Thank you Bruce. It's, it's great to be here. Welcome everybody, and, thank you for joining me for a subject that I'm particularly passionate about of hypertension and in, in particular, approaches to fluid therapy in that realm as far as, resuscitation goes.
So, let's, start at. Beginning, when did therapy first come into vogue to find that we have to go back to the pole epidemic of London. So right back in 1870s, that he was going to boil up.
Interesting thing about about that in that you you remember when you first graduated and you start to to try new regimes or new drug protocols for the first time, you're very conservative in your approach, you don't necessarily go for the the upper limit, you usually do things to effect. But before I get on to that, I just wanted to indulge this great description from which The latter wrote to The Lancet, after he had administered this, lacta ringer's solution to a periare woman. Soon the sharpened features, sunken eyes and fallen jaw, pale and cold, bearing the manifest imprint of deathyet, began to glow with returning animation.
The pulse returned to the wrist, and in a strong voice, the woman declared that she was now free from all uneasiness. I, I, I love that, and I think it's . It's, it's, it's a great, very apt description.
Unfortunately, the, the woman, while she was clearly feeling quite quite well after that infusion, did die, of her disease two hours later. What I, what I want to take away from, from Doctor Latta's approach though is that like any new therapy, when he started to implement this new novel treatment of, intravenous fluid. Therapy.
He did things incrementally. He did it ounce by ounce and diligently monitored the patient's signs. And unfortunately, things have changed.
This approach has changed. We've moved from a time of giving ounce by ounce with diligent attention to detail of clinical signs and response in our patients to giving litre after litre without much due care. And so I'm, I'm really encouraging this old approach, and what, what is the problem?
So, basically there is a growing evidence of the harmful effects of liberal intravenous fluid strategies. And by liberal intravenous fluid strategies, I'm not talking about . Very far outside the box.
So I'm talking in the realms of the 10 mL per kg per hour, and as we'll elucidate later on, perhaps even approaching the 5 mL per kg per hour could be considered to be excessive in many of our patients. What I'm gonna be encouraging is the administration of fluids, with clear, defined objectives and goals. So, a lot of the problem is, aligned with some of the dogma that exists in our, our veterinary industry, you know, I remember, in general practise being in sitting in many consult and listening to, My colleagues say, well, you know, we're gonna put your pet on intravenous fluids and that's going to assist with things like hypertension and and so forth, and now the evidence is kind of pointing to that not necessarily being a full truth in itself.
So, why have we been getting away with it or seemingly getting away with it for so long? Well, the, the reality is that the vast majority of our patients, with the exception of those that may end up in the post-operative period with some congestive heart failure, or, or the like, some, you know, heart lung complications. The majority of the patients are really good at.
The, the fluids. And it's not usually until day 234, postoperatively, by which stage that patient is normally at home, that, that fluid which was in the intravascular space is now out into the interstitium and that fluid along with all the excess amount of sodium starts to do its worst. And what we see is increased complications as far as .
Decreased wound healing and ostomosis breakdown, as well as the classical, heart lung complications and increased risks of pneumonia and so forth. So I'd like to just step into some of the the human literature briefly to start with, and in a landmark multicenter study by Brigitta Branstra and colleagues, 172 healthy human patients were randomised to receive either a restrictive or a standard intraoperative fluid regime. Now the restrictive group received a mixture of crystalloids and colloids, and the standard group received on average about twice the volume, predominantly crystalloids.
The authors demonstrated a significant dose response relationship between complications and increased volumes of intravenous fluids, while the restrictive group, which had fluid rates approximating 3 to 4 mL per kg per hour, had significantly less minor and major complications such as the anastomosis, leakage, pulmonary edoema, pneumonia, wound infections, and the like. So here's another study, 156 healthy people undergoing elective abdominal surgery, randomly selected to receive either restrictive, in this case around 4 mL per kg per hour fluid regime, or a standard more traditional, regime of around 10 mL per kg per hour. And the restricted group gained less weight perioperatively, experienced fewer surgical complications, and retained better GI motility.
So this notion in particular in this study, this notion of post-operative weight gain is something that has been well documented in, in humans, and it's not uncommon for a 70 kg average human patient going for an elective procedure to end up weighing. Anywhere between 5 to 10 kg more post-operatively than they did before they were anaesthetized. A large part of that is to do with normal stresses of anaesthesia and surgery that do result in, perhaps up to anywhere between 5 to 10% of the intravascular fluid norm normally translocating from that intravascular space, and that will eventually go back into the intravascular space, but that is compounded and those.
Physiological factors which enable that the return of that fluid back into the vascular are often retarded by excessive or perhaps current fluid administration regimes. So this is a I I introduced this study because it's a, it's an old one, but it's it's kind of applicable because it's it's related to to our animal patients. Here we have a anastomosis study where we see that, And during normal manipulation of an enteral anastomosis, it can result in a significant increase of around 5 to 10% in interstitial water load around that anastomosis.
But, in this particular group they had, so they had the control group which wasn't administered . Intravenous fluids, and then they had the treatment group, which were administered what we would consider to be a relatively restricted fluid regime of 5 mL per kg per hour. They noticed that those patients that received that intravenous fluid administration rate had double the edoema due to that surgical anastomosis site and those that Hadn't received those fluid rates and didn't receive any at all.
So what's the problem with edoema at the anastomosis site? Well, with edoema comes an inability to perfuse, to heal, to remove inflammatory mediators from that site, and so you do end up with a higher increased risk of breakdown and consequent infection. Now this, this particular study is quite a a a a landmark paper.
Indeed it's, it's probably a study that wouldn't have gained legs in the first world. So, what this particular study did was, a question, well, as far as its ethics goes, they took 3,141 children in Sub-Saharan Africa, that were diagnosed with severe sepsis. And they were randomised to either receive a restrictive fluid regime, which involved a maintenance fluid rate.
And the the other proportion would have received the standard fluid regime for people, children with sepsis, which involved a regime of colloidal support and in this situation, albumin, along with an increased rate of maintenance crystalloid fluid support. So here we have a situation which just seems completely crazy where we have children who would would classically be in need of fluids were actually deprived of of that regime. The interesting thing in this study was that after 48 hours, those children that received the restrictive fluid regime had a significantly reduced mortality rate.
And here we go, here's here's a study that is veterinary specific and ties in nicely with our our concept of of hypotension. And I'd like everybody to to really focus in on the, on the highlighted portion here, where we say high volume rapid rate administration of an isotonic crystalloid solution, so . Lactated ringer solution, Hartmann's the equivalent, was ineffective in counteracting isofluorine-induced hypertension in nomobulimic dogs at a deep plane of anaesthesia.
So what that statement is actually telling us is that the administration of intravenous fluids for the correction of hypotension, which has been directly caused by our anaesthetic gases, our anaesthetic agents, Is an ineffective strategy, and we really do need to to take that on board and then we'll elucidate that a little bit in a while. But the key concept here is fluids do not correct vasodilation. So what's the problem?
Well, essentially what we, we have been doing, and I, I like to, to call iatrogenic saltwater drowning, As, as mammals, as humans, and indeed our veterinary patients, we're very good with with dealing with hypovolemia, dehydration and so forth, we can, Increase our sympathetic nervous system activate our renin angiointestin aldosterone system, and we can compensate with that quite readily. What we're not adequately able to deal with is hypervolemia and particularly this iatrogenic hypervolemia. So what happens from a physiological sense, well, I'll just walk you through this slide, so essentially, With increased or excessive amount of fluid administration, we end up with hypervolemia, we have an increased cardiac stretch that results in that, and in response to that, we have the release of naritic peptides.
Two that are released, atrial natic peptide from the atria and brain natritic peptide as well from the vegetables, we're gonna focus on atrial natritic peptide, AMP to start with, and it does a couple of things. So the first thing would seem, Physiologic, we have excess amount of fluids, so AMP will act on the kidneys to increase urine production, which is great, it gets rid of that fluid to some extent. But it also does some negative things as well.
And then there's this, what it does, it acts on the endothelial glycocalyx, so don't be concerned if you haven't heard of the endothelial glycocalyx, we'll get to that in. A Little while. It's certainly the, the buzzword at the moment with, criticalists and, intensivists, and, it's to do with, it's a little bit of a lining of the endothelium, but as I said, we'll deal with that in a minute.
What AMP does on the endothelial glycocalyx is it increases vascular permeability and increases edoema. Now the AMP also acts on our lymphatic drainage. So the lymphatic system is similar to the cardiovascular system and whilst unlike fish and, some, reptiles, we don't have lymph pumps or lymph parts as such.
Our lymphatic system does have a, a systematic way of returning, fluid that has gone from that intravascular to the extravascular space into the lymphatic system, and it kind of, has a pulsatile action that returns that. Translocated fluid back to the intravascular space, and what AMP does, it actually retards the ability of the lymphatics to promote that, that healthy return and to the intravascular space, and so once again causes an increased interstitial edoema. So here we go, this is the endothelial glycocalyx, you can see it's this, this fluffy, this gel-like structure around here and principally, as, as far as intravenous fluid therapy goes, it's the main site for the control of the trans-capillary fluid movement.
It also has some some integral functions as far as a vascular barrier, it prevents platelet aggregation and and also has some inflammatory mediating aspects as well. But as far as the context of the talk today, it is the major component which presents, which prevents excessive fluid translocation. So, there are multiple things, it's not just, anaesthesia, we do have the option to, to blame our surgical, colleagues as well.
So certainly the stress of surgery will result in a, triggered shedding of the endothelial glycocalyx, other factors like protease release, sepsis is a classical pathology, that will result in some shedding of the endothelial glycocalyx. And other oxidative damages will also incur a loss and a shedding of this layer as well. But certainly from an aesthetic point of view, our main goal is to try and reduce the production of atrialometritic peptide and so by reduce the iatrogenic acute hypervolemia.
So it's all about protecting the endothelial glycocalyx. So, back to the, the, the clinical realm, what we really need to do is to readjust the way we think. It does require a a paradigm shift.
We need to ask what are we giving this fluid for? Is it routine maintenance? Is it replacement, or is it resuscitation, or is it just habit?
With anaesthetized patient, therefore, the patient must be going on 10 mL per kg per hour or 5 mL per kg per hour. And, and what we're going to do over the next few slides is actually step through and use draw on the scientific literature to try to find a more justifiable fluid rate for our our routine procedures. And the way that our historic 10 mL per kg per hour was originally calculated, did involve the concept of what I like to term these three Rs, so routine maintenance, replacement and resuscitation.
So if we look at the top here, we're gonna work through routine maintenance, we're gonna add what routine maintenance would represent to replacement, and then we're gonna end up with a, a total fluid administration rate that, in my opinion, is justified much more strongly by the literature. So let's firstly look at routine maintenance. The routine maintenance is essentially the basal fluid requirement based on metabolic demand, and first thing you'll notice if we look at, this is the the recommended rate from the literature here.
You'll notice that that is reduced from what you might consider to be classical, maintenance rates if you're talking about medicine or ICU classical rates, and that's because the patient is necrotized. So by default, metabolic rates are reduced to some extent. And there is a bit of a difference as far as the the categories and the weight of the patient goes as to the metabolic requirement in terms of the mLs per kg per hour.
So if we first look at patients in the weight range of 10 to 100 kilogrammes, probably the most appropriate, maintenance rate for these patients will be around 1 mL per kg per hour, and if we look at those smaller patients, so patients less than 10 kilogrammes, it's likely to be double that, so around the 10 mL per kg per hour. So that's this portion dealt with, routine maintenance, let's move on to the replacement. And for me, replacement is the, the portion of the overall fluid calculation that has has evolved the most, and I think with with new evidence, we've certainly re-evaluated this component the most.
So let's look at replacement, and there's some dogmas within replacement that I just want to touch on. So firstly, the notion of fasting. It's quite commonly said, and I've heard it mentioned, frequently, if our patients are fasted, so if our dogs and cats and so forth are fasted, they, they tend not to drink.
And so, as a result of that, they are going to be a little bit under volume, they're gonna have a little bit of a deficit in their intravascular volume by the time they get to, anaesthesia. Well, that just really isn't supported by the literature. There is good evidence to support the fact that, human patients which have been, faster, and actually more than fasted, so nail by mouth, for a period of 10 hours, had no significant change in their intravascular fluid volumes.
And just to, to, to put that into context, what are our recommended fasting regimes for dogs and cats. So if we look at adult dogs and cats, the fasting recommendations are 6 to 8 hours, you look at young and geriatric patients would recommend around 2 to 3 hours, and, it goes without saying that providing that the particular Circumstances around the, the surgery perhaps that they're going for, or if they're going for gastric surgery, then, or if they have other comorbidities like meroesophagus and and the like, then perhaps you would want to restrict fluids a little bit earlier, but for the vast majority of elective patients, they should have access to water up until the time of pre-medication. That's fasting, so dehydration, you are going to have patients which are dehydrated and require anaesthesia, so what about them?
Well, I guess the the the key for the aspect of dehydration is that in the anaesthetic context, We don't really have the opportunity as far as the time aspect goes, to be able to correct a significant portion of that dehydration. And if we do try to correct that dehydration too aggressively, this notion of, of fluid loading and so forth a couple of hours before induction of anaesthesia, then what we do end up with is a lot of Extraverssation of that fluid, we end up with a lot of bogging of the, interstit with excessive amounts of fluids, and a lot of the comorbidities that we spoke about in those first earlier slides. So, the recommendation is that we do not replace greater than 70% of the fluid deficit in 24 hours, and I think that's very important.
So don't look at the anaesthetic period as a time to, To replace those dehydration losses, really we should be managing our patients before they get to surgery, or indeed, maintaining them in hospital afterwards to adequately adequately rehydrate them to a, to a healthy point and not using that immediate perioerative period to try and do an excessive amount of of stabilisation in regards to fluid loading and administration of fluids. So how about replacement? Well, I don't know whether you of you out there might have heard the term, third space.
Well, it's a, it's a mystical term, it, it actually doesn't exist. I joke with my, with my colleagues that it's the space between the surgeon's ears, but, the reality is that, the third space does not exist. It was a concept that was, designed to try to try to categorise the fact that we did realise that, about 10% of the fluid was leaving the intravascular space during surgery, stress and anaesthesia.
We didn't really know where it went. So we now know that that 10% is generally going into the lymphatic system and providing the lymphatic system hasn't been overwhelmed, as in with the situation of hyperbulimia and retarded by ANP providing the lymphatic system is acting healthy, that 10% will just enter lymphatics and will return to the intravascular space quite happily. But what we what we have had is an increasing of the fluid rate historically, and hence where the 10 mL per kilo came from, to try to compensate for this fluid shift.
And so what we were actually doing was compounding the situation, we're actually overloading our lymphatics and actually retarding the ability of that regular system to be able to function normally. And that was really quite detrimental and in many circumstances continues to be quite detrimental. OK, so further along the lines of replacement, there are insensible fluid losses.
I, I hate that term, it's kind of insensible in itself, but basically what insensible fluid losses are, they're things like perspiration, and, loss due to urination and so forth. If we look at things like perspiration, and we consider a patient that perhaps, is, for example, just going to, Radilogy, you're getting some some radiographs taken, there's no skin incision and so forth. The amount of loss of fluid just by the the desiccation of of of the airways, is in the vicinity of around 0.5 mL per kg per hour, so we can add that 0.5 mL per kg per hour to our replacement section, in addition to our existing routine maintenance number.
So what about surgery? Well, it wasn't too long ago, and not just in in veterinary medicine, but if you had an open abdomen, people thought that you actually had to give at least 20 mL per kg per hour to try and ward against the the viscera and all the loss of And drying and perspiration that was incurred with major exteriorization of of bowel and so forth. But the reality is that there is actually, very little, fluid loss from the intravascular space due to major surgical exteriorization.
And this study by Lenke, and you can see it's not even an old study, it's back in 1977 was a particularly interesting study. So they took a bunch of human patients, and they had 4 rabbits, by the way. And what they did, they created these little biodomes over the abdomens of rabbits and over the abdomen.
Of, of the human, participants. And they had 3 degrees of surgical incision. So firstly, they had the minor surgical incision, which was literally an incision into the abdomen, and there was no parting of the skin.
So there was no visualisation of the the intraabdominal contents at all. So that was the minor degree of incision. Then there was the the moderate degree of incision, which meant that the skin was actually parted and you could visualise the the intraabdominal contents.
And then there was finally the major degree of incision, which involved full exteriorization of the viscera. And startlingly, the the most amount of fluid loss that occurred was only 1 mL per kg per hour with major steriorization of all of the of the internal abdominal viscerra. And, and so that is dramatically less than what has been practised for many, many years.
So we can add this 1 kg per hour, 0.5 mL per kg per hour to our replacement section. And if we add those combinations up, we see if we combine routine maintenance and replacement, that intravenous fluid rates rarely need to exceed 3 mL per kg per hour.
Anything above that is the requirement of resuscitation. So I'm gonna move on now to resuscitation, but as far as routine maintenance plus replacement goes, our, our number should approximate 3 mL per kg per hour, and that is across both dogs and cats. OK, so, resuscitation, resuscitation involves things like blood loss and dehydration, and it's really important to be able to categorise these.
So we can do some of these these clinically, but certainly, your patient might present with a with a clinical history that does suggest that it is. That it might on physical exam classical signs of depression also on some blood work have indices of hemo concentration or the like. It might have hematocrit changes, it might Have total protein, BUN electrolytes, urine output, blood gases, pH, the, the plethora of, of, of clinical picture that might fit with either blood loss or dehydration.
So it's important to be able to categorise that. It's important to be able to categorise that because it's important to be able to treat it appropriately and we'll get to that in a in a while. So if we just look at dehydration, I will routinely, as a, as a minimum for all of my patients before I anaesthetize them, get a PCV, TP, UFG if, if possible, as well as a good, physical exam and, and patient history, which will really.
Give me a good index, of suspicion as to whether I'm dealing with a dehydrated patient here and whether, I'm likely to experience, hypertension that in particular could be related to, decreases in intravascular, fluid volumes. Remember that by the time that you have decreased blood pressure and increased heart rate, you're probably at a point which is very, very difficult to treat, so we know that for example in in blood loss that you need to have lost at least anywhere between 30 to 50% of your total blood volume to start to see changes in blood pressure and heart rate. What we need to do as clinicians is practise meticulous attention to detail.
So for this this resuscitation component, it relies on a, a very diligent physical exam. Basic blood work will also assist with that. And intro procedure, we need to practise meticulous.
Attention to detail, so that involves communication and quantification. We need to be able to have a communication with all perioerative staff to be able to gauge how much is being lost from that intravascular space. The notion of a 4 by 4 gauze being 10 mils, a lap sponge being 100 mLs, we need to have, Clear instruction that reservoirs should be checked, suctions should be checked, and irrigation volumes should be known to be able to accurately quantify our losses and to be able to treat those at the time when they occur, not at the time when we start to see our clinical response to our patient, because by that time, We're already well and truly down the track.
OK, so, as far as resuscitation goes, and fluid responsiveness, which is this little part that I'm gonna be talking about now, the goal of intravenous fluid administration in the resuscitation, context is this. It's to increase our venous return, increase our stroke volume, and increase our cardiac output, which will ultimately increase oxygen delivery to our tissues. The kicker is that, and the problem, the ultimate problem, is that only 50% of hemodynamically unstable patients, as in patients which, in the context of this lecture, 50% of patients with hypertension, And 50% of patients which are actually under volume as far as their intravascular volume goes, will be responsive to to fluids.
So, as, as a case in point, if, an elderly person were to fall over and have a, an arm fracture or say a long bone fracture, and they've presented to an emergency department, one of the things that they will do will be to put an echo on the heart and. They will, instigate what we call passive leg raises, so they'll have the patient raise their legs, 15 to 30 degrees, and what that does, it simulates approximately 400 to 500 mL bolus of blood to the to the right side of the heart. Simultaneously, they'll be measuring echo and stroke volume, and if they see a a relative increase proportional increase in stroke volume with that increase in preload from that fluid bo so that relative fluid bolus, then we know that that particular patient is fluid responsive.
Unfortunately, we haven't broadly progressed that far in veterinary medicine, so what we do have is this this concept of, of fluid responsiveness to, to deal with somehow. So, basically a fluid responsive patient is a patient where and here we have the, the Frank Starling curve. So they're, they're a responder is a patient on this inclining part of the Frank Starling curve, and they're a patient where if you increase their pre-load, they'll get a proportional increase in stroke volume.
But if they're up on this plateau of Frank Starling curve, You can increase their pre-load as much as you like, but you really won't see a a clinically significant increase in stroke volume. So why does this happen? Well, we know from the from the human literature that it can happen for a raft of reasons.
It can, happen, for, obvious clinical, disease, so, heart disease, renal disease, remember these, these patients might already have a a actively engaged renin angiotensin aldosterone, . Sequelae, that would mean that they already have a fairly substantially full intravascular space and so relatively they're not going to increase their stroke volume anymore, but what we're also finding is that they might have subclinical heart disease or subclinical, Cardiac structural anomalies that that just means that they aren't able to respond to to a fluid challenge. What we do know is that you need to have a healthy, both a healthy left and a right ventricle to be able to respond to fluids, and often perfectly healthy people just don't fit into that category and the same is is held for our veterinary patients as well.
So what can we do, if we don't have this, you know, this diagnosis tool of echo readily available, what we do have is the notion of a a fluid challenge. What a fluid challenge is, it's about giving a rapid bolus of fluid over a period of a rapidly, you know, small amount of period, so 5 to 10 minutes, and promptly assessing the hemodynamic response. And in, in the context of of of hypertension, we could consider responders to be those patients which improve their blood pressure significantly.
So there, there are various ways of being able to challenge our patients, we have both colloids and we have crystalloids at our disposal, and just from a, I guess a hydrostatic pressure point of view. If we, if we're talking about colloids, and I'll deal with the difference between colloids and crystalloids in a minute, but certainly, colloids, you're going to require a lot less, so probably more around the 3 mL per kg, over 5 to 10 minutes for a colloid to see if a patient is a fluid responder, versus around the 5 mL per kilo over 5 minutes for a crystalloid. OK, so, some of the differences between crystalloids versus colloids, colloids, particularly our, ethyl starches have received a fair bit of, negative press, in the, in the human and also now in the, in the veterinary, realm, and that's largely to do with acute kidney injury and a lot of those circumstances.
Evolved out of ICU patients where you, you did have, constant rate infusions of colloids, not all of them, but a lot of them did, unfortunately, certainly in my part of the world and in many other parts of the world, we don't have good alternatives, so we don't have, certainly, locally here, canine. Elements, the Gelman, as a, as a physiological colloid to draw on. So, in the absence of more, species-specific colloids, we, we still, in my opinion, do have, a, a need for some of our ethos starches, in particular, hydroxy ethyl starch.
So why are they, why are they good? Well, in the context of blood loss, blood in itself does have a colloidal property, and so if we're losing a colloid, we, Ultimately, need to replace it with something that's going to fill that colloidal force with that hydrostatic hydrostatic force, and colloids, you need, you can give a lot less colloid than than the comparable crystalloid to replace that deficit. So we once used to think that, if we look at crystalloids, for every 1 mL of blood loss, we could replace that that component with about 3 mLs of crystal.
Lloyd, we've now kind of revised that to, to, to the, to the level of 1 mL of blood los loss will probably equate more to around 5 mLs of crystalloid to to replace that. And that's getting up to a large volume. And if you think about some of the problems with extra cessation of fluid, then you can see that that colloids still do have a place to a role to play because the replacement.
Ratio for a colloid is probably more of a 1 to 1 with blood loss of 1 to 1.5, so for every 1 mL of blood, it can ultimately be replaced with 1 mL of of colloid. Here's a diagram, which, basically summarises the the amount here.
I'm not going to go into it, in, in an excessive amount of detail, but it's essentially, if we have, blood loss, we need to replace that loss with something. We need to replace. That hydrostatic pressure loss with either a crystalloid, if we're going to use a crystalloid, we're looking at around 5 mL per kg for each 1 mL of blood loss.
If we're talking about a colloid, it's gonna be in the vicinity of 1 to 1.5, 3 to 1 mL of blood loss. And below that I've got the recommendations as far as when to transfuse and when not to transfuse because ultimately when you get into the realms of a patient with a hematocrit of less than 20% or the equivocal haemoglobin of of less than 60 grammes a litre, then certainly a transfusion is a reasonable option.
And as far as resuscitation goes, if we're talking about correcting intravascular losses that are non-blood related, so in the realms of dehydration, we want to make sure that we test whether our patient is actually a fluid responder or not. And so the options here are summarised are crystalloid, so, 3 to 5 mL per kg or a colloid in the same realm as I say we're probably looking at around more closely to the 3 mL per kg per hour if we're talking about hydroxye starch or the trade in volume and at least in this part of the world. I, I will make a note that I do cap my total volume of colloid to 20 mL per kilo for 24 hours.
And certainly, I do not use a colloid in in certain patients, and I'll just briefly touch on that now, so certainly patients which are which are likely not to have an intact endothelium. They're patients where you're likely to get an extra cessation of colloid, and that colloid will stick around in that interstitial, so septic patients, I tend to avoid, colloids in, in those patients and and go towards more of a a repressive therapy response. OK, so what about if your patient is, is a fluid responsive?
Well, yes, crystalloid or colloid. If a patient is fluid non-responsive, you don't have much of an of an alternative other than to go to basepressive therapy. We'll get into that a little bit more detail when we deal with hypertension.
Here are the key points from this, part of, of the lecture. So elective patients should have hydration optimised before anaesthesia. Do not replace greater than 75% of fluid deficits in 24 hours.
There's significant evidence to support a more restrictive perioperative fluid strategy to avoid this harmful effect of hypervolemia. And in crystalloids should be used to replace losses due to insensible perspiration and neurine output. And colloids are perhaps the therapy of choice to replace acute blood loss, which is above the transfusion order.
Fluid resuscitation should ultimately be guided by an by an assessment of fluid responsiveness. OK, so moving on to hypertension. What is hypertension?
Well, classically it is a mean arterial pressure, which is less than 60 millimetres of mercury. Well just on that, it's the most common per-anesthetic complication in veterinary patients and ultimately, why do we measure it? Well, it's really important to maintain our perfusion to our vital organs, so the heart, brain, and the kidneys in particular, and this mean arterial pressure of 60 millimetres of mercury is the arbitrary amount which is considered to be the minimum perfusion profession, minimum perfusion pressure to ultimately to live without oxygen.
So this part is about treating hypertension, and this slide is a little bit compressed, but I want to sort of walk you through it. Cardiac so non-invasive blood pressure and even invasive blood pressure is essentially the, the poor person's cardiac output. If we had a way of actually ultimately measuring or an indicy that was best aligned with the fusion and delivery to the tissues, it would be cardiac output, but it's invasive, it's often cost prohibitive, and so we, the, the next best thing is, is cardiac is non-invasive blood pressure.
So what are what these components here are all the factors that contributed to cardiac output or blood pressure. We have heart rate, we have contractility, we have filling pressure which is composed of blood volume and venous tone. And this slide, I just want you to focus on the the blue parts, so these are essentially the causes of hypotension.
So we have decreased heart rate, we have decreased contractility, we have decreased pre-load or feeling pressure. And then there's this one down here which we'll ignore a little bit at the moment, but I'll get to it in a minute. So essentially we have decreased heart rate, that's going to be often caused by vagal stimulation or some of the anaesthetic drugs that we use.
We have decreased contractility, some of our anaesthetic drugs will also do that. Arrhythmias are a particular cause of decreased contractility, and then there are less common things like cardiac tamperide. In the decreased preload or filling pressure, we have the two categories of absolute hypovolemia, so real loss from the intravascular space, so blood or plasma, and then we have relative hypovolemia, so that's to do with decreased vascular time.
Decreased venous return, so GDB is a classic example of that. Or maybe mechanical ventilation where we have increased intrathoracic pressure and maybe decreased venous return because of compression of some of those big vessels of the chest, like the vena cava, for example. So to touch on this one, this is a bit of a anomaly, so certainly, Increase afterload, if we have increased afterload as in compression of the aortic side of the heart, then you are going to ultimately have decreased, cardiac output.
So things like alpha 2s, so our meatomidine, our dexametotomidine, our xylazine will all increase our afterload and will obviously result, as a result of that we will decrease our cardiac output. Unfortunately, we have kind of fallen into the, the, The damaging pathway of not engaging with physiology when we treat hypertension, and I'm sure some of these will ring true as as the way you were perhaps taught at vet school. So we teach our students and it's very common for this still to occur to firstly check our anaesthetic depth, decrease our isofluorine, give an intravenous bolus of fluid, and then give atropine, and if that doesn't work, well, you might start a vasopressor.
And the problem with this is that unless you were outside having a coffee while your patient was anaesthetized, the vast majority of time your patient is at an appropriate anaesthetic desk. And, and so what I often see is that people will check the anaesthetic death, and they'll often turn down the anaesthetic gas. The patient wakes up and then they end up having to give a bottles of propofol or alfaxolone or whatever, .
Have to increase the level of of isoflurane, for example, and then the patient becomes more hypertensive. Often, these are a little bit superfluous. Yes, you should be diligently checking anaesthetic depth, but that's just part of your normal anaesthetic monitoring.
And then there's give fluid bolus, well, As you've already learned, only 50% of patients are actually going to be fluid responsive. And you've also learned about the, the harmful effects of excessive intravenous fluid administration. So, so really giving a a fluid bolus is probably not the best bang for your buck at this stage.
And get atropine. Well, yes, certainly if the heart rate is is low, and, and blood pressure is low, then, an antimuscarinic is probably a good choice. So anti atropine or glycopyrolate and yes, if there's vasodilation, a vasopressor is appropriate.
But this is a this is largely an unphysiological approach. So what do I do? Well, if I.
When I'm supervising an anaesthesia, if I walk into a theatre and I, I see a hypertensive patient, The first thing I do is look at the pre-GA exam, so pre-anesthetic exam. I turn the anaesthetic form over and I look at what that patient's physiological parameters were before I threw anaesthetic at that patient, before I threw a pre-med at the patient. I want to look at things like it's heart rate and so forth.
I want to look at its PCVTP to see whether it is a patient with potential intravascular fluid losses. And then I, I treat only the probable cause of the hypertension, so if the heart rate is low, I, I know that a 30% decrease from normal will result in decreased blood pressure. Is the patient hypovolemic?
So, is there, is it absolute hypovolemia, so I look in the abdomen, is the patient bleeding, is there any evidence of dehydration, Is there an increased PCV, increased GP, or is this relative hypovolemia? Have I given vasodilating drugs like a romazine or is it my general anaesthetic gases perhaps? Then I look at contractility.
Contractility is quite an easy one to, to assess or quite rapidly to assess. I look at my ECG. Are there any, anomalies?
As I say, certainly excessive depth of anaesthesia will result in that, but the majority of times the patient is perfectly, at a, at a stable point of anaesthesia. And then I treat which one of those was the most likely cause. And then I learned from my failure.
So just like you would with a medical consult, you can use, you know, a treatment trial. If I increase my heart rate to normal and that fails to improve my blood pressure, then I work through the algorithm and the only other alternatives are going to be hypovolemia or contractility. And then I treat the next most probable cause.
So just to, to finish up, I just wanted to talk through a couple of case examples. Here we have Leon, sorry to interrupt you. Yeah, we, we only have about 2 minutes left.
OK, fantastic. I'll I'll go through one example and then that we should summarise it. Thank you.
So, here is a, here's a case of routine ovarian hysterectomy, 8 month old kelpie, pre-medicated with methadone and aromazine induced with alfaxolone maintained on isoflurane, oxygen, and intravenous fluids. So this is the my patient monitor. Here I see a mean arterial of 50 millimetres of mercury so definitively we do have a situation that needs to be treated.
So what do I do? I firstly, I look at my pre-GA exam, what has changed or is abnormal. I look around here and, and the most striking thing is a decrease in the heart rate.
I can see here that I have a heart rate of 50 and before the patient was anaesthetized, the heart rate was around 80. And so I treat that. I treat it with glycopyrolate or atropine intravenously, and then I look and see what happens.
And, and we can see here, heart rate has returned to a relatively normal, and we have, a mean arterial pressure which has returned to 70 metres millimetres of mercury. I also look at my other indices. So I look at, if I go back a slide and I look at my my entitled CO2, I look here and I see that when my patient was hypertensive.
30 millimetres of mercury. CO2 here, when my patient is normally intensive, is around 45 millimetres of mercury. Now, CO2 is a very good indices of of cardiac output as well.
And there's only 3 things that can contribute to entitled CO2, metabolism, circulation, and ventilation. And if any of those are decreased, so in, in this case here we had a decrease in circulation or cardiac output, we had a decline in my entitled CO2, and then when we see that the main arterial pressure has improved, we have an increase in that. So do look at your other parameters too, just to confirm that you're on the right track.
I'm bearing in mind that I'm running out of time, but the key point here is essentially to to get back to looking at what the patient was like before it was anaesthetized and treat the most likely indicator. How are we going for time, Bruce? I'm Leon, as much as I'd like to sit here and listen to you, I'm absolutely riveted.
We are out of time. No, that's fine, that's fine. Thank you.
I appreciate the time. Yeah. Leon, sorry, as I say, that was absolutely riveting and I'm sure everybody that's attending would agree with me.
We could be spellbound by your insights and certainly by your shaking of our mental furniture and rattling of it. I know I certainly will be looking at anaesthetized patients a lot differently from from tomorrow. But thank you Leon.
Much appreciated and all those multiple letters behind your name certainly show up in your, in your teachings. So thank you.