo chemoreceptors like we discussed earlier, in those patients they become less sensitive to the changes in CO2, and they're quite, they're quite commonly hypocapnia under GA. Really, really severe, whereas patients can convert to what we call the hypoxic drive, so where the oxygen receptors take over their drive to ventilate, and then we go and place these patients on 100% oxygen.
And they go completely apic. I've only seen it a couple of times and it is really, really severebo as patients. The majority of them are just often really hypercapnic on the GA.
They still, ideally we should be initiating ventilation if they get over the 60 mark, because essentially they will still release catecholamines, etc. And overtake the myocardium. But essentially we expect these patients to be hypercapnia once we've induced anaesthesia.
The biggest CT tube we need possible, we know that anyway, because we don't want to create any resistance, but obviously if we need to ventilate these patients, especially we need to give them a good airway, and we don't want any mucus plugs completely obstructing as well and the tube. They may need to have an increased expiratory time, so a big, big patient, Frenchy, some of these French bulldogs now are really, really big, dogs, but essentially if they're only able to have placed a 5.5 ET tube.
That's a huge tidal volume to put into the chest and allow to expire essentially through a straw. So we need to often increase our expiratory time for that to happen. And I just thought I'd say blood pressure is often affected in brachycephalic anyway because they have high vagal tone, so they often have lower heart rates, for example, so we can often make blood pressure much worse with, with ventilation.
So these are the ones that need blood pressure support. Asthma and bronchitis, so most won't require ventilatory support, but I just thought I'd mention it because bronchoconstriction is a risk. They're a risk anyway, being asthmatic, but especially when we intubate that patient and especially when we, potentially ventilate this patient.
They might require longer expiratory pauses for the exact same reason as I discussed with the brachycephalic, so we need to allow that time for that tidal volume to come back out and especially if they're a little bit bronchoconstricted. And we want to use lower airway pressures than normal, so around that 8 to 10 mark for a cat, for example, and a higher respiratory rate to achieve adequate ventilation because we don't want to upset those airways and cause any more inflammatory reaction. Laryngeal paralysis and tracheal collapse, most won't need ventilation support, but the ones that do is if the trachea is collapsed beyond the point of the ET tube.
They're also prone to bronchoconstriction, so you can obviously see the dyspnea and the resistance on lung expansion like you would in asthmatic patients, and they can desaturate. And it can look like an obstructed idal CO2 trace as well. So that's with the asthmatic patients and these patients.
Plural space disease, so I'm gonna talk about pneumothorax separately. So fluids accumulated in the pleural space and prevents those lung expanding fully. So ventilation will be affected, obviously the more increased volume you have in the plural space, the more ventilation will be affected.
Aytosis, which is collapsed alveoli, is very common and especially with chronic cases that gets worse. Most do require some ventilation support during anaesthesia. Especially when we induce anaesthesia, those compensatory mechanisms that increased respiratory efforts, will, will go when we induce anaesthesia.
But emergency thoracocentesis is obviously in the cases that need to be prepared for that at the induction, so have everyone there ready. It is very much a bit of a toss up a balance between low respiratory pressures to prevent this what we call what I called before re-expansion, pulmonary edoema or reperfusion injury. So we don't want to upset the alveoli too much and re-expand them too quickly or too firmly, but we equally don't want any more alveoli to collapse and cause even further atylaxis, so it's, it's a balance there.
So we're aiming for 10 to 12 centimetres of water roughly and a respiratory rate of 10 to 20. Pneumothorax, ideally we should allow to breathe spontaneously. IPPV can make pneumothoraxis worse in some cases, especially tension pneumothoraxis.
So we're going to be pushing air into that plural space when we're forcing air into the lungs. So ideally let these patients breathe spontaneously. Ruptured buller cases as well can have really friable alveoli, so we could potentially rupture more as well, so we don't want to do that.
But obviously sometimes, in some cases they do need ventilation. So, ideally don't avoid, don't go over a peak in spiritual pressure of 10 centimetres of water and 8 to 10 breaths per minute. We're just trying to maintain normal apnea, and a normal oxygen saturation, or at least over 90 with these patients until we've dealt with the problem.
So we don't need to go too hard and too heavy with this, these patients. We just need to keep them a little bit more stable. Fractured ribs and flail chests are often, often unable to ventilate normally.
And the fly segments pulls back in during inhalation as well. Require ventilation until the segments can be surgically repaired. Lower tidal volume again and higher respiratory rate in order to achieve your normal apnea.
Ensure really good analgesia as well because these patients have got fractured ribs. So we need to make sure that we support them with analgesia. And always observe for signs in your thorax because fractured ribs can puncture the lungs.
Therematic hernias, organs are compressing the lungs and therefore preventing the full expansion. They often have pneumothoraxes and other comorbidities, it's usually from an RCA for example, but it could be a . One where they've had, sorry, completely forgot the words when they when they can be born with diaphragmatic as well, but that's quite rare.
So it's usually from some kind of trauma, so they often have other comorbidities. The inflammatory response can cause pleural fluids and contusions, and then they, they're almost always present to some degree. So these have got a greater risk of re-expansion pulmonary edoema and the reperfusion injury.
Because often the cat that goes missing for a couple of days and comes back, it's it's obviously been quite chronic, and they are at greater risk or the congenital ones, that was the word I was looking for, congenital er ones have got a greater risk of that as well, so we just need to be really careful. Tilted boards can aid ventilation as well, so we tilt them slightly and the organs that are within the chest can sometimes . Sometimes they can fall out a little bit back into the abdomen, but at least they're not putting too much pressure on the lungs.
Lower tidal volume and peak inspiratory pressure and the higher respiratory rate again to avoid re expands and those alveoli too quickly. OK, blood gas analysis then. I appreciate that that was a lot of information to take in.
And blood gas analysis, can be a little bit more tricky, but, I'm hoping that I've sort of made it a little bit easier for you. And if you have got the option to sort of grab a coffee, then please do. So why do we use blood gas analysis?
So we use it to assess acid-based status, and we use it to assess respiratory function. We are also able to assess dependent on the machine because they're getting better sort of every year, I suppose they they can measure electrolytes, glucose, lactate, and our machine now measures kidney parameters, so they can be a great tool to just use for a quick overall picture of that patient. This helps us to treat the patients appropriately and it can allow us to develop a diagnosis or rule one out.
And it can also assess response to treatment. So if we put treatments in place and we want to assess the response, it can be great for that as well. Two types of samples, so we've got venous and arterial.
So Venus is the most common that we use, and we're going to focus on arterial today, but I thought I've mentioned that venous can be used for most things, acid-based status, so you can still use it for acid-based status and electrolytes. It just can't be used for respiratory function. It can be used to assess oxygen extraction, but I think if we want to look at the oxygenation of a patient, we often take an arterial blood sample.
So the arterial one it can assess adequacy of ventilation, so how well you're performing your ventilation. It does require though a sampling of an artery, and it requires a heparronized syringe with the air bubbles removed and then run immediately, so you need to be able to run this immediately in order to get the most accurate results. So I'm just gonna show you a little video at the moment of an arterial blood gas being taken from an arterial cannula that has been placed.
We need to take it really slowly and over a good few breaths in order to get a full picture of what's going on. I'm just gonna show you this. So we're just taking it really slowly.
This is the patient before actually that I showed you was being ventilated. So we've just removed. Sorry, we should always remove a small amount of blood first, and then this is now our heronized syringe being connected, and this is where we are actually now gonna take the sample.
My apologies for that. So we're just removing a little bit of blood first and then we will take our sample in our heronized syringe, slowly over a few breaths as you can see. Closing our three-way tap.
And we're now gonna make tables this year. So we need to get rid of those air bubbles in order to accurately measure what's going on. So they don't affect our results in any way.
So the dorsal pedal artery, which is what that patient had the cannula in, is the most common site to use. You locate and palpate the pulse, so we're not gonna visualise anything. You're not gonna raise anything and you're not gonna see the artery in any way.
You might occasionally see it in a greyhound's pulsate. We're gonna clip and prep the area for sampling. And with the blood gas syringe and needle, this one has a cannula in the video I showed you, but you can use a needle.
We're gonna insert the needle, using, as I say, palpation technique for a pulse and take a sample of at least two respiratory cycles, ideally a little bit longer. Place a pressure bandage for 1 to 2 minutes after the site because obviously it's an artery so we don't want to cause any haemorrhage in any way. Just make a note that that does need removing as well.
We don't want to put too much pressure on that for too long. Now what you should always do when you, when you're taking an RCO blood gas sample is to note the Nidal CO2 on your catnograph at the time and also your inspired oxygen. So whether you're taking this on room air, maybe it's a very sick collapsed patient, or usually our patients are on 100% oxygen during anaesthesia, so you just put, make a note that they're on 100% oxygen.
For those that have gas analysis, you can note the exact figure of FIO2, so that's fractional inspired oxygen. It's usually anywhere from 97 to 98 to 99, so it often doesn't really make that much of a difference, but if you want to be exact, you can do. If you're using an arterio cannula, as I said in the video, we withdraw a small amount first and then discard that, and then we attach our syringe and take the sample.
Common errors, so if the sample is left uncapped for any reason, or PACO2, so the carbon dioxide within the blood can decrease and the pH can increase. You can get a large air bubble as well if we leave that in. Our oxygen can increase and CO2 will decrease.
And if it's left unchilled, so if it can't be run immediately, you can put it on ice, but if we just leave it sort of on room temperature, the oxygen can decrease and the CO2 can increase. I wouldn't necessarily focus on what can increase and decrease, but it's just to let you know that we need to cap it, get rid of any air bubbles, run it immediately, or put it on ice. And then essentially when we're looking at specifically the blood gas analysis, what we're looking at is these three things.
So we're looking at PH, PACO2, and PAO2. So our pH is important for normal cellular function and the homeostatic mechanisms within the body keep the pH within a tight range for a very good reason. The pH for cats and dog and sort of mammals is 7.35 to 7.45.
That is the normal reference range. Death is associated with a pH of less than 6.9 or more than 7.8, so.
You can appreciate that that is not that sort of far away from the normal reference range, so this is why we need to keep, keep acid-based balance normal. So we do need to respond really quickly when the pH is less than 7.1 or getting towards the 7.65 mark.
So we need to be really responsive to this because we know that death can be associated with a sort of slightly less or more than that. If we have a pH of less than 7.35, this is known as acidemia.
And if we have a pH of more than 7.45, it's an alkalemia. So our PA CO2 is the one that we're gonna look at next.
So we looked at, we've looked at RPH and we know whether there's an asidedemia or an alkalemia. So we've already got half of the answer that we need. The CO2 is the only respiratory gas that affects pH so oxygen doesn't.
Ventilation is responsible for CO2 levels like we discussed. So if the pH is less than 7.35, there's an asidedemia, and if the aide is too high, so it's over 45 millimetres of mercury, we have a respiratory acidosis because we know that we're acidotic, and we know that it's caused by the respiratory system.
So it's a respiratory acidosis. If we have a pH of more than 7.45.
So that we've got an alkalemia and a CO2 of less than 35, so low, we know that we have a respiratory alkalosis. So we've got our first answer because it's alkalotic and we've got our second answer being the respiratory system being the problem. If we have a pH of less than 7.35, so we are acidotic again, so we have an asidedemia.
But actually the CO2, it could be normal or some quite often, it's less than 35, so less than what it should be, so low. This is often a compensatory response to metabolic acidosis, so I'm not going to go through the metabolic acidosis values, because that involves bicarbonate and base excess and stuff, so this is just about the respiratory system. But if you ever notice that, it's usually a compensatory response to the metabolic problem.
So it's a metabolic acidosis is the problem, and we're trying to blow up a bit more CO2 in order to try and correct this pH. If the pH is more than 7.45, we are alkalosic and the CO2 is more than 45.
Then obviously this is high, so this is not quite marrying up with a respiratory problem. It can be a compensatory response to a metabolic alkalosis, so slow our breathing down and try and increase, . RCO2 and therefore decrease this pH.
The oxygen and SPO2 I wanted to talk about, so that's the promise that we're gonna look at, sort of lastly with our respiratory, blood gas analysis. So SAO2 is the saturation of oxygen bound to haemoglobin in arterial bloods, and that makes up 97%. Of our, how our oxygen is sort of transported if you like.
And then our PAO2 is the partial pressure of oxygen that is dissolved in plasma and that's only 3%. It's still a very important 3%, but there's very small amount that then is dissolved in plasma. Now our PA02, when you're looking at an arterial la gas sample, should be 5 times the fractional inspired oxygen, so 5 times the oxygen they are inspiring.
So room air is 21% oxygen, so you should have a PAO2 of around 100 millimetres of mercury. When we move to 100% 02 that we're delivering with our most of our anaesthetized patients, we should have a PA02 of 500 millimetres mercury. This is obviously if all is well and the patient is healthy.
However, what I wanted to go through is that on the next slide is there is very little difference between an SAO2 or SPO2 reading. Of 90 to 100% which I explained on the graph. Despite this correlating to a PAO2 of 60 to 500, I'm gonna go through that because that's a little bit confusing on the next slide.
But it's just to demonstrate that actually SPO2, when animals are on 100% oxygen. Isn't reliable until there's a massive, massive problem, so let me just explain that slightly. So this is the oxygen disassociation curve.
So this essentially is SPO2 on here, and along the bottom here is our PAO2. So it's just showing you the relationship between those two. So if we had a PAO2 of 100, so we're on room air, we've got healthy patients, we go up to here.
And our SPO2 should be around 98%. 98, 99%. OK.
Then we place this healthy patient on 100% oxygen and we should have a PA02500. And we go up there and again SPO2 should be 99, 100. So, essentially between here, there's very, very little difference.
So if we've got a patient that has got, is on a 100% option. But actually they're struggling a bit with the respiratory system. You won't necessarily see it on your SPO2 yet, but you would see it on your arterial blood gas analysis.
So it might be that you take a a sample and the patient has a PAO2 of 200. So a lot less than what it should be, it should be 500 in the healthy patient. We've got it at 200.
Your SPO2 will still say 99 to 100% because there isn't a problem. The only time that your SPO2 will detect a problem is when we get to less than 100 and it massively falls then. So even when we are around 90, we've got around an SPO2 of the, sorry, the low 90s there.
It's only when we get to less than that it massively dramatically falls. Why I wanted to say this is just because a respiratory patient might be fine on the GA and it's only when you get into the recovery period, when you place them back on room air, that you will get a problem, that you will see a problem. So it's really important to monitor SPO2 throughout anyway.
So I'm not saying SPO2. It is invaluable during anaesthesia, it is because it will definitely detect the problem if there's a problem with that patient, even things like someone's knocked the flow metre off, etc. So it will definitely detect the problem, so always have it on your patients.
But also, whilst you're recovering that patients and taking them off oxygen. You should be monitoring the SPO2, especially for respiratory patients. You should be able to see if they can cope on back on room air before you then move them to the recovery period, because often what they need is oxygen support in that time.
So I just wanted to sort of demonstrate that that SPO2 and PA02 relationship. This is a table that I I made I don't know if you want to take a picture of it. It's just a little bit of ease when you're looking at an arterial blood gas analysis sample.
So, just gives you the indications of whether the whether even if respiratory acidosis, this is what you should see, and a spiritual alkalosis as well, and I have thrown some metabolic things in there as well. As I say, we haven't got time this evening to go through that, but that is on the chart. And in summary, so to initiate mechanical ventilation, we, it would be if the patient is moderately hypercapnia, so over 60, 50 to 5 having a cat, moderately hypoxemic, moderately, sorry, metabolically acidotic.
Open chest surgery, increased integrated pressure, a question marked neuromuscular disease just because they don't all need support, but you should monitor that respiration really closely if they do have neuromuscular disease. And adjust ventilation settings in line with the disease of the patient to maximise the outcome and prevent any further damage. And utilise arterial blood gas analysis to assess your patients and response as well because it can be really important to assess what's going on, as I say, there can be differences in the respiratory patients.
So, even though you're entitled CO2 might say. It has an entitled CO2 of 35, you take a blood gas and it might be a lot higher than that because the CO2 isn't able to be expired because there's a problem within the lungs, so it can be really valuable to see what's going on with those patients. And thank you and hope you enjoyed the session.