Thanks, Bruce, for the introduction. So the learning outcomes for this session are to, give you a better understanding of how to describe how, the depth of anaesthesia can be assessed, to define the normal ranges for commonly measured parameters in conscious and in anaesthetized patients. To understand how an altering physiological status might be reflected by changes in these parameters, to discuss the practical uses, limitations and benefits of various monitoring modalities.

And to give you a better understanding of how to identify commonly seen abnormalities in a range of monitoring modalities and how and when we need to treat them. So anaesthetic monitoring. So the American Society of anaesthetists, basic monitoring standards require us to monitor our patients for oxygenation, ventilation, and circulation.

And there's been a number of, studies and research undertaken into monitoring modalities and how they can help us look after our patients under anaesthetic. And they have found quite clearly that monitoring our patients during anaesthesia decreases the odds of anaesthetic death. And similarly, a lack of monitoring can increase the odds of anaesthetic death or, morbidity or mentality rates by 5 to 35 times.

So just actually applying some monitoring, whatever you've got available in your practise can actually really decrease the odds of a problem occurring with your patient. So what equipment can you use? So yourself, I mean, you are probably the best, you're the key item for your patient under anaesthetic.

There's no point in having lots of equipment attached if we don't know what they're telling us and we don't know how to interpret it. But also just having someone that's responsible for that patient that's overseeing it is gonna be the most valuable tool that that patient can have under anaesthetic. We have a variety of, equipment modalities that we can attach to our patients now.

They could be as simple as a stethoscope, but there are some much more sophisticated monitoring, machines now that we can attach to, just to help us during this anaesthesia period. And they could be multi-parameter monitors, like the one on the left here, which gives us a wide range of monitoring options. Well, you can get standalone machines, which are normally a little bit cheaper, but they're more likely to be kind of individual.

You can see this one on the left is actually a pulse oximeter, but it does have the added bonus of the Capnograph. So it really kind of depends on what availability you have in your practise as to what you can use. So if we start by looking at how we can monitor the depth of the anaesthesia, we're looking at having kind of a 4 stage approach to anaesthesia in general.

So we go from stage 1, being awake to stage 4, which is very deep. So what we're looking At when we're anaesthetizing our patients is to maintain an anaesthetic depth, kind of in the mid-range. So we're looking for a happy medium.

So that being kind of stage 3 medium plane, where we've got a nice ventral medial rotation of our eyes. We have probably just an absent palpable reflex with a kind of diminished response to surgical stimulation. You can see as we go up the stages into deep and very deep, our eyes start rotating back to the ventral, the central position, sorry.

But you can see the pupil has dilated, whereas when your patient is too light, that the, you still have a central eye position, but you can see a bit of a pupil constriction. So that's kind of how you can kind of determine where you are. So how can our kind of monitors help us during anaesthesia?

And we've only got kind of about an hour to talk about it. So I'm gonna just overview kind of the common common parameters or monitors that we can use that are kind of common in our practise. So we'll go over ECG, we'll talk a little bit about pulse oximetry.

We're gonna overview the capitalnography and some catnograms and what they're telling us and how we can interpret them. And finally, we'll talk a bit about blood pressure, how you can monitor it and what you can do to kind of respond to changes in in our blood pressures in our patients. So what is an ECG?

So, it's basically also known as electrocardiography, which is a vault metre that records the electrical activity of the heart. And what it's doing is it's recording the activity of, of kind of heart cycles. So, as the, in order for the heart to contract and maintain circulation, we need to have depolarization and repolarization of the heart muscle cells in order for it to pump blood around the body.

And it does this by means of positive and negative electrodes. So why would we want to take an ECG or why would we use that during our anaesthetic? So it's basically going to give us a heart rate and a heart rhythm.

And knowing the heart rate's normal is key to making sure that we've got cardiovascular stability, but also knowing the rhythm of our hearts is gonna give us a really good indication of any abnormalities which could compromise our cardiovascular system and result in a cardiovascular collapse or a cardiopulmonary arrest. So, as well as heart rate and rhythm, our ENG can also tell us if there's a chamber enlargement. Maybe there's evidence of myocardial disease.

Some electrolyte disturbances, such as, hyperkalemia or hypokalemia can, can present with ECG changes. Some certain drug toxicities can result in ECG changes. Patients with pericardial disease or myocardial infarct or ischemic.

So if they've had periods of absent blood flow to part of the tissues, we can also sometimes be able to kind of see that on an ECG because it results in an abnormal trace. So how is the ECG formed? So we're looking at the middle at a normal sinus complex.

So we've got a P wave, our QRS complex, and our T wave. So this is kind of what we will, compare all of our ECG rhythms to. So when you look at how the ECG is formed, the P wave is basically representing the sinoatrial node firing, which is basically the heart's pacemaker.

So that's what controls the heart rate. And what happens here is the sinoatrial node fires. The electrical signal kind of spreads across the atrium to force or to initiate atrial contraction.

We've got a little gap there between the P and the QRS, and this is basically called the PR interval, which then allows the blood to flow through the right atrium, through the atriums into the ventricles, and then allows that electrical signal to reach the atrial ventricular node. Now, the atrial ventricular node is there where the, electrical signal kind of starts, and that's what initiates our ventricular contraction. And the QRS complex kind of represents entire ventricular contraction, but it can be broken down into Q, R, and S waves.

The Q wave being the ventricular septum depolarizing and contracting, the R wave, which is the downstroke, is representing the, the outside of the ventricles contracting, and the S wave is looking at the top of the ventricles just contracting, but it all happens so quickly that it all kind of happens all at once, and you kind of get this nice QRS complex. And then finally, we're looking for a T wave, which represents repolarization. So that's the relapse of the heart, the reset of the electrical circuit to allow the next heart cycle to take place.

So when we're looking at interpreting ECGs, there's a number of steps that we can follow to make sure we look at it in its entirety. So the first thing you want to do is look at the heart rate. So determine whether that's normal first.

Then you look at the rhythm, and you're looking to see the rhythm of the complexes to, to see if they're kind of regular, or if they're regularly irregular, or if they're kind of all completely all over the place, and we would then call it irregular. When you look at each individual complex, you then need to make sure that it's got a P wave for every QRS. So that's the first kind of wave which shows us that that's a sinus complex because it's originated from the sinoatrial node.

And then is there a QRS for every P? So if you've seen lots of P waves, is there a QRS complex associated to show us that that signal has then reached the X-ray ventricular node and therefore, we've got our ventricular contraction. And then lastly, do the waves look normal?

So are we actually able to compare that to this normal ECG which is on the screen here? Does it look normal or do the waves look abnormal, which again can tell us that there is a problem. So we look at these common common sinus rhythms, and we can tell they're all sinus rhythms because they've all got P waves.

We've got bradycardia, which is basically a slow heart rate. So you can see on the top, the heart rate is 40, but all the complexes are normal. They've all got PQR, S and T waves.

There's a P for every QRS, there's a QRS for every P, and the shape looks normal, it's nice and regular. So that's a common sinus rhythm called bradycardia. Tachycardia is basically an increased heart rate.

So you can see here, the heart rate is 200 beats per minute. All of the complexes look the same. And you can see there's a P for every QRS, a QRS for every P.

Although the T wave, I think because the heart rate is so fast, we're kind of just losing the T wave a little bit, just into the P wave. So you can see there's kind of a little, a little, A a little bulge and then the big pee wave starts again. And then lastly, we've got sinus arrhythmia, which, again, all of the complexes look the same, but we've got an irregular rhythm, but it's regularly irregular.

So if you look at this, you can see there's. A slowing of the heart rate, and then an increase of the heart rate. And it's quite regular.

So we've got 4, sinus complexes, a bit of a pause, and then we've got 4 sinus complexes and a bit of a pause. And what happens here is as the animal's breathing in, the heart rate increases, and as they exhale, the heart rate slows down. So do we need to treat these?

So if we start with the sinus bradycardia, I think the first thing you need to do is look at your patient's depth and see if the animal's depth is too much, and you can reduce, the volatile agent or whatever maintenance agent you're using. We typically see sinus bradycardias when patients are a bit too deep. Evaluate your blood pressure alongside, the heart rate to determine whether you've got adequate perfusion of the tissues.

Because if your heart rate is kind of around 40 and above, then we're normally happy with maintaining them heart rates, as long as our tissues are still getting the, the blood that they need. So we've got adequate blood pressure to deliver oxygen to the tissues. I think we need to be concerned when the heart rate starts to reduce below 40 beats per minute.

And in that case, we would need to kind of treat to increase that heart rate, because kind of lower than that, we're kind of bordering on, problematic where it could just kind of collapse at any stage, or if the blood pressure drops, we're gonna be in some trouble here. So you can increase the heart rate with anticholinergics, and the anticholinergics work on receptors within the heart, which increase the sinoatrinode firing. So we can treat with atropine or glycopyrelate.

And both drugs will work to increase the heart rate, and alongside, you'll probably see an increase in blood in blood pressure. You just need to be a bit careful by increasing the heart if you've got a reason for the bradycardia. So we expect to see a low heart rate, if we're using medoomidine.

And that's because we get the intense phase of constriction from using the drug, and then the, the body actually recognises an increase in blood pressure, and that's why the heart rate starts to drop. So increasing the heart rate at this point would probably just cause more problems and you just increase the workload of the heart because the vessels are still construct constricted, sorry, with Medoramidine. That we would more likely be better off to antagonise or reverse the effects of the mediomidine if we're worried about heart rate and blood pressure in these patients.

You can see bradycardia if, patients are becoming hypothermic. So you might find that if you're trying to treat bradycardia with drugs, that they might not work if the patient's temperature is too low. So increasing body temperature and mono and kind of maintaining normothermia as much as possible is probably gonna help here.

And then treat the underlying cause. There are kind of various reasons why we can get sinus bradycardia, such as a patient with electrolyte disturbances or some, some primary kind of heart conditions. So knowing the reason for the bradycardia, you can treat it by treating the underlying cause.

Sinus tachycardia. Again, check anaesthetic depth. We normally see increase in heart rates if depth is too low, so the patient has become too light.

You see an increase in heart rate if patients are painful. So checking the anaesthetic depth, increasing that or providing additional analgesia is gonna help here. Check your blood pressure.

Make sure that your blood pressure is not too low because you can have a reflex increase in heart rate. Because the blood pressure is too low and that's the body's compensatory mechanism. So check for blood loss, speak to the surgeon, check your suction and make sure you haven't just had a massive haemorrhage that you then need to treat with fluids or increase in the vascular volume.

You can also see increases in, heart rate if your patients are, have a low PCV. So if they have a low haemoglobin level within the blood, they're unable, or they increase the heart rate in order to deliver oxygen to the tissue. So in these, these cases, if you've got anaemia, you might find your patients have tachycardia as well.

And then sinus arrhymia is a normal common arrhythmia in dogs, and we don't need to treat it, but you can do by increasing the heart rate. So conduction abnormalities you can have, and that's where you have an interruption of, the electrical circuit or a delay. So your first degree AV block is an increased PR interval.

So that's just a delay between the signal reaching the AV node from the sinoatrial node. A second degree AV block, you can see where we have loan P waves. So we don't have QRS complexes for every P wave here.

And then a 3rd degree AV block. It's a complete heart block. So we've got no, we've just got PE waves.

We've got no associated CRS complexes. And what you can see on the screen is called an escape complex. So this is a ventricular ectopic beat, which doesn't occur, or doesn't originate from the sinoatrial node, and that's basically the heart trying not to kind of collapse and not arrest.

So what do we need to treat? So the first degree IV block is not normally clinically significant, but you can check your electrolyte levels because sometimes that can cause, first-degree IV block. And normally, actually, we probably wouldn't even notice this first degree AV block on most of our monitors.

Just monitor your heart rate and blood pressure. Your second degree IV block is treatment isn't always necessary, but increasing the heart rate is going to alleviate this. The same goes for the bradycardia treatment with atracrine and glycopyroli.

But again, be careful with your mediomidine induced AV blocks. You'd probably be better here to use atipamazole if you're concerned, but if your blood pressure is normal, then this block isn't normally, a problem as long as it's not increasing in frequency. Your 3rd degree IV block is your problematic conduction abnormality, in which case this patient is gonna need a pacemaker because there is a complete block of electrical signal into the, the ventricles.

So at some point, we're gonna have an issue with this patient either kind of fainting, collapsing, or having a cardiopulmonary arrest. Ventricular rhythms, you can see are basically ectopic beats. So again, they're not originating from the normal course of the sinoatrial node.

So if you look at the top ECG, we have a range of normal complexes. So we've got a normal heart rate, the rhythm is normal, we've got, lots of Ps with associated QRS's, but you can see this one in the middle. Hasn't, is abnormal.

It's wide and bizarre, and there's no associated P wave. And that's telling us that we've got a ventricular premature contraction. And that's a contraction that that's occurring early within the heart cycle.

So the sinoatrial node hasn't fired this. So this is just kind of a random depolarization of, of, of the cells within in the ventricles. The bottom rhythm is called ventricular tachycardia, and that's defined when you've got a run of 3 or more ventricular premature contractions.

So what do we need to treat? So BPCs or ventricular rhythms can occur with primary and secondary heart disease. They can occur in sepsis.

You can get them with pain. So trying to kind of localise and find out the problem or what's caused it is gonna help you treat it. So treat the underlying cause.

Infrequent VPCs can be monitored. They don't usually affect cardiac output, blood pressure for too long, but more, as they begin to become more frequent and then kind of proceed into ventricular tachycardia, you're then gonna have an issue with maintaining cardiac output and maintaining blood pressure. And usually we've got high heart rates here, so we have a problem with kind of blood flow within the heart to be able to deliver adequate volumes.

Treatment of ventricular arrhythmias is with lidocaine, and you can If you've got maybe infrequent VPCs, you could treat it with just a bonus of lidocaine, but it's kind of normal for us to need a CRI of lidocaine in order to treat ventricular tachycardia. And the problem with sustained ventricular tachycardia is that you can end up with ventricular fibrillation, and this is where your patient arrests. We've got no heart rate, we've got no blood pressure, and at this point we would need to initiate CPR.

So moving on to pulse oximetry. So pulse oximetry is a noninvasive monitoring modality, and it measures the Boston saturation of arterial blood. And what we're looking for is a saturation of more than 95%.

It'll also give us a pulse rate and a pulse rhythm, and you can use this alongside an ECG if you have one, to look for, any pulse deficits. So it's gonna tell us if we've got, a difference in heart rate and pulse rate. So, looking at them both synergistically is gonna tell us if we, if each heartbeat that we've got, it has an associated pulse with it.

Pulse oximetry works by using red and infrared light, and it measures the difference between light absorption, basically within in the cells. So oxyhemoglobin, so that's oxygen-rich haemoglobin, absorbs more infrared light. And and haemoglobin without oxygen, so deoxyhemoglobin, absorbs more red light.

So it looks at them both and then it, measures the difference between the two and then gives us a percentage, result, saturation result. I think it's important to know with pulse oximetry that it's not an indication of our partial pressure of oxygen within our arterial blood, but it is useful to alert us that we could have a problem with low oxygenation. And you can look at the oxyhemoglobin dissociation curve here to kind of determine the level of hypoxemia as your pulse ox kind of value reduces.

So the normal PAO2 of a patient, breathing room air, which is 21%, we're looking at as a rule of thumb about 5 times the inspired concentration. So room air, we're looking at a PAO2 of around 100 millimetres of mercury. So as the PAO2 starts to drop, we can have a very normal SPO2 right up until the point where we get down to around kind of 60 millimetres of mercury, with oxygen saturation within our arterial blood.

And that's kind of indicative of quite, quite severe hypoxemia. So, It's a good tool for, for alerting us that there could be a problem, but it's not gonna overall tell us whether we've got a, an oxygenation issue. The only kind of only way that we're gonna know that for sure, is by doing an arterial blood gas, measurement.

That's not to say that it's not useful, and I use it all the time in like, my, recoveries for patients just to check for oxygen dependency. There are some limitations with pulse oximetry, so if you've got a patient with vasoconstriction, maybe we've given the meatomidine, you're less likely to get a good trace. If you've got a patient that's hypertensive, in which case they're normally vasodilated, and then we, it might struggle to, to locate kind of haemoglobin.

Patients with pigmented mucous membranes, or if you've got a patient with a dry tongue, you might get a reduction in signal. And they have shown that using a wet swab in cases where you've got a low, a low saturation or not a very good trace can increase the signal and therefore you get a better trace. But I think with pulse oximetry, Because it's, most of them are on a spring, you're likely to see a reduction in the saturation over time, and in which case, I tell people not to panic, maybe just replace it to a different part of the tongue, and then kind of make sure that it is actually a true reading.

If it is starting to become low, then we need to investigate why that patient might be hypoxemic. So catography is a continuous and non-invasive piece of monitoring equipment, and it was introduced by Doctor Loft in 1943. So it's been used for a long time and it was developed as a monitoring tool for use in anaesthesia and intensive care, and they used it for a lot in kind of ventilated patients in the ICUs.

Used in its basic form will give us a respiratory rate and a, and a rhythm. And it will also give us a measurement or partial pressure of carbon dioxide, and that's expired CO2 or and inspired CO2. So expired CO2 is abbreviated to Nidal CO2 or ETCO2.

So how does acanograph work? So it uses infrared technology like the pulse ox, and carbon dioxide absorbs infrared radiation. So a beam of infrared light is passed across the gas sample and onto a sensor, and the presence of CO2 in the gas leads to a reduction of the amount of light getting to the sensor, and then the sensor is able to kind of determine the result, as an entoal CO2 region.

And it's presented on a graph as ntidal CO2 plotted against time. So size stream or mainstream, so a mainstream catnograph, it goes between the ET tube and the breathing system, and that's going to give us an end, a true end tidal real-time idal CO2 level. It will also give us a respiratory rate.

Side stream takes a portion of gas from the breathing system and delivers it to a monitor. So you've normally got a bit of a delay in, in your trace from that breath, if that makes sense. So it takes time to get back to the machine.

However, you'll also normally get a catnogram with a side stream monitor, whereas the mainstreams, they're really small, and they're on the breathing system, so you're less likely to get such a good catnogram trace that you can then see lots of other issues with. So what other information do we get from acapnograph? So it tells us about carbon dioxide production.

So that gives us an indication of cell metabolism, because carbon dioxide is a waste product of oxygen metabolism. It tells us about gas exchange, and that's really important in monitoring oxygenation and ventilation in our patients. So, if we've got tidal CO2, if the patient is actually breathing out carbon dioxide, then we know that we've got perfusion to our lungs, and we know that we've got ventilation because the gas has been exchanged from the blood into the lungs to be exhaled.

It can also tell us if we've got an intubation error, so we won't get an entitled CO2 if we've intubated the oesophagus. It can also tell us about some breathing system failures and whether that's anaesthetist error and how it's set up, or maybe there's a an equipment malfunction, such as a problem with our rebreathing system. The last thing that it can also tell us is about cardiac output.

So it gives us a really good indication about circulatory status of the patient. So, you know, as I said, carbon dioxide production is from using oxygen. So all the oxygen has to be delivered to the cells in order for carbon dioxide to be, to be made, basically.

And then it then needs to be delivered back to the lungs. So it tells us a lot about how well our circulatory system is working. If you've got good entidal CO2 or normal entidal CO2, then we're, we're probably more than happy that our cardiovascular system is working efficiently enough to remove the CO2 from, from the body.

And reductions in cardiac output will result in decreasing CO2 levels. So what's normal? So we're looking at normal being 35 to 45 millimetres of mercury in a conscious patient.

Hypocapnia or low tidal CO2 is represented as less than 20, and high or hypercapnia is represented as more than 50 millimetres of mercury. Often in cats, particularly with side stream monitors, we find that their tidal volumes are quite small, so the portion of gas that's taken out of the breathing system is diluted with some, some kind of normal oxygen and anaesthetic agents. So often in cats, it's normal to see slightly lower end tidal CO2s.

But are we always going to see normal under anaesthetic? No. So most patients under anaesthesia will have a degree of respiratory depression, and that's down to.

Being anaesthetized, all of the drugs that we use, a lot of the analgesics that we use will provide respiratory depression, as well as putting them in positions, maybe on their backs or on their sides, putting, positioning aids and all of that kind of thing on them is going to result in them not being able to ventilate as normally as they would do if they were awake. So we're looking really to aim for values between 30 millimetres of mercury and 60 millimetres of mercury under GA. And it can be quite normal to have a slightly higher tidal CO2 because of this respiratory depression, and it doesn't always need us to do too much about it.

So outside of the range. So if you've got increase in entidal CO2, so CO2 level is increasing, then that could be a result of decreased elimination, which can tell us maybe that our patient isn't ventilating well, or if our circulation isn't taking the CO2 back to the lungs to be eliminated. You can have an increase in CO2 inhalation.

So therefore, therefore, we're doing something wrong, our breathing system is not working very well, in which case, they're rebreathing, basically, the CO2 that they're trying to get rid of. Increase in entitled CO2's above normal level can result in cerebral vasodilation. They can, you can see changes in the blood pH, and you can end up with respiratory acidosis.

So the pH become very low and very acidotic, and you can have an increased risk of cardiac arrhythmias. If your end of CO2, excuse me, is dropping, then it could be because you've got decreased cardiac output. It could be that you've got increased CO2 elimination.

Or it could be an equipment malfunction. But if you've got a, a decreasing entidal CO2, you could have your patient then start to awake because you've got increased elimination, and that could result or could be because they're too light. It does result in cerebral vaso constriction, so the blood vessels in the brain start to constrict, which can can kind of compromise blood supply.

And it could tell you if it drops off very quickly that you've got an impending cardiac arrest. So if we look at the normal catnogram, 0 being inspiration. Phase one is the beginning of exploration and this is where all the gas that hasn't been involved in gas exchange.

It's called dead space gas is removed, so that's all the stuff that's sitting in the, the, the ET tube and the breathing system. Phase 2 is where the alveolar gas, so that's the gas that's, been involved in gas exchange, starts to mix with the phase gas, so it's gonna be a bit diluted. But what we're actually looking for is this phase 3, and that's gonna give us a true indication of our Nidal CO2 level.

And that's where the expired gas consists mostly of alveolar gas. And this is where we get the, the end tidal CO2 reading from. So how do we analyse catnographs?

So this is a completely normal catnogram. The first thing you want to look at is CO2. Is that normal?

Again, like ECG look at the frequency of breathing and see if that's normal and regular or regularly irregular. Is the, the rhythm the same? Is it correct?

Is the height of the catnogram good? Is there a good shape? Does it meet baselines?

So that will give us an indication of whether we've got rebreathing. And the shapes, so we're looking at this being normal and like ECG we kind of compare catnograms to this as normal, to be able to determine what the problem is and where it's originating from. So we'll start with hypercapnia, so we know that that is a high end tidal CO2.

So if we look at this, the endidal CO2 is 54. The respiratory rate is 15. The rhythm is normal.

The height is a bit high. It does meet baseline. We haven't got any inspired CO2, and the shape is relatively normal.

So we've basically just got hypercapnia, which is normally caused by hyperventilation. And again, we depress the ventilation with anaesthesia, a lot of the drugs that we use. So it's normal for us to see slightly higher CO2 levels under anaesthetic.

So it could also mean that if we're manually ventilating our patients that we're not doing enough, or it could be that our patient is spontaneously breathing, but actually they're not doing enough. And in which case we then might need to think about increasing our IPPD or starting IPPD. Patients that are hypothermic are likely to be hypercapnic, and patients with hyperthyroidism can also present hypercapnia.

So how are we gonna treat it? So, sometimes we don't need to treat it. So, as I said before, we're happy with entidal CO2 up to about 60 millilitres of mercury, as long as they're breathing well and you're happy that their ventilation is mostly normal for what we're expecting them to be under GA.

You could look at the anaesthesia depths to see if you can reduce that. Or if you're really concerned, or if it starts to increase or continues to increase, then we might need to think about mechanical ventilation. Hypocapnia is defined as a low entidal CO2 level.

So you can see on here the Nidal CO2 is 15. So that, this is actually reading it from kind of the lowest point at the right of the kenograph. So, the frequency, so the respiratory rate is, is relatively normal at 20 beats breaths per minute.

The rhythm is normal. The height is abnormal. So, we've got a fluctuation in, in these, levels.

We are meeting baselines, so we're not inspiring any, expired carbon dioxide. And the shape is relatively normal. But what we're looking at here, and we're really kind of focusing more on kind of the right-hand side of the catagram trace to determine the fact that actually this patient's got low idal CO2.

And the causes here are, could be a low cardiac output, and that's actually what this this catnogram is telling us, cos that's gone from normal to abnormal very quickly. So that's a quite quick profuse drop in cardiac output. Patients with kind of continuous hypocapnia can be hyperventilating or maybe we're over ventilating for them if we're manually IPPD.

Hypothermic patients, patients with hypothyroid can be hypercapnic. And if there's a leak or a disconnection with on our breathing system, then you can get hypercapnia as well. So the treatment here depends on the cause.

So if they're hyperventilating because of an inadequate anaesthetic depth, then increase your anaesthesia depth, so increase the volatile or provide more analgesia if they're feeling pain. If you're ventilating your patient, then decrease your manually, your manual ventilation a bit because we're probably over ventilating slightly. If you've got a significant drop in in Nidal CO2, it's probably indicative of a, a drop in cardiac output.

So assess this alongside your blood pressure and your heart rate to, assess the cardiovascular status, really. And, or just check your breathing system at this point, because it could be that you've got a bit of a disconnection. So rebreathing is where the patients are rebreathing the expired CO2 that they've, we're trying to eliminate.

So if you look at these, this. Capnogram on the left here, you can see that when we look at the CO2, it's relatively normal. The the the respiratory rate is normal, the rhythm's normal, the height is OK, but we're not making baselines.

So this is where our abnormality is. And you can see here we've got a fresh inspired CO2 of 7 millimetres of mercury. The shape is normal.

So this is caused here by an inadequate fresh gas flow on our non-rebreathing system. So we're not actually removing the waste well. You can also have this as an inefficient rebreathing system because your CO2 absorber is exhausted, or maybe, like in this picture at the bottom, you've got a problem with your unidirectional valves.

They're either stuck they're stuck open or stuck closed, which is allowing stuck open really, because they're allowing kind of movement of gases and mixing of inspired and expiratory gases. So the treatment here depends on what what breathing system you're using. So increase your fresh gas flow if you're on a non-rebreather, and then check your circle system if you're on a rebreathing system to make sure that your absorber is, is fresh and not exhausted and your unidirectional valves are working well.

So cardiogenic oscillations are basically seen with low breathing rates, so you can see the frequency here is low. Our end tidal is still normal. The shape is a bit wrong, isn't it?

So we've got these fluctuations during expiration, and it's basically caused by the heart beating against the lungs, and it kind of results in the breath to be released in stages, which is represented on the catnogram here. It's completely normal, and we don't need to do any treatment for this. It does look a bit abnormal and it can be quite scary to start with, but we're not inspiring any expired CO2.

We've got normal CO2, so we're happy with our cardiac output. And although our, our respiratory rate is low, it's still kind of adequate if you've got kind of a large breed dog. So here we're looking at airway obstruction, and you can define this by the shape of the catnograph.

So if we look at the, all of the other parameters, the CO2 is kind of normalish. This is a cat, so we're happy with the entire of 33. The the respiratory rate is 20, we've got no fresh inspired.

We're making baseline. The shape's just a bit, abnormal, and this is a typical shark fin kind of presentation if you've got an obstruction within your airway somewhere. And this can be caused by a mucus plug in your ET tube, which is quite common in cats.

You can get it if you've got bronchoconstriction, maybe your patient's got feline asthma. You can get it if you've got an airway obstruction, which is a foreign body or a mass. Have a look at your ET tube and see if it's kink, because sometimes if you've got the head in an abnormal position, you can kind of compress the ET tube, which can look like an obstruction or cause an obstruction.

And again, if you've got a patient with feline asthma. So, you can treat this by suctioning the ET tube, maybe given a bronchodilator, if you've got a bronchial constriction. Again, check the position of the ET tube, check the breathing system.

There isn't maybe a, a sandbag or something that's kind of over one of the hoses, which is compressing it, and check the, the, the kind of, position, the position of the patient's head to make sure we're not kinking around too much, which has caused an obstruction. So if we look at this catnogram on the, the right, we've got a problem with a leak here. So if we Evaluate all the parameters.

Our CO2 is normal. The frequency is fine, a respiratory rate of 15 is fine. The rhythm is normal.

It's quite regular. We've got a good height to our capnogram, and we're making baselines, so we are removing all the waste gases, but the shape again is abnormal, and you can see it looks a bit like a kind of pyramid pose, a bit very tenty, and this is true kind of significance of there being a leak within our breathing system. And the causes of leaks are leaky ET tube cuff.

Maybe there's a hole in your rebreathing bag or a hole somewhere in your breathing system. There could also be a hole in the Capnograph line, or maybe we've just got a loose connection somewhere, which is causing a leak. But really, the only treatment for the leak.

Or to find the leak can fix it. And sometimes we just kind of have to admit defeat. We can't find it, so we changed the breathing system and we changed the ET tube.

And it's probably easier in these cases to change the breathing system before you start reintubating patients under anaesthetic. So if we look at blood pressure monitoring, and so blood pressure is the force applied against the walls of the arteries as the heart pumps blood around kind of the body. And the pressure is determined by the force and the amount of blood and the size and flexibility of the arteries.

So the equation for blood blaster is cardiac output multiplied by systemic vascular resistance. And cardiac output, looks at the, the kind of contractility of the heart and the volumes. And then the systemic vascular resistance kind of looks at again, volume within our vascular system.

And then the size of the, the arteries. So this is where we're looking at vasoconstriction and vasodilation. Normally, we've got vasodilatory problems under anaesthesia, and these are what cause kind of hypertension.

You can monitor blood pressure by a non-invasive or an invasive monitoring method. So it depends on what you've got available within in your practise. So a Doppler is a non-invasive blood pressure monitor, and it's very good for cats and small patients, it's quite reliable.

And what it does is you've got a Doppler flow detector, and it's involved with the placement of an ultrasonic probe. And it's got, a piezoelectric crystal, and you place that crystal over an artery. And what happens then is there's a frequency of sound reflection from one crystal to another, and it's looking at moving blood within the arteries, and then it's able to convert a shifting frequency from one crystal to the other into an audible sound.

It's quite clever. And when we use a Doppler, you place the probe over an artery until an audible pulse is located. And typical placements for Doppler probes are kind of ventral metacarpal, and you're there for, locating the median palmar artery, the ventral metatarsal area, and that's the medial plantar artery, or the dorsal metatarsal, where you're then locating the dorsal pedal artery.

So a lot of people spend quite a lot of time placing a probe and then placing the cuff and then you lose, you don't take the probe in place. So I think once you've So the first thing I do with the Doppler, basically, is I will get a piece of tape, put some ultrasound gel on my probe, clip up my artery, and locate it, and then tape the probe in place, and then turn the Doppler on. And 9 times out of 10, you're probably gonna be in the right place.

But if you're not, then you can just kind of tweak the tape a little bit until you hear the pulse, come through on, on the Doppler. Once you've got an audible pulse, you then select an appropriate size cuff and place that proximal to the, to the probe, because you want to actually inflate the cuff and then stop blood flow, basically, in order to then represent blood flow so that we can determine the pressure. You select the appropriate size blood, pressure cuff by looking at the circumference of the limbs.

So most of the pressure cuffs that you've got have got a, an index line on them, which is on the side, and then you just kind of wrap that around the limb and look, you're looking for basically that to measure 40% of the circumference. You then attach your sigomeinometer and then inflate the cuff and then until you can't hear the pulse anymore, and then slowly release until the audible pulse returns. And the doctor is gonna give us a systolic arterial blood pressure measurement.

However, there have been various studies into these because a lot of the time we see slightly lower than what we would like to be systolic. So they have looked at, what, Is what they're actually telling us, and they've compared invasive blood pressure monitoring with the Doppler to see what kind of results we're getting. And they have found that in smaller, smaller patients, they're less than 5 kg, which is kind of true of most of our kind of cats and small dogs, that actually it's given us more of a mean arterial blood pressure.

From a Doppler. Oscillometry is another non-invasive method of monitoring blood pressure, and this is good because it will give us a systolic, diastolic and mean arterial pressures. So you attach a cuff to a peripheral limb, inflate, press the button on the machine, which then inflates the cuff until the artery is occluded, and then it Deflates and the blood pressure is monitored is measured when oscillations are detected.

So it uses air and as the cuff deflates, the pulse then oscillates up the blood pressure lead into the machine and then it's able to calculate a blood pressure measurement from that. It's less reliable in smaller patients. They're gonna have smaller pulses, so the, the, the signal kind of gets lost up the lead.

Or patients with vasoconstricted low heart rates or arrhythmias, you're less likely to get, kind of an accurate reading from them. However, they've started, marketing and they've developed, a high definition oscillometry. So the accuracy of this is improved as it actually looks at pulse waves on a screen and we estimate the accuracy of the blood pressure measurement that it's got, depending on the size of the pulse and how well they think, how accurate they think it is, basically.

So if we're gonna monitor blood pressure invasively, it's the gold standard. It's the most accurate way of monitoring blood pressure, but it does involve placing an arterial catheter. The typical arteries that we use are the dorsal metatarsal artery, the coccygeal artery.

You can have a surgical placement of a femoral catheter in our smaller patients if the, the dorsal arteries are very tiny. The good thing about it is it can be also used for sampling arterial blood, so that we can actually monitor, arterial blood gas if we've got an in-house machine. But it does take a lot of, it takes skill and practise.

So it's probably not something that you're gonna start doing on very critical patients because it's gonna take some time. So you're gonna start practising placing arterial catheters. I would start using, placing them in our healthy patients before we then start moving on to our, Critical patients, because you don't really want to increase anaesthesia time by trying to locate an artery in order to, monitor blood pressure.

But with practise, you can actually place arterial catheters. Technically, it's as easy as placing a peripheral intravenous catheter. And it doesn't take a lot of equipment.

So, it is something that you can do relatively simply. Arterial catheters shouldn't be used to administer drugs. What you then need to do is have a blood pressure transducer and a, and a monitor, basically.

So you connect your arterial trace up to a blood pressure transducer, which is zeroed at atmospheric pressure. So that denotes the pressure at 0, which is at the level of the heart. And then pressure is recorded and displayed as a continuous wave form.

Along with a systolic, diastolic and mean blood pressure. And it is real time. It's consistent.

So every time you get a change in blood pressure, it will be displayed on the monitor. So it is gonna give you a real-time, good indication of what that patient's blood pressure is. With the non-invasive methods, you have to keep pressing go, or you have to wait for them to kind of recycle.

So this is kind of real time, it's continuous. So it's really good for our patients that are critical, where we need to be much more careful with maintaining blood pressures in. You need to flush these catheters because they're arterial blood, so you do get clot formation, and that can give you an inaccurate results.

So we do have these kind of hooked up to a saline flush system, which we just use to kind of flush out the catheter if we see kind of a reduction in our pulse quality on our monitor, which is going to indicate that we've got maybe a clot or a problem, within our catheter. So a normal blood pressure in our patients depends really on breed. So one size doesn't fit all, and this, table I took from the new BSAVA manual, the anaesthesia and analgesia, manual.

Which is all evidence-based. So if you look at it, there's a different, a few different, Papers that they've used to kind of research into what's normal in in pressures in cats and dogs. And they found that as the cat gets older, that it's normal to have a slightly increase in pressures than if a cat's younger, and patients in hospital are likely to have increasing in blood pressures.

So the systolic arterial blood pressure is a pressure during systole, and so that's the maximum pressure as the left ventricle contracts. The diastolic arterial pressure is the pressure at at diastole, which is the minimum kind of background pressure between heart cycles which prevents the cardiovascular system from collapsing. So if you've got a vasodilated vessel, you're more likely to have a lower diastolic arterial pressure than if you've got a razor constricted vessel, you're gonna have a higher diastolic arterial pressure.

And then the minimum, the mean arterial pressure is the average arterial pressure and there's a calculation which works out the mean between the two. And even for under anaesthesia is to avoid periods of hypertension. So mild Hypertension is classified as a mean arterial pressure of 45 to 60 millimetres of mercury.

Severe hypertension will classed as a mean arterial pressure of less than 45. So we were, we're looking to maintain, Oxygen delivery and profusion of our tissues. So we need to try and maintain a, a, a mean arterial pressure of 60 millimetres of mercury in order to maintain perfusion to all of our vital organs.

So, prolonged hypertension can result in, damage to the tissues. So if we're going to treat hypertension, we need to kind of decide on how we treat it. And deciding on the treatment depends on the rate of onset.

So how quickly has that hypertension occurred, the severity, so is it mild or have we got severe hypertension? And then we need to find out the cause. So is it volume related?

So have we got a decrease in circulating volume, which has caused hypertension? Have we got a decrease in cardiac output? So is our contractility of the heart reduced for some reason?

Which is resulting in hypertension. We've got a vasodilated vessel, and it's really normal under anaesthesia to see vasodilation. All of the anaesthetic drugs that we use cause a degree of vasodilation.

So we're looking really to try to counteract that. And you're more likely to see drops in blood pressures as the patient becomes more critical under anaesthetic or if they've got concurrent diseases. And the treatment options will depend really on what disease process that they've got, because you need to be careful, for example, if you've got a patient with cardiac disease, you don't want to be using loads of fluid to correct hypertension because they're not gonna be able to kind of process that increase in circulating volume unless they've had a bleed and they've got a deficit.

So how do we treat a hypertension? And it, again, it really depends on the cause and what you've got available in your practise. But the first line treatment that we'll use is try and kind of decrease anaesthetic depth as much as possible.

So check depths and see if you can reduce the volatile agent, if you can, if the patient is becoming hypertensive because they're becoming too deep. If you can't reduce anaesthetic death, Then you can use fluids to treat hypertension, and it's normally to treat volume-related hypertension or vasodilation. So if you've got a normal healthy patient that's vasodilated because of anaesthesia, you can increase vascular volume quite safely by giving a crystalloid, as a bolus or as an infusion.

It's quite common for us to use fluid therapy under GA. Now, as your volume issue kind of becomes more critical, maybe the patient's had a bleed or is septic or has, kind of hypoalbummania or something, or a low red blood cell count, you then kind of depend or decide whether the replacing volume with the crystalline is probably not the best thing to do because you're just gonna dilute or make the blood kind of more watery. So then we look at maybe blood products.

And again, it really depends on what you've got available in your practise, and what the patient actually needs. So if you're looking for, if the patient has become hypercaragulable, if they're starting to bleed, then we're gonna need kind of a whole blood product, or we're gonna need a plasma to give clotting factors back to the patient. Or if that patient has had a bleed and They've got a low PCV then we can increase volume by giving pack red blood cells, and that's gonna increase the oxygen carrying capacity to be able to deliver more oxygen to our tissues.

If we can't give fluids, or we're already giving fluids, then the next treatment we can use is an anticholinergic. So if, as I said before, when we were looking at the bradycardia, anticholinergics, such as atropine and glycopyrolate are good to, to treat legally mediated bradycardia. So they act directly on the sinoatrial node, which, to increase firing, basically to increase heart rate, and they will also increase blood pressure.

So atropine is, is, has a short onset time, so it's very quick and it's got quite a dramatic increase in heart rate and blood pressure, whereas glycopyonium is a slower acting drug and you don't get such a dramatic increase in heart rate and blood pressure. And the anticholinergics are probably better for your kind of mild hypertensive it's kind of a treatment for mild hypertension. As we start getting into more kind of more severe hypertension, we then need to look at.

Why, what else we can do, what other drugs we can use if we're using fluids and we tried an lonergics and they're not working, we can then look at. Increasing heart contractility by providing an inotrope, or if we've got a really low diastolic pressure and we can't use loads of fluids to increase vascular volume, then you can use a vasoconstrictor. So the inotropes will increase the heart contractility of the heart, and there's a drug called dibutamine that you can infuse that will do that.

And then you can get, you can give a vasoconstrictor which will treat vasodilation and cause initiate vasoconstriction. And them drugs are called, that drugs called enylephrine or vasopressin. If you've got mixed kind of a reduction in cardiac output and vasodilation, so if a patient is very critical, maybe they're very septic or you've got a GDD or, or a hemoadol or something where you're having trouble, with anesthesia-related hypertension, as well as volume-related hypertension, you can pick a mixed onotrope and vasoconstrictor, such as dopamine, noradrenaline, adrenaline ephedrine.

And these will all be given as infusion and They can help increase blood pressure in, in these patients. I think, again, you don't have all of these options all the time in practise. So it's trying to find the cause, for the hypertension.

So why, why is that hypertension occurred, and then knowing what kind of options that you've got. And it's a really good idea to kind of investigate what you've got in your practise. Think about the risk of anaesthesia in these patients.

And then have kind of a plan from start as to how you're going to treat hypertension in order to preserve kind of perfusion and oxygen delivery to our tissues, so that we don't have any ischemic kind of hypoxic events where we then start having damage to tissues. And normally the first things that we start to damage are our kidneys, and they can result in acute kidney injuries or kind of worsening kind of renal failure. So how do we approach treating hypertension?

So mild hypertension, again reduced depth, provide fluid therapy. If they've got a low heart rate, I'd probably look at an anticholinergic. If that didn't work, then we're gonna use kind of a, a dopamine or dibutamine to increase contractility or prevent vasodilation.

If you've got severe Hypertension, then you need to be a bit more aggressive. So reduce your inhalation or even turn it off if you're kind of acute severely have a drop in blood pressure. Be more aggressive with fluids and bloods, and then be more quicker to start using ionotrope.

In vasopressors to, try and support, support the cardiovascular system as quickly as possible because these low blood pressures are what we're gonna find with damage to tissues, but also we might find that we have a collapse of our circulatory system at these points. So in conclusion, appropriate monitoring reduces the occurrence of anaesthesia related morbidity and mortality rates. Recognising that monitors have limitations that can be misleading is really important.

So don't rely on your monitors. They will lie to you. So, understanding what the monitors can tell us and how to interpret them, and when to treat problems is key to making anaesthesia as safe as possible for our patients.

And again, that's why we're all there. We're doing our best to have successful outcomes. Compare and use checklist before induction, Making sure that you've got kind of plans in place to know the steps that you're going to take to treat these problems, to make sure that you've prepared all your equipment before you've anaesthetized your patients.

You don't want to be kind of fumbling around and increasing anaesthesia time because you haven't prepared well enough. And use what you have available. I, I hear it quite a lot of times, nurses or practises saying, oh, they've got Dopplers sitting in the cupboard, but they don't use it on patients under anaesthetic.

And I just can't understand why that's the case. If you've got it there, get it out, practise using it, and it's gonna make anaesthesia much more safer for your patients. Thank you for listening, and I hope you found that, interesting and useful.

I'm happy to answer any questions. Lisa, that was absolutely incredible. Your, your explanations and simple, no-nonsense approach to, to this subject of monitoring and modalities was, was fantastic.

So thank you for your time. Thank you. And I love your mug, by the way, I think that's fantastic.

Folks, if you've got any questions, you, you feel free to, to pop them into that Q&A box. At the moment, Lisa, I think you've done such a fantastic job that you've covered everything. Nobody has got any questions for you.

And, yeah, I did, I did like your point about trust yourself and know your limitations of your monitors. . You can't just watch the monitor and think everything's OK.

No, no, and that's what I try and teach the students at at work is they, they, they actually can get a bit, transfixed by the monitor, and they stop looking at their patients. And I think assessing depth of anaesthesia is really key to making sure that the monitors are actually telling you the right thing. So don't, the monitors can be used to help.

Don't kind of rely and then forget that there's a patient there that can tell you a lot of stuff as well. Yeah, and I think we, we are so lucky in this country with the fantastic RVNs that we have available to us, that they really just, they outweigh any, any monitors, trust themselves and use the monitors as a backup is, is the best advice, I think. Yeah, absolutely.

Fantastic. We've got no questions coming through, Lisa. So it's my pleasure to just once again thank you for a fantastic presentation and for your time and I sincerely hope we see you back on the webinar it.

Great, thanks for having me. Thanks folks for attending to Peter, my controller in the background for making everything work seamlessly. Thank you very much.

And from myself, Bruce Stevenson, it's good night.