Hi everybody and welcome to tonight's webinar. My name is Sophie McMurray, and I have the pleasure of chairing tonight. So before I go on to introduce our speaker, I'd just like to point out that you can ask questions throughout tonight's webinar, and in order to do so, just hover over the toolbar.
It'll either be the top or the bottom of your screen. Click the Q&A box and type your question in there. They'll come through to me.
They won't disrupt the webinar at all, so you can send it at any time. And then I will stop at the end and I'll ask the questions to our speaker then. So tonight we have the wonderful Michelle Moran.
She's a registered veterinary nurse and she also has a veterinary technician specialty in anaesthesia and analgesia. She works at Northwest Veterinary Specialists, and she's in charge of the nursing, she's a supervisor of the nursing anaesthesia team there as well. And I've had the pleasure of working with Michelle for about 12 years, and I can assure you you're in good hands tonight.
So I'm really looking forward to tonight's webinar and I'll hand over to you, Michelle. Thank you, Sophie, for that introduction. So tonight I'm gonna be talking to you about monitoring blood pressure during anaesthesia.
I've picked this topic because I think it's really important that we should be monitoring these patients, every patient, during your anaesthesia period from beginning to end, ideally, not just your critical patients. So we'll go on and we'll begin. So what is blood pressure?
So it's known as the driving force of arterial blood flow, so perfusion to your organs and that supplies your oxygen to all those organs and tissues within the body. The pressure at which that blood flows determines how well that's achieved. And all of those vital organs such as your brain, heart, lungs, liver, kidneys are really dependent on that flow to function, and any dramatic changes can be really detrimental.
They say now monitoring blood pressure should be a minimum standard of monitoring anaesthesia, so not just done in referral hospitals or in the sick cases, it should now be a basic monitoring tool that we use each day. So I'm gonna just talk to you about what controls blood pressure. So it's regulated by the medulla andlogata in the brain, and that's in your hindbrain, if you can see on the picture there.
And it's under the control of the autonomic nervous system, so you're sympathetic and parasympathetic nervous system. And there's also some humeral local control mechanisms which we'll go through in a second. So changes are detected by the bi receptors and they're located in your carotid aortic bodies in those walls of your arteries basically.
And that information is sent to the medulla and then they adjust accordingly. The cardiac centre will increase or decrease your heart rate and that's via your sympathetic and parasympathetic nervous system. So your sympathetic nervous system will increase your heart rate and your parasympathetic nervous system will decrease it.
There's also a vasa motor centre, and that will increase or decrease your systemic vascular resistance. Don't worry too much, we're gonna go through that in a minute what that is, but it's basically the tone of your vessels, so whether they're vasoconstricted or vasodilated, and that controls that. And then these humour on local control mechanisms, basically like chemicals in your bloodstream.
So you've got adrenaline, no adrenaline, you've also got something called nitric oxide, so that's a vasodilator, so that all helps. And then if that's prolonged or it's insufficient in any way, the Renan angiotensin system's activated. And unfortunately we haven't got time to go through all of that system tonight, but I just thought I'd mention it.
So where do we want to monitor this parameter under anaesthetic? So it's one of the most important measures of cardiovascular function to the anaesthetist. And it's the best tool we have at the moment to provide us an indication about that tissue perfusion.
Many of the anaesthetic drugs that we use on a day to day basis, both injectable and inhalational, will cause a decrease in cardiac output or systemic vascular resistance, and we're gonna go through that in a moment. All patients, big, small, young or old, will experience some hypertension during anaesthesia. So why is that low blood pressure a concern?
So hypotension is classified as a mean arterial pressure of less than 60 millimetres of mercury, or a systolic arterial pressure of less than 90 millimetres of mercury if you're using in a Doppler. The perfusion of the vital organs becomes inadequate at this level, and that means the oxygen delivery is reduced and the waste products that are metabolised and carbon dioxides produced are not removed. Which then obviously can cause hypo hypoxia and hypercapnia.
And ultimately leads to organ dysfunction or failure. So prolonged hypertension to more than 15 to 20 minutes, which isn't actually that long when you think of something that's prolonged, can lead to nephron damage and later renal failure or play a role in renal disease in later life. And it also decreases your liver metabolism of drugs, it can lead to central nervous system abnormalities and even cause a transient blindness in recovery as well.
As you can see, all of these factors are involved in blood pressure and tissue perfusion. So that mean arterial pressure on the top there, we're gonna look at the cardiac output of CO and systemic vascular resistance. Because everything else falls under that category.
So those are the two determined factors of mean arterial pressure. So your cardiac output and your systemic vascular resistance, or sometimes in some books, it's called peripheral vascular resistance, but it's the same thing. I'm gonna go through those now.
So cardiac output, so it's the combination of heart rate and stroke volume, it's the amount of mLs of blood that's ejected from the heart each minute, basically, that's what cardiac output is. And the heart rate is obviously the number of contractions per minute. And your stroke volume is the volume of blood ejected with each of those contractions.
So you get cardiac output. So the mLs of blood per minute from those two factors, heart rate and stroke volume. Stroke volume is dependent on three factors, so pre-load, so that's essentially they sometimes call this end diastolic volume.
All that means is that it's the amount of blood in the ventricles before that next contraction. So you obviously need a good amount of that before you're going to get a good strig volume, so you need a good amount of blood in those ventricles ready. The after load, so that's the force against the heart during the contraction, so that correlates with the tone of the vessels basically.
So if you can imagine a 20 mil syringe of saline is your heart. And your vessels are your sort of pink maybe IV catheters. And then if your ves are constricted, that's gonna go to a yellow, and that would you'd need a lot of force to get to eject that blood out and around the body.
Or if you have a green catheter that obviously when you're vasodilated, it's much easier to get that blood out and around the body. So that's what after load is in a more of a simple term. And then the contractility is just the heart's ability to be able to generate that force as well.
The systemic vascular resistance, it's just the resistance to blood flow in that vessel. So artery or capillary bed. So it's just the tone of that vessel, so it's just three pictures there to demonstrate that.
So vasoconstriction goes really narrow, your kind of yellow catheter, normal, and then vasodilated. These are your normal blood pressure values under anaesthesia in dogs and cats I must stress under anaesthesia. Up to 120.
You mean arterial pressure 60 to 100. And diastolic arterial pressure of 55 to 90. So your systolic arterial pressure is the peak pressure that occurs within those arteries when the ventricles contract.
And that's determined by a combination of these factors, stroke volume, which we talked about, systemic vascular resistance, which we've talked about, and the contractility. And your diastolic arterial pressure is the minimum pressure within the arteries when the ventricles relax and that ventricular filling happens prior to the next contraction. That's primarily determined by the systemic vascular resistance, so the tone of your vessels is what determines diastole.
And you mean arterial pressure is derived from both of those systolic and diastolic arterial pressures, and it's basically the average perfusion pressure. OK, so what value does that mean arterial pressure needs to be in order to adequately profuse those organs. It needs to be more than 60 millimetres of mercury, but you want not aim for just around 61, 62, you want to be aiming for 70 and above.
And if it falls below this value, that's classed as hypertension and your perfusion of the vital organs starts to become inadequate. Short term effects are less than 15 minutes, a really, really short time frame. You can get a metabolic acidosis, there's an increase in oxygen demand, there's an increase in glucose demand, and then there's an increase in cardiac workload there.
Prolonged hypertension, as I said before, it's only longer than 15 minutes, not very long at all, really. You're gonna get ischemic damage which the kidneys are particularly susceptible for, and that can lead to nephron damage and later to renal failure, as we discussed before. It can also worsen any hypoxemia that there already is and decreased liver metabolism of your drugs, you're gonna get a slow recovery and it can lead to central nervous system abnormalities and blindness like we talked about earlier.
It is important to recognise that a normal mean arterial pressure measurement doesn't always imply that there's adequate cardiac output and adequate perfusion to those organs and tissues. So that's because the body is, as we talked about earlier, really good at changing things in order to meet the requirements. So adrenaline's released to cause vasoconstriction and shock.
That doesn't mean that they are having an adequate perfusion state to all those organs and tissues. So it's important to look at the animal as a whole, assess it as a whole and its condition, and apply all of that knowledge and what you're seeing on the monitors as well. So there's loads of causes of hypertension during anaesthesia and I'm just gonna quickly Pop these on the screen, but we're gonna go through them on an individual basis now.
Most of the time it's to do with your anaesthetic drug administration that's what we're gonna go through first, but we're also gonna go through the others as well. So these are gonna be the commonly used drugs that we use on a day to day basis during our anaesthetic periods and that are gonna affect your blood pressure. First of all, how do they affect our blood pressure?
So they produce a dose-related depression of myocardial contractility, so they decrease the contractility which will in turn decrease your cardiac output. They cause vasodilation. So they widen those, those vessels and that is also known as a decrease in systemic vascular resistance.
The reduced ventricular filling as well, that will decrease your cardiac output too. And they also depressed the bar receptor reflex as well. Soacopromazine is often used on a day to day basis.
So that causes vasodilation, which will decrease your blood pressure and also at the same time decrease your body temperature too. It's difficult obviously to correct that because there's no reversal agent. And it does cause a reduction of up to 20% in hematocrit in your PCV due to this, the spleen dilating as well.
The alpha 2s, your dormito, dexomitor that causes vasoconstriction, so your, your vessels go narrow and that increases your blood pressure initially. And then that does start to decrease to normal values or slightly lower than normal at times, although clinically we don't see that that often. But yeah, that's on in a dose dependent manner, so I couldn't give you a time frame on when that occurs, but it, it is dose dependent.
Obviously the higher the dose, the longer that initial increase in blood pressure will last for. It does cause a bradycardia, but it is a reflex bradycardia. It's in response to that high blood pressure.
So those bi receptors that we talked about in the carotid and aortic bodies will detect such high pressures and drop the heart rate to compensate for that. A decrease in cardiac output is seen with an alpha 2 just because the heart rate is lower, but in an animal that's got a normal cardiovascular function, it doesn't affect the delivery of oxygen to the organs. Propofol, this is something that we use each day too, so this is caused as a global vasodilation, which decreases your cardiac output and systemic vascular resistance, so causes causes vasodilation and that will also drop your blood pressure.
It's worse with rapid injection. And it's most severe, 2 minutes post-injection. The heart rate increases slightly as a response to this fall in blood pressure.
And the reason why it only increases slightly is because it also affects that bar receptor reflex that we have. So it's not the most, the first choice with your hypovolemic patients. Halfaxolone does exactly the same as propofol, except that it doesn't affect that bi receptor reflex.
So you will see a more of an increase in heart rate to try and compensate for that blood pressure drop. Isofluorine and sevofluorine are two of the inhalation agents that you use on a daily basis. So they decrease myocardial contractility, which decreases your cardiac output.
And they also cause vasodilation as well. So both of them together, decrease your blood pressure in a dose dependent manner. The more you use, the worse that is.
Ketamine, so this actually stimulates the sympathetic nervous system, which will increase your heart rate. And therefore it increases your cardiac output, and therefore will increase your blood pressure. However, it's important to know that it will, you're asking the heart to increase, so when you ask the heart to increase heart rate, increase cardiac output, contractility.
It will increase the cardiac wear clothes and oxygen demand, so it's not suitable for those cardiovascular patients. Midazolam, I just thought I'd put this in there just to note that this sometimes ideal for the cardiovascular unstable patients because it doesn't have any effects whatsoever on blood pressure, so it can be a really nice agent to use in those critical patients. I just wanted to briefly touch on the non-steroidal side of things when we're talking about blood pressure cause we often use these, especially in our routine cases.
So COX 1 and COX-2 inhibitors, most of CO2, and the COCOX enzymes in the blood in the bloodstream in the body convert rachaonic acids into prostaglandins, and they maintain GI mucosa, renal blood flow and platelet function. But they also cause pain and inflammation, that's why when we use the non-steroidal anti-inflammatory COX-2 inhibitors, that's why we use them mainly for that pain and inflammation. However, That GI mucosa then and the renal blood flow and platelet function can be compromised.
So they must be avoided in liver and kidney disease, hypovolemia. Any likelihood of haemorrhage or anything, low blood pressure, or patients with GI disease? Some non-steroidals are licenced for pre-op use.
However, the manufacturers, if you read the data sheet, really thoroughly recommend that they're only given if fluid therapy is going to be administered throughout the anaesthetic period and blood pressure is monitored throughout, which I thought was really interesting. In the hydrated healthy patients, the probability of a non-steroidal related renal dysfunction is low, but obviously if it, it's given to a compromised patient. Or a patient that's in, in renal problems already or at risk of, then obviously your risk massively goes up there, but if we're not monitoring blood pressure and you have a hypotensive periods, then this can be a problem.
OK, so we've talked about the drugs there, so we're just gonna go on to other causes of hypertension during the anaesthetic period. So cardiac arrhythmias can affect the, the blood pressure. So that can be from anaesthetic drugs or concurrent disease or volume states of the patient.
More common than you think. And the effect blood pressure, they either don't allow enough time for the ventricles to fill, or they, because they haven't come through that normal conduction pathway, then the contraction doesn't happen as well. Fluid deficits, so blood loss preoperatively or perioperatively, you're gonna maybe have dehydration, maybe you've got a patient that's PUPD or foreign body, vomiting, diarrhoea.
Any third space losses, so have you got any peritonitis or protein losing enteropathy? All of those conditions basically can cause a fluid deficit and therefore cause you to have some hypertension. So ideally we want to correct these with crystalloids or colloids or blood products, whatever they need.
We should ideally correct that loss before we anaesthetize these patients or give them perio-operatively in an emergency situation. So intravenous fluid therapy should be provided to all the patients during the anaesthesia to compensate for losses and hemodynamically to support that patient through its anaesthetic period. 3 to 5 mL per kg per hour is recommended on the healthy patient, 3 mil being more towards the cat than the small dog, and up to 5 mL per kg per hour for the for the sort of medium to larger size patients.
They should be assessed obviously on an individual basis though and tailored accordingly. So if you ever give IPPV or you've got a mechanical ventilator, that can also decrease your blood pressure. And that's because increases in intrathoracic pressure when you overinflate the lungs, or maybe you've got a closed APL valve, hopefully not, but this, you know, it has happened.
Can increase the pressure in that pleural space, and it will, all of these things, even a tension pneumothorax, will decrease your venous return to the heart and ultimately that will decrease your cardiac output and essentially could be fatal in some of these cases. So if you are using a mechanical ventilator, you can check your airway pressure and tidal volume and decrease as necessary. If you're doing manual IPPV and you notice the blood pressure drop, just ease off on the, on the amount of pressure that you're, you're given.
You just want normal chest excursions there. You don't need anything overinflating and as long as you're achieving normal apnea, then you'll be fine. There you go, that's, and then just obviously observing your SPO2 reading as well.
And obviously if you've suspects tension pneumothorax, then don't, that's the time you don't perform IPPV as it can make things much worse. Always check your APL valve as well before any anaesthetic on every circuit and check again if you're experiencing any blood pressure problems. So tachycardia and bradycardia, so an increased heart rate and a decreased heart rate can both equally affect your blood pressure.
So tachycardia can be a numerous reasons why this happens, but it can also be a response to falling blood pressure as the patient tries to compensate. And high heart rates as well cause our blood pressure to fall. That's because there's not enough time for those ventricles to fill.
So the cardiac output decreases with each beat. And the bradycardia can be due to again, lots of reasons for bradycardia join join an anaesthesia, but they obviously decrease your cardiac output as well because when we discussed cardiac output earlier, we, we know it's a combination of heart rate and stroke volume. If you see any patients with sepsis or SAS, they have a loss of vascular tone, and they're often in a vasodilated state, and they produce excessive levels of nitric oxides, excessive levels of nitric oxide, and that causes vasodilation.
They're really, really difficult to increase the, these guys' blood pressure. They also have a have a deficiency in vasopressin. And that endothelial layer is also affected and they often third space or have edoema as well.
So all of those problems. Can cause a low blood pressure. Any concurrent disease like cardiac disease will affect your cardiac output.
Any arrhythmias, any endocrine diseases, maybe poorly controlled diabetes. They're also at risk of a low blood pressure as well. Pause the systemic shunts as well, they have an increased production of nitric oxide, which is, as we've talked about before, it's a a vasodilator.
Renal disease as well that can cause blood pressure problems. They're unable to regulate what's going in and out. And any patients with ascites, peritonitis, edoema, protein losing enteropathy, any other fluid losses above normal are all at risk of developing some degree of hypertension or maybe it's even already there before you've anaesthetized these patients.
Vagal nerve stimulation. So the vagal nerve innervates both the the sinoatrial node in the heart and the atrioventricular node. It's part of your parasympathetic nervous system and it slows down your heart rate.
Stimulation of this in some surgeries can induce a drop in heart rate and therefore hypertension. So laryngeal tie back and ocular surgery, do that, brachycephalics are also really prone. They have what's called high vagal tone, so they're at an increased risk of hypotension and bradycardia, even though they've got no other disease process going on.
Anaphylaxis, it's, it is quite rare, but it's life threatening. It's another, it's another possible cause of your hypertension. It's seen more commonly with IV contrast, but it can be with any drug that you've given.
Usually they go tachycardic and then hypotensive. They, they have severe vasodilation. They may or may not have respiratory changes.
Sometimes asking the owner if they've got any allergies on admission will help you be more prepared for that situation if it does arise. They they're, they're at a higher risk of that happening to them. So pericardial effusion is another possible cause of hypotension.
Hopefully we'll have picked up on this before we anaesthetize this patient. So it's the presence of an abnormal amount of fluid in that pericardial space and that decreases the ability of the heart to dilate and fill with those, that blood. So therefore that leads to a drop in cardiac output and a drop in blood pressure, because those ventricles aren't able to fill as adequately as they should.
And then sometimes it's as simple as some surgeon or equipment pressure. The large abdominal retractors can decrease venous return if too much pressure is applied. Surgeons' hands on major vessels can do this.
Any large abdominal masses, pregnancy, pyometra, any positions, especially the caudal vena cava can be occluded as well, especially during a caesarean section when they're on their back. And they all can decrease the cardiac output and therefore the blood pressure. OK, so what to do.
I've put that little cartoon on the right there. It, it is all about communication, about talking. To, to your vet, and I'm communicating what's going on.
So mild, that's classified as a mean arterial pressure of 45 to 60. You want to look for the cause and treat to all of those causes that we've just talked about, you ideally hopefully want to recognise a cause and ideally treat that. Treat any bradycardia with atropine or glycopyrelate providing they're not in that vasoconstrictor phase using an alpha 2.
Which if they're in that vasoconstrictor phase, you shouldn't have a problem with your blood pressure, but I just thought I'd mention that. Turn down your inhalational agent if you can, and treat any tachycardia. So if you're struggling to turn down your inhalational agent, you might want to give some analgesia and then you can turn that inhalation agent down cause that is a really potent vasodilator.
So even small changes on that vaporizer setting can't have a dramatic effect. Treat any arrhythmias if they're present. And you could consider a fluid therapy bolus of 10 mL per kg or 2 to 5 mL per kg bolus of colloids if you needed to.
And the drugs that we most commonly use during mild hypertension are ephedrine and dibutamine or dopamine as well. And obviously if you are given IPPV you just may need to reduce that tidal volume a little bit or just back off on those on those chest excursions. Moderate to severe is classified as a mean arterio pressure less than 45.
So this was a real blood pressure reading on the right there. So you wanna, you wanna get help, you, you wanna communicate this information quite fast and you wanna look for the cause and treat it. Treat any bradycardia, treat any arrhythmias, potentially even turn off the inhalational agent, which is what we did with this cat on the right hand side, that blood pressure.
And a fluid therapy bolus if you think that there's a massive volume lost for whatever reason. Drugs, we tend to skip out the ephedrine that's normally used for the mild hypertension cases. So dibutamine, dopamine or noradrenaline is what we usually would go to for severe hypotension.
And definitely check your APL valves. OK, so we've understood. How blood pressure?
Is controlled, we've understood all of the causes of low blood pressure, and now we're gonna find out how we monitor the blood pressure. So how can we monitor blood pressure? We can do it invasively, so we can do it direct from an artery or non-invasively, which is sometimes called indirect.
So non-invasive blood pressure, there's two commonly used methods, Doppler and the oscillometric device. They all tend to underestimate the actual blood pressure slightly. But regardless of the method used, the cuff selection is really, really vital for obtaining an accurate results.
So the width of the cuff should extend to 40% of the circumference of the limb in dogs, and they say around 130 in cats. There's often a mark on the cuff that should be placed over the artery as well. If it's too big, it can underestimate your readings, and if it's too small, it will overestimate your readings.
The cuff should ideally be placed at the same level as the heart. And usual cuff occasions are forelimb, tail and hind limb. That's just a photo to explain on the left hand side how to measure the cuff.
So that's about right for that dog on the left. You're looking, it's about 40% of the circumference of the limb. It's quite difficult to see there, I suppose.
And on the right hand side picture, that dog is on its back and that that cuff is at the level of the heart. If you're using Doppler in practise, the cuff should be connected to a sygo manometer. And the Doppler ultrasound probe is placed over the artery distal, so below that cuff, ideally using some ultrasound gel to improve the signal and get any hair off that might be causing any interference.
You do that until you hear an audible whoosh sound, so essentially that's your pulse rate. And then you inflate the cough until that week she's no longer heard. And then the cough is gradually deflated until you hear that whoosh sound again.
So that value at which you hear that woof sound corresponds to the systolic arterial pressure in dogs. In cats, and really, really small dogs like your chihuahuas and your Pomeranians, it's often closer to the mean arterial pressure or somewhere in between the systolic and mean arterial pressure. That's just an example of two separate dopplers.
You've got advantages and disadvantages of using a Doppler. The advantages are they're quite relatively inexpensive out of all of the blood pressure equipment that there is available. It's easy to perform once your technique is practised and you're used to accessing and locating that pulse.
And you can tape it on if you need to and hear the pulse throughout of that anaesthetic period, which can, you can sometimes hear pressure changes like a drop or you can hear arrhythmias or sometimes the heart rate is increasing or decreasing, especially if you're busy opening suture material and things like that for your surgeon. The disadvantages are it only gives the systolic blood pressure reading. So systolic blood pressure of more than 90 doesn't necessarily mean that the mean arterial pressure is more than 60, and that's just because the diastolic arterial pressure, it can be quite low and bring that mean arterial pressure down.
So that's a major disadvantage of the Doppler and it can be more challenging in really small patients to locate the arterial pulse. Oscillometric devices, so this kind of does everything for you. You determine all of those three arterial pressures.
And they do that by detecting pressure oscillations at different points as the cuff is deflating. They often display a heart rate with it as well, and that can be a good indicator whether you believe that reading or not, if that heart rate matches. They may be inaccurate as well, or take some time to read, especially when the animal is hypotensive, or if you've just given an alpha 2, so such as your dormitor or your dexteritor, you can really struggle to read within those 1st 5 to 10 minutes of giving that alpha 2.
That's just an example there, you've got your systolic arterial pressure at the top left and next to your diastolic, in the middle, you've got your main arterial pressure and then at the bottom there you've got your heart rate or your pulse rate. So there's advantages and disadvantages again. So the advantages are it measures and displays all three arterial pressures for you.
Really easy to use, just click a button. And it can be put onto cycles to measure however many minutes you want and you don't have to keep pressing the button. You can just get it to cycle every so many minutes.
The disadvantages are they fairly expensive. And they can be inaccurate at times, more so with smaller patients or when they are hypotensive or in those vasoconstrictive states that we've just talked about. So, What I thought was important to understand is if, if, because it's not always possible to place the cuff at the same level as the heart, but if you understand the effects it has and if you need to adjust your readings accordingly, then you can do.
So if it's too low, if it's below the level of the heart, it'll overestimate your reading. And if it's too high, so if it's above your heart, it will underestimate your reading. Now for every 10 centimetres difference, that's quite a large amount really.
You either add or subtract a value of around 7 millimetres of mercury, so it's not too much, but it can be the difference between you thinking an animal is hypertensive or not. And now we're gonna talk a little bit about invasive blood pressure, so direct blood pressure measurements. Ideally, it's for patients that are really sick or compromised in any way or patients that are having surgery that are at risk of major blood loss.
You might also place an arterial catheter. And monitor invasive blood pressure if you have a respiratory patient as well because you can then assess blood gas analysis too. It does require a catheter to be placed in an artery, and that is then connected to a transducer using non-compliant tubing.
This is then filled with saline or heparinized saline and it's connected to a pressurised continual flush system. And that avoids clots and prevents the wane form from what we call dampening, it gives so it prevents it from dampening and it gives a nice trace. It provides reliable and continuous information throughout so it's a real time.
Continuous information. And it's considered the gold standard way of monitoring blood pressure. It's often done in referral hospitals.
This is just an example of a catheter placed in the dorsal pedal artery on the hind limb, and it's connected by a three-way tap to non-compliant really stiff plastic tubing. Which is then connected to a transducer, so that, that, that blue thing in the middle, and then the fluid line is connected and on the right hand side you see the pressurised bag to help keep that continuous, very small amount of continuous flush going through that artery. This is a video just to show you that it is a real-time waveform any changes are second to seconds.
And as you can see, the waveforms match the ECG which matches the heart rate and the SPO2, everything correlates. So there's advantages and disadvantages. So the advantages are it's a reliable and continuous waveform.
It gives really valuable information, it's second by second, as you can see on the video. And it can be used to collect repeated arterial samples if you need to assess any blood gas analysis. And it is considered the gold standard technique for monitoring blood pressure.
The disadvantages are that it's really expensive, the equipment that you need, and it requires technical ability and the risks, it's not risk free when you're placing an arterial catheter. Pulse quality, this is something that I feel quite strongly about that you should be doing, ideally every day in practise, something that you can teach yourself in the conscious and anaesthetized patient. What I would say is that get used to doing it on really healthy patients first of all, so that you know what's normal.
So assessing peripheral pulses, seeing what the quality is like on all those healthy patients, and then you can maybe assess during anaesthesia. Or on sick and compromised patients and that will help, really, really help you during your anaesthetic period. It can be obviously applied then that skill during the anaesthetic periods.
We ideally with blood pressure monitoring, but if you've only got one Doppler machine or you've maybe got one multi-parameter monitoring machine, you've got 2 or 3 anaesthetics going on at once. This is a little bit like a backup. So the pulse pressure, so it's the difference between systolic and diastolic arterial pressures.
A really strong pulse equals a large pulse pressure. And a weak pulse equals a low pulse pressure. There's a theory as well, which I'll go through in a second.
. How well you can include the pulse can also give you really vital information. So there is a theory that can be applied to a peripheral such as a metatarsal pulse. If you can't palpate it.
Then the main arterial pressure is likely to be less than 60 millimetres of mercury. If a central pulse such as a femoral can't be palpated, then the main arterial pressure is very likely to be less than 40 or they're in cardiac arrest. So it's just a really nice skill to teach yourself, ideally do it on the conscious, healthy patients first, then progress through to the anaesthetized patients and then maybe to compromise sick patients.
And this is just a case example of an anaesthetic that I, I did not, not too long ago. So that the full stops the heart of the heart rate. And the, the, the crosses are the main arterial pressure.
So as you can see, as we're going along, oh, and also if the animal's being ventilated, so the respiratory rate doesn't change because it's being ventilated. So as you can see by the crosses. The, the, that's the main arterial pressure, that, that's fairly stable, fairly stable, and then it just starts to decrease below 60.
If you can see as well, the heart rate is increasing. And that's in response to that drop in blood pressure. So what I did with this case is I decreased my isoflurane, and that's over the course of a few minutes slowly started to respond and the blood pressure started to come back up to normal.
I thought it was a really good case example to use just because an increase in heart rate doesn't always mean they're light and that they maybe should be increased on the isoflurane. It is sometimes the body's response to a drop in blood pressure. So if you weren't monitoring blood pressure and all you had was an increase in heart rate.
Then your natural response might not be to decrease the isoflurane, often people might increase it or look for another cause of an increased heart rate when all it is is a drop in blood pressure. So I thought that was a really good case example to use. And thank you.
That, that's everything for tonight. Brilliant, thank you very much, Michelle. Absolutely brilliant webinar.
I've made plenty of notes. If any of you do have any questions, just pop them through, hover over the toolbar at the top or bottom of your screen and click the Q&A box and just send your questions through so I can ask Michelle. I do have one question, Michelle.
So you mentioned about pulse quality and if you, that you can compress the pulse peripherally. So if you do compress the pulse, does that mean that it's low blood pressure? Yes, yes.
So if you can occlude the pulse quite easily, that's not a good sign. So in the healthy patients, it should be really, really hard for you to press down and occlude that pulse. If you try most of the time on your healthy patients, you'll still feel it on your fingers, obviously a little bit weaker because obviously you are compressing it, but you, it should be still strong enough that you can still feel it on your fingers.
If you can easily occlude that pulse, that's usually a bad sign. OK, brilliant, really good, good little tip. We've got a couple of comments coming through just saying what a fantastic talk this was and saying thank you so much.
That's really nice to see. And up to now, ah, we have one question. OK, it says.
So is it possible to estimate blood pressure with body temperature? No, not usually, just because if you're, if you're in a vasoconstrictive state, it could be for many reasons, it might be that you're shocky. It might be that you've given an alpha 2 like Dexamedatomidine or meatomidine.
Which will also vasoconstrict you, so your, your peripheral body temperature or certainly rectal might drop, but you might actually have a really high blood pressure, so it's, it's not really an indicator really, unfortunately. It'd be ideal if it was. OK, brilliant.
And that seems to be the end of the questions. So on that note, I'll just say thank you for everybody for listening tonight and thank you very much, Michelle for a brilliant webinar and I'm sure we'll see you back on here soon. Thank you very much.
Perfect. Thank you very much. Bye.