Thank you for the introduction. So, yes, tonight we're gonna be talking about hemodynamic monitoring, so looking at the cardiovascular system. And you can see from this basic outline that there are actually a number of different ways in which we can monitor the cardiovascular system of our patients.
I'm gonna go through each one of these, starting with some of the more basic, everyday things that we would probably do without really thinking about them too much, all the way down to some of the more complex, and in-depth methods. But to start off with, I'm just gonna say a couple of words about patient assessment. An assessment of our patients is essential in order to understand what their condition is.
And the information that we get from assessing our patients also allows us to form plans and implement those plans. A thorough patient assessment involves a combination of a physical exam, monitored parameters, and laboratory data. But all too often I think we tend to focus on the monitored parameters and the laboratory data.
And it's really important to make sure that we're not gonna miss the woods for the trees, because we can actually gain a huge amount of information from just simply performing a clinical examination on our patients. And I find this quote quite useful that it helps remind us that although monitoring of our patients is really important, whether that be under anaesthesia or in the critical patient in a sort of an ICU setting, it's important to remember that it's not just the monitoring alone, which is beneficial or protective. Rather, it's the interpretation of that data and our actions based upon the changes in the monitored parameters.
Our patient monitoring should be targeted to the individual and avoid use of routine monitoring. The type and frequency of monitoring should be based upon the patient's underlying disease, their physiological reserve, and the degree of clinical suspicion that we have for things that could go wrong. The monitoring plan needs to allow us for early detection of any derangements while preventing excessive tests being performed which will waste resources, might be unnecessary for the patient and can make things quite expensive for the owner.
And again, just to highlight that monitoring monitored variables are only useful if an alteration is linked to an intervention, which affects the outcome. So if we're going to be monitoring our patients, but we're not going to do anything with that information that we get, then we really should be thinking twice about performing that particular test. So moving on to the cardiovascular system, we all know that the cardiovascular system is responsible for circulating blood throughout the body.
It's responsible for delivering oxygen and nutrients to the tissues and removing waste products. So therefore it's really important that we maintain cardiovascular stability because the cardiovascular system is essential to life. Many conditions can affect the cardiovascular system, and they, they can affect them in a number of different ways, including, the autonomic function, vascular tone, heart rate, and contractility.
And when we're monitoring the cardiovascular system, what we're really aiming for is to try and maintain stability, to, to avoid any extreme swings in the patient's cardiovascular state. In terms of how we can go about monitoring the cardiovascular system, as I said, we have the, the relatively basic ways in which we can monitor the, the, the cardiovascular system. And then we have some more, more specialist or in-depth ways.
And the reason I've put, CVP or central venous pressure and cardiac output at the bottom in brackets is because, while this is a way of monitoring the cardiovascular system, both of these are slightly more invasive, not necessarily performed in routine clinical practise, and they can be quite complicated, to perform. So starting with the most basic of things, it's looking at the patient's heart rate and rhythm. And this is something that we do every day in every single patient.
And we can assess the heart rate, heart rate and rhythm in a number of different ways, including auscultation, pulse palpation, or by a variety of different monitoring equipment. But what I would say is that we always really should be assessing our patient's heart rate in combination with their pulse rate and the pulse rhythm. Because this is just going to give us a little bit more information.
For example, it can give us a bit more information about potentially peripheral perfusion or whether there are any pulse deficits present. And something which will cover a little bit more when we talk about ECGs, but it's worthwhile mentioning here, is that if we're using an ECG to look at a patient's heart rate and rhythm, we do need to remember that the ECG is simply showing us electrical activity of the heart, and it doesn't necessarily mean that we have a contracting heart. The other thing that we need to remember is that heart rate is actually really quite non-specific, and we must take it in context with what else is happening.
So, as a simple example, this box here indicates some of the multiple reasons for why tachycardia may be present in a patient. And we need to play a bit of detective work when it comes to things like this and try and rule in or rule out different reasons for why the patient may be tachycardic. In terms of what is normal for a heart rate, this obviously varies across species, but what people often find surprising is that patient size often has very little impact.
What has more of an impact is the patient temperament. And although I've written a range of what most people would consider a normal heart rate for for dogs and cats. Obviously, this is going to vary massively depending upon both the individual patient and the circumstances.
So for example, if we had a highly stressed cat coming into the clinic with a heart rate of 140 to 160, I would consider that to be slightly abnormal, because we would expect a highly stressed cat to be somewhere up near 220. Now, we've mentioned assessing pulse quality and how important that is in terms of assessing it at the same time as looking at our patient's heart rate and rhythm. And we've already said that this can give us indication of whether there are any pulse deficits present and also gives us an indication of perfusion.
And when we're feeling for pulse quality, what we're actually feeling for, or what we can actually determine from the pulse quality is what's known as the pulse pressure. The pulse quality does not indicate blood pressure. The pulse pressure is simply the difference between the systolic blood pressure and the diastolic blood pressure.
So our pulse quality will feel good if there is a large difference between these numbers. But we can have a large difference between these numbers, at the lower end of the scale or a large difference between these numbers at the high end of the scale, and equally we're still going to feel like we have a good pulse quality, but we might have a low blood pressure. Although it's very crude, we can assess mucous membranes in terms of both their colour and capillary refill time.
And that'll give us an indication, about some features of the cardiovascular system, but also potentially other body systems. Obviously, in a normal healthy patient, we would expect the mucous membranes to be of a salmon pink colour, be moist and have a capillary refill time of between 1 to 2 seconds. We should be aware, however, that, apparent mucous membrane colour is influenced by ambient light.
So, probably the best example, we can use is the use of heat lamps. The red colour of the heat lamps makes interpretation of mucous membrane colour almost impossible. So, it can be useful to make a note of how the mucous membranes look, underneath the particular lighting either in the kennel environment or the theatre environment, prior to, for example, anaesthesia.
So we're gonna have a baseline for comparison. And as I said, obviously, appearance of mucous membrane colour can give us an indication of, conditions with the cardiovascular system, such as anaemia, shock, or blood loss. But it can also give us an indication of other problems such as, hypoxia, liver disease, or hemolysis.
In certain circumstances, there are going to be changes to mucous membranes, which, what we would maybe expect. So, for example, if we have a patient in a state, or we administer them drugs, which causes vasodilation, we're going to have mucous membranes which are pinker than we would sometimes expect. And the reverse is true.
So if we administer drugs. Or we have a patient in a state of vasoconstriction, then they're going to have paler mucous membranes. And again, one of the best examples that we can give of this is when we administer an alpha 2 agonist to the patient.
And I'm I'm sure you've all seen where after we administer a large dose of an alpha 2 agonist, the patient's mucous membranes look very, very pale. And then as soon as we administer the attipamazole, they become a lot pinker again. And it's actually, it's kind of highlighted in the colour of the original bottles of the original, Metaomidine with dormito and antecedent where the dormitor was a blue coloured bottle and the antecedent was a red coloured bottle.
As you said, normal capillary refill time is 1 to 2 seconds, and, capillary refill time can give us an indication of peripheral perfusion with a prolonged capillary refill time indicating vaso constriction and a shortened capillary refill time indicating vasodilation. However, we do need to be aware that this is not particularly sensitive, and we can see in this video here a patient which appears to have a relatively normal capillary time, but this patient is actually dead and had been euthanized about 5 minutes before this video was taken. So, while it capillary refill time does give us some useful information, we do kind of need to bear in mind its limitations.
So I've mentioned perfusion quite a lot already and ensuring adequate peripheral perfusion or blood flow is critical in any patient, whether they be conscious or anaesthetized. And very often we measure blood pressure and we, we're using this as kind of a surrogate marker for perfusion. But it's really important to remember that blood pressure does not necessarily mean that we have a good perfusion.
If we have a patient with what we would deem to be good blood pressure, which usually means a high blood pressure, this may simply be because they have excessive vascular tone, which is actually limiting blood flow. However, as we'll come on to, blood pressure does give us an objective measurement, which is relatively simple to achieve. So in terms of how we can actually assess perfusion, it's really can be quite difficult and it's also quite subjective.
And there are 6 parameters which we can use clinically, at least in the conscious patients, to help us assess perfusion, and that includes mentation, mucous membrane, colour and capillary refill time, heart rate and pulse quality and extremity temperature. But as we've already seen, these factors are not particularly sensitive and can be altered by a number of different things. And then when it comes to sedated or anaesthetized patients, these subjective parameters become even more difficult to assess due to the inevitable alterations that we're causing in hemostasis.
So it has been shown that global markers of anaerobic metabolism, such as a negative base access or a high lactate, are more sensitive indicators of perfusion when compared to either blood pressure or a physical examination and the subjective parameters. And they could also prove useful for anaesthetized patients as well. In the human literature, it has been shown that up to 80% of hypovolemic patients that were treated to an end point of a normalised heart rate, blood pressure and urine output were actually still considered to be hypo perfuse based upon evidence of anaerobic metabolism.
So these sorts of things are something which maybe we can start thinking about if we're trying to assess a patient's perfusion. But as I said, we often measure blood pressure and use that as kind of a surrogate marker for perfusion. And this is because of the limitations of peripheral perfusion assessment.
Repeated blood pressure measurement is, is relatively easy. It gives us an objective measurement and it allows the trends to be observed over time. It does provide us with a crude indication of cardiac output and perfusion.
But as we've already said, there are caveats associated with this. So if we look at this little box here, we can see that mean arterial blood pressure is roughly equivalent to the product of cardiac output and systemic vascular resistance, that is vascular tone. And cardiac output in itself is equal to stroke volume, so how much the how well the heart is contracting and heart rate.
So we can see from this that if we increase our systemic vascular resistance or our vascular tone, we are going to be increasing our blood pressure, and that makes sense. But as we've already said, this may worsen perfusion. Having said that, we do require a minimum blood pressure in order to perfuse our tissues and remove our waste products.
And normally speaking, we are looking for a blood pressure, a mean arterial blood pressure above 60 millimetres of mercury. And hypertension is defined as anything less than that, and hypertension is defined as anything with a mean arterial blood pressure over 110 millimetres of mercury. And there are a number of different ways in which we can measure blood pressure.
We can have non-invasive methods including the oyometric and the Doppler methods, and we can have invasive blood pressure monitoring and that requires placement of an arterial catheter. We most commonly encounter hypotension in our anaesthetized and critical patients. And generally speaking, we would define mild hypotension as having a mean arterial blood pressure, between 45 and 60 millimetres of mercury.
And while this is common, particularly in anaesthetized patients, it doesn't mean that we shouldn't take steps towards correcting this, in order to try and minimise morbidity of our patients. And severe hypertension is defined as anything less than 45 millimetres of mercury, and this definitely requires prompt diagnosis and management. When we're thinking about blood pressure and in particular, alterations in blood pressure and then deciding how we go about treating it, often it's quite useful to have an understanding of the contributors to blood pressure because that can help us, troubleshoot and problem solve as to what's actually causing the problem and how we can best treat it.
So we've already seen that mean arterial blood pressure is roughly equivalent to the product of cardiac output and systemic vascular resistance. And so from this we can think, well, if we have a low systemic vascular resistance and vasodilation, this means that our mean arterial blood pressure is gonna be low. So does the patient have vasodilation that we can treat?
Do they have a mal distribution of blood flow or a reduced preload? And can we help solve this by providing fluids to our patient? Do they have a reduced cardiac contractility or a reduced stroke volume, which is contributing to a reduced cardiac output?
And do we need to try and improve cardiac contractility with a positive inotrope? Or do they have bradycardia and it's a reduction in heart rate, which is affecting the cardiac output and therefore may not tell your blood pressure. So if we work through this in a logical fashion and take things back to first principles, it can actually go quite a long way to helping us solve problems.
In terms of how we measure blood pressure, first off, we have the solemetric blood pressure monitoring tools. This is a non-invasive method, and it's useful because it, measures systolic, mean, and diastolic blood pressure. It's quite useful because it can give us trends.
But unfortunately, it does also, or it can, suffer from a number of inaccuracies, particularly if the patient is hypotensive, hypertensive, if they've got arrhythmias, or any extremes of heart rate. So basically, our symmetric blood pressure, is going to give us a good reading when everything is nice, normal, and working fine. But if something starts to go wrong, then we're gonna potentially suffer inaccuracies with this.
One thing I would say, which is useful to remember, is if you have a stand-alone symmetric blood pressure monitoring, tool, that provides you with a pulse rate as well as blood pressure. Check the pulse rate that the machine is giving you with the patient's pulse rate when you take a pulse. And if they match, it's more likely that, you're going to have an accurate or more accurate reading.
If the pulse rates are widely different, then, I would be a little bit cautious about interpreting what the blood pressure reading is that we're getting. In terms of how we use an oylometric blood pressure monitor, we need to place a cuff on either the patient's limb or the tail. And that cuff is inflated by the monitor to a pressure which is above systolic arterial blood pressure, and the monitor then gradually deflates that cuff.
As the cuff is deflated, vibrations will start within the arterial wall, and they will be detected by the monitor. And as you can see on this graph here, the vibrations start, Around about systolic blood pressure. They gradually get larger and larger and larger, and they reach peak amplitude at mean arterial blood pressure, and then they gradually get smaller and smaller and smaller until they disappear at diastolic blood pressure.
So that's how our monitor will determine systolic, mean, and diastolic blood pressure. Whenever we're using a symmetric blood pressure monitoring, it's really important that we get the right size cuff for the patient. And in order to determine what is the right size cuff, we're looking for a width to be approximately 40% of the limb or the tail circumference.
If we're using a cuff which is too small, the blood pressure will overread, and if we're using a cuff which is too large, it will underread. Sometimes it's not possible to get the perfect size cuff. However, if we move the cuff to different parts of the limb or a different limb, then this can help optimise the, the size that we're using.
High definition oylemetry is a new type of monitor, or relatively new. Again, it's a non-invasive monitor, and it uses an internal processor to manage and monitor, the valve, which releases the pressure in the cuff, and can do this over a very wide range of around 5 to 40,450 millimetres of mercury. It allows a very linear cough deflation with real-time scanning and analysis.
And if it's used with the computer programme which goes with it, it can allow real-time data acquisition and analysis, and as we can see with the screenshot here, it can present a beat by beat presentation of the pulse waves. This allows the user to help determine whether or not the reading is acceptable or not, is accurate or not. But unfortunately, in a clinical setting, use of the monitor in combination with the, the computer programme is a little cumbersome.
And without use of the of the computer, then it, it becomes kind of a little bit more like a standard, a symmetric blood pressure monitoring tool. Use of a Doppler can be extremely useful, and often they're available in even the smallest of veterinary practises. They provide a continuous auditory signal, which automatically provides us with information on heart rate and rhythm.
And if the Doppler probes are placed over an artery and have a inflatable cuff placed proximal to to the probe, then combining that cuff and anemometer, with the Doppler probe, it will allow us to get blood pressure readings from the patient. It kind of works in a similar way to the oyometric blood pressure monitoring in that that we use a manometer to inflate the pressure cuff until we no longer hear the audible signal. And then as we gradually release the pressure in the cuff, when we hear the sound reappear, that is determined as our blood pressure.
In dogs, this is fairly reliably known to be systolic arterial blood pressure. But in the cats, the jury is still out as to to what exactly this pressure reading is. So, The, the thinking now is that actually this, this reading in the cat is somewhere between systolic and mean arterial blood pressure and actually probably falling slightly closer to the mean than the systolic.
So personally, when I'm taking a Doppler blood pressure reading, my sort of cutoff levels for hypotension in the dog, I use 90 millimetres of mercury because I'm treating that as, systolic blood pressure. Whereas in the cat, I tend to use a slightly lower cutoff of around about 80 millimetres of mercury because what I'm kind of telling myself is that we know that in the cat, the, the, the reading we're getting is less than systolic blood pressure, but actually it's also probably higher than mean blood pressure. So I kind of split the difference and use 80 millimetres of mercury.
Invasive blood pressure is considered to be the gold standard way of measuring blood pressure. However, it can be technically more challenging and it does carry some risks, because we have to place an arterial catheter. However, we can justify its use in certain situations, so particularly if a patient is going to be hemodynamically unstable, and therefore require continuous blood pressure monitoring, or if the patient is likely to need multiple arterial blood gases to be taken.
The use of invasive blood pressure monitoring can provide measurements even in the presence of arrhythmias or extremes of heart rate, and as we've already said, it can provide beat to beat information on blood pressure. And when we're using it as we can see in this picture here of the the monitor, we also get a pressure wave trace. So it gives us an indication about what the pulse character is doing as well.
In order to perform invasive blood pressure monitoring, as I've already said, we need to place a cannula in a peripheral artery. We can use a number of different, arteries. The most common is the dorsal metatarsal artery, although we can also use the radial planter metacarpal, aricula and coccygeal arteries as well.
Once we've placed the arterial cannula, this needs to be connected to a saline-filled manometer line and pressure transducer, which we can see an example of that here. And then that pressure transducer is connected to a monitor and we perform what we call zeroing. So we're telling the computer what atmospheric pressure is and therefore what zero is.
And we're also zeroing this at the level of the patient's heart. So this transducer needs to be level with the patient's heart. As I said, there are some risks associated with invasive blood pressure monitoring, some potential complications, which can include serious haemorrhage.
So obviously this cannula is attached to an artery. So if they're going to bleed out, they can do so much more quicker than with an artery. And you can see in this picture here, I placed an arterial cannula in the dog, and unfortunately, the sliding clamp, which was used on the T connector, shed through part of the T connector, and this was under drapes at the time of surgery.
And so I didn't see for a little while that, the, the patient was bleeding through this, hole that had been made in the T connector. So it is, it is a risk that we need to be careful of that, haemorrhage can occur. Obviously, we can have complications such as air embolism and thrombophlebitis, which tend to be a slightly greater problem if they occur in an arterial catheter compared with the venous catheter.
And we can also get distal ischemia and necrosis because, depending upon where we place the cannula, some of the vessels we use might be end arteries and supply tissue that where there is no other collateral circulation. When we place arterial catheters, we should always, and we, we're planning on keeping them, them in longer term. They should always be flushed around about every 1 to 2 hours to try and prevent the likelihood that a clot is going to form, and they obviously should always be labelled as an arterial catheter to avoid inappropriate drug administration.
As I've already said, when we place an arterial catheter and are using invasive blood pressure monitoring, we tend to get a nice arterial pressure wave form trace that we can see here. And this arterial wave form can give us information about different parts of the cardiac cycle. So we can see I've labelled here, we can get an indication about systole, the pressures which are occurring during cystole, and also during diastole.
And when we look at the arterial wave form, qualitatively, we can get an indication about different aspects of the cardiovascular system. So it can give us an indication of myocardial contractility and stroke volume, and also whether the patient is hypovolemic or vasoconstricted. Now, from simply eyeballing the arterial waveform, we don't get necessarily any quantitative data.
We don't get actual numbers that we can write down, but we can get an idea of, of how the patient is doing. And if we, perform changes, so for example, we were to give the patient a fluid bolus or we were to give them vasopressors if they needed it, we can see visually changes that happen in the arterial wave form in response to this. Now, we said that invasive blood pressure is considered to be the gold standard, but it is still possible to get artifactual measurements when we're working with invasive blood pressure monitoring.
And these are often known as either an over damping or underdamping, and we'll discuss each of these on the next couple of slides. Most of the time, these over damping or under damping occurs because of equipment problems. And the best way to try and minimise distortion of, these waveform traces and artefacts, is to use the correct equipment, because it, this kind of takes us back to our, sort of GCSE and A level physics where, we, we were thinking about resonance and all of our different waveforms.
Being created. But basically on a practical level, in order to minimise distortion of the way informed traces, we need to have equipment which is short, wide, and stiff. So we need to have catheters, which are as short as practically possible and as wide.
So as larger gauge is practically possible. And the manometer tubing that we're using to connect the catheter to the transducer needs to be a stiff and noncompliant. Over damping is the most common thing that we tend to see, the most common artefact with invasive blood pressure monitoring.
What we tend to see with over damping is an unnaturally smooth wave form. So a falsely low systolic arterial pressure and a falsely high diastolic pressure. But usually the mean arterial blood pressure is still correct.
So if we look at the examples down here, this wave form on the left is considered to be normal. Whereas the wave form on the right here, is considered to be over damping. And that can occur due to a number of different reasons.
We've already mentioned that it can occur due to technical problems and problems with the equipment, but it can also happen as a result of changes in our patients status as well. Under damping is the other extreme. That's where we have an exaggerated wave form with a large amplitude.
So we have a falsely high systolic arterial blood pressure and a falsely low diastolic arterial blood pressure. But again, usually the mean is still correct, and we can see that here in the middle. This is a middle wave form is an example of an underdamped waveform.
And again, this can occur with technical problems, but can also occur as a, as a result of changes within the patient. What we're actually looking for is a balance between over damping and under damping. We want to avoid excessive resonance and excessive damping.
And this is what's going to give us the most reliable measurements. In order to to qualitatively assess the amount of damping which is present within the monitoring system, we can perform what's known as a quick flush test. If we flush the arterial line with a normal saline at a pressure of over 300 millimetres of mercury, basically over systolic arterial blood pressure, the trace should oscillate, both positive and negative for 2 to 3 cycles before settling on a wave, before settling on what will give us the waveform.
Anything more than 2 to 3 cycles indicates under damping and anything less over damping. So we can see here, this is an example of a normal quick flush test. So we, when the pressure is consistently high here is when we're flushing it, we release the, the flush and we get a cycle of, 2 to 3 times.
In the middle here, we have an example of under damping, and on the left here, we have an example of over damping. And this is something we can quickly do in the clinic to get a, a qualitative idea of how, how reliable our results are going to be. Moving on to central venous pressure, this is basically the, the pressure measured within the right atrium of the heart.
It's influenced by a number of different things. It's a a influence of a balance of the cardiac output, and venous return. And people do use it as a crude indication of the patient's volume status as to whether the, the patient is hypovolemic, normovolemic or hypervolemic.
It requires a jugular catheter to be placed and ideally that jugular catheter needs to be at the level of the right atrium. So it is a little bit more invasive because obviously jugular catheters are a little bit more challenging to place some peripheral catheters, and they have to be done in an aseptic manner. And then when the jugular catheter is placed, traditionally, central venous pressure was measured with a, a YouTube manometer, but in reality, nowadays, we use a, a pressure transducer like we've already seen for the arterial blood pressure.
The normal reference range for central venous blood pressure is between 0 to 8 centimetres of water. And generally speaking, a low central venous blood pressure is often taken to mean that the patient is hypovolemic and a high central venous pressure as the patient is volume overloaded. But actually what's probably more useful than just looking at individual numbers in particularly numbers in isolation, because it can be affected by so many different things, including stage of the cardiac cycle, intrathoracic pressures, so whether the patient's breathing in or out, if they have plural space disease or whether positive pressure ventilation is being applied.
What's more useful is looking at the patient's response to a fluid challenge. So what you tend to do is, look at the, original central venous pressure, give a fluid challenge of, let's say 5 to 10 mL per kilo of an isotonic. Crystalloid solution rapidly and then see what the response of the CVP is.
And we can see here that in normal volemia, the CVP will rise slightly, but fall back to normal after about 15 minutes. In hypovolemia, the CVP should rise slightly, but rapidly fall again, and in hypovolemia, the CVP rise and remain high. Now people do still use this, but actually, as I've already kind of indicated, CVP is affected by so many different things, and there are actually so many assumptions that are made when we're using it, that actually, it's usefulness is, limited, and actually because it's a little bit more invasive to do, it personally, I, I don't really use CDP much anymore.
Pulse oximetry provides us with two useful bits of information. Firstly, the patient's pulse rate, and then secondly, the saturation of haemoglobin with oxygen. Assuming a patient is not suffering from pulse deficits, again, that the pulse rate on the pulse oximeter should match the heart rate, but this does need to be clarified in each individual patient.
In a normal, healthy conscious patient who's breathing room air, arterial haemoglobin saturation should be equal to or above 98%. But obviously, when we anaesthetize patients, we can cause a whole host of changes within the ventilatory system. We can cause hyperventilation and ventilation perfusion mismatches, which may result in a haemoglobin, saturation level slightly lower.
So, anything sort of like down to 95%. Pulse oximeters are very useful, but they can also be quite frustrating, particularly if we don't have an understanding of what the limitations are. What's really important to appreciate with pulse oxim, pulse oximetry is that it is measuring oxygen saturation of haemoglobin.
It does not measure total oxygen content of blood. And to kind of understand this a little bit more, we need to think about how oxygen is transported around the body. So 97% of our oxygen is combined with haemoglobin, and only 3% is dissolved in plasma, and it's just 3% which is dissolved in plasma, which is known as our PAO2.
So if we're taking an arterial blood sample and we we're looking at the PAO2, which is what we often use to define hypoxemia in our patients, that is only representing 3% of our oxygen transport through the blood through the body. So therefore, haemoglobin is really, really important and it actually increases the oxygen carrying capacity of our patients by around about 60 times. Which means clearly an anaemic patient can very easily suffer from a reduced oxygen delivery.
And as an example, I've got this slide here where we can see, two different dogs, a healthy Labrador, who's got a PCV of 40 and a slightly low SPO2 of 94%, and a spaniel with IMHA, so a low PCV of 15%, but an SPO2 of 99%. Along the top of this table here, we can see a pretty complicated equation. It's basically, Here is how you go about calculating total blood oxygen content.
And when we plug in these figures for the two different dogs, dog 1 and dog 2, what we end up seeing is that the total blood content is vastly different. So dog 1, who has a normal PCV but a low SPO2, actually has way more oxygen within the total oxygen content within the blood and then dog 2 with a low PCV. So despite having a higher SPO2, dog 2 has a much, much lower blood oxygen content.
So when we're using our pulse oximeters, it's important to remember that although our saturation may be good, so we may have a good reading on the pulse oximeter, in an anaemic animal, a normal SO2 reading doesn't guarantee that the blood contains enough oxygen to meet the patient's requirements. Going back to our physiology, we've got the oxyhemoglobin dissociation curve, and this curve, which we can see in the graph, describes the percentage of haemoglobin saturation with different partial pressures of oxygen. And we can see how, because it's got a sigmoid shape and S shape, at the normal end of the curve, we have, if we have small decreases in our saturation, so for example, between the green line at about 98% to the red line at 90%, we will end up with very dramatic decreases in our PAO2.
However, because the shoulder here at 90% correlates with a PAO2 of 60 millimetres of mercury, which is what is defined as, as hypoxemia. These small decreases in, in SPO2 between 190%, don't actually actually really give us an indication of whether the patient is hypoxemic or not. However, below 90% of SPO2, this does give us a very sensitive indicator that the patient is hypoxemic, because below 90%, we fall below the 60 millimetres of mercury and we fall very, very quickly.
So less than 90% SPO2 does give us a sensitive indicator that our patients hypoxemic and we should be doing something about it. When we're using pulse oximetry, we need to attach the probe to an unpigmented, bit of tissue and a bit of tissue which is pulsatile. So normally we use the tongue, but if this is not possible, so for example, a chow who has a pigmented tongue, there are other places we can use, including the prep use, vulva, potentially the ear, sometimes the upper lip works in anaesthetized patients, anywhere that is unpigmented.
The pulse oximeter machine sends, red and infrared light at about 30 times a second through the tissue and then measures it via a sensor on the opposite side of the tissue, and measures the amount of light which has been absorbed by that tissue. And as I say, and I'm reiterating that it's important to appreciate that pulse oximetry measures oxygen saturation of haemoglobin, it does not measure total oxygen content of blood. We do have limitations associated with pulse oximetry.
As I said, they are frustrating bits of kits sometimes. And I've listed here a number of reasons for, potential artefacts. So if you do have a low pulse oximeter reading, the first thing to do is not necessarily assume that that is true, but maybe look to why you may be getting artifactual readings.
Moving on to the ECG, as I've already said, the ECG simply provides information on the electrical activity of the heart. So it gives us information about whether the patient has any abnormal cardiac rhythms, or also conduction abnormalities. What it doesn't do is provide us any information on cardiac outputs.
We do not know if our heart is contracting simply by looking at the ECG. The other thing we need to be aware of is that when we're using the ECG to look at the patient's heart rate, we need to check that that heart rate given by the ECG is correct. Most of the anaesthetic monitors that we're using, are designed to be human monitors, and so they sometimes struggle with our patients and their slightly different ECG complexes.
So they sometimes will double count the heart rate because normally they're looking at the R wave and they're using this as their way of determining heart rates. But our patients can sometimes have very large T waves and sometimes even very large P waves. So sometimes it can either double count or even triple count the heart rate.
Also, for cats, certainly most of our anaesthetic monitor ECG's struggle with cat ECG traces, just simply because they're so small, and they sometimes read that the cat is in asystole, which obviously we know not to be true. However, having said that, ECG is the gold standard for cardiac rhythm assessment, and we do need it for definitive diagnosis of arrhythmias. In terms of when arrhythmias are detrimental, this is something that we kind of need to assess in our patients because not all arrhythmias, particularly under anaesthesia, not all of the arrhythmias that we see are pathological and detrimental to the patient.
And my sort of kind of guideline is to to when it's starting to become detrimental or pathological is firstly, if we're starting to see pulse deficits in the patient, but also whether that abnormal ECG rhythm is starting to affect our patient's blood pressure. If our patient is starting to be hypertensive with an arrhythmia, then for me, that's ECG is becoming clinically more important. In terms of how we attach the ECG we can either have a 3 lead or a 4 lead ECG and if we're wanting to properly look at the ECG, interrogate it and perform measurements, then we really do need to be attaching the ECG leads in this configuration.
However, having said that, depending upon what a patient is having done when they're anaesthetized, it may not be possible to attach the ECG in this configuration. So if they're having 4 limb on both, sorry, surgery on both for limbs, we can't use potentially either for limb to attach the ECG. We have to improvise.
And in that case, I would, try and turn my ECG upside down and I'd maybe have an ECG lead on both back legs and one on the nose or the ear, for example. So we can get a little bit creative in anaesthesia when it comes to using. And positioning of ECGs.
Basically, we're looking for a nice, a nice size of, trace and one which, we can recognise what is happening. In terms of the ECG complex, we can break it down into kind of three main sections. We have a P wave, which represents atrial depolarization, which we would hope is followed by atrial contraction, but not necessarily so.
We have the QRS complex, which represents ventricular depolarization, hopefully followed by ventricular contraction, and we have the T wave, which represents ventricular repolarization. We do not see atrial repolarization because that is hidden within the QRS complex. Whenever I'm looking at an ECG complex, I think in order to recognise an arrhythmia, we need to look at the PQRS complexes in a systematic fashion.
And I always tend to ask myself the same four questions, and that is, what's the morphology of the ECG? Can I identify all of the different parts of the complex? Are the complexes uniform?
Do they look the same? Are they regular or irregular? And also something that you can't tell by simply looking at the ECG you have to look at the patient as well.
It's whether there is an output associated with the complex. Is there a palpable pulse for each complex? So I'm sure you're all aware of what normal sinus rhythm looks like.
We have identical R to our intervals, which indicates a regular rhythm. There is a P wave for every QRS complex, and there is a QRS complex for every P wave, and all of the QRS complexes appear normal. And if we were to palpate for a pulse, there would be a pulse for every complex.
This is an example of sinus arrhythmia, and what we can see is that there is a normal complex morphology and that they are all uniform. Again, there's a P wave for every QRS and the QRS for every P. However, the complexes are irregular, and there are variable R to our intervals with some shorter and some longer, but this is an irregular pattern.
And it's likely that in this case, every complex will produce a pulse. And obviously, we all know that sinus arrhythmia is where the heart rate is linked to to respiration, and it can be completely normal in dogs, particularly those with a high vagal tone, so our fit, healthy dogs, or particularly brachycephalic dogs, those which may have concurrent gastrointestinal disease or after drugs such as an alpha 2 agonist. However, in cats, sinus arrhythmia is abnormal, particularly if it's detected within the hospital environment, because, cats are basically small balls of sympathetic, stress, and so we would not expect them to have high vagal tone.
So they should not have, sinus arrhythmia. This is an example of 2nd degree AV block, and when we look at it, we can see that there is a normal QRST complex, and all of the QRST complexes are uniform, but some P waves do not have an associated QRST complex. The complex frequency is irregular, with a longer R to our interval where the P waves don't have an associated QRS complex.
And if we were to feel for pulses, there would be a pulse deficit, obviously where the QRST complex is missing. The cause of second degree AV block is basically not all of the waves of depolarization from the atria are being conducted through the AV node. And again, this can occur due to high vagal tones, so our brachycephalics, our athletic dogs, .
Dogs with the gastrointestinal disease, or it can be drug induced. The, the big one is alpha 2 agonists, and we very regularly see this, under anaesthesia if we were to administer an alpha to agonist. And it can also incur due to primary cardiac disease, such as fibrosis of the AV node and also electrolyte imbalances.
Ventricular complexes, result in abnormal morphology of some of the complexes, so we can see here and here. There's no discernible P wave and the QRS complexes are wide and bizarre, which indicates that the polarisation is occurring in the ventricles rather than the sinoatrial node. And so they are known as a ventricular complex.
The abnormal complexes in this example are uniform, but they may not be. And if they are not uniform, it's indicating that they are originating from different parts of the ventricle. In, in this case, the irregular complexes, come slightly early, so they, they, these would be known as ventricular premature complexes.
And with these ventricular complexes, there may be a pulse deficit. The list of reasons for why we can have ventricular complexes is huge. So we can have structural heart disease, they can occur with abdominal disease.
It can be drug-induced hypoxia, due to anaemia or uremia. The list is huge. And in terms of whether they are becoming clinically significant, again, personally, I tend to look at whether they're causing pulse deficits and more importantly, whether the patient is becoming affected by them and having changes in blood pressure.
Ventricular tachycardia, is basically, long runs of ventricular complexes with a heart, a high heart rate. And usually ventricular tachycardia is defined as having a heart rate in dogs of over 160. If they're showing ventricular complexes and long runs of ventricular complexes, but their heart rate is less than 160, this is often known as idioventricular rhythm.
And is less, worrying because, generally at a heart rate of less than 160, even with, ventricular complexes, the patient can generally maintain an appropriate, output. But in this instance, when we're looking at ventricular tachycardia, we can see that the complexes obviously don't have a normal morphology. Again, there's no discernible P wave and the complexes, the QRS complexes are wide and bizarre.
Again, in this instance, the abnormal complexes are uniform, but they may not be, and the complexes are regular. Depending upon the heart rate, we may or may not have pulse deficits. The reasons for ventricular tachycardia are pretty much the same as the reasons for isolated ventricular complexes, and they can be numerous.
So again, we might have to play a little bit of detection work to find out the, the underlying cause. Now this is an example of atrial fibrillation. All of the complexes have an abnormal morphology.
There's no discernible P wave, but there is, but they are the QRST complexes are supraventricular, they're not ventricular. Atrial fibrillation may or may not have an irregular baseline and you can see that here it's got a wibbly wobbly baseline. In this instance, the CRST complexes appear uniform, but the rhythm is highly irregular, and often, at least when it's first diagnosed, atrial fibrillation has a high heart rate.
And this patient is likely to have pulse deficits. In terms of what causes atrial fibrillation, generally it's a structural heart disease, but if we have giant breed dogs, it may be, I, when I say normal, I say that in inverted commas, because in these dogs, they may, the, the giant breed dogs, they may not have structural heart disease. It's simply because they have such a huge heart that the size of the atria will allow atrial fibrillation to set up and be continued.
It can also be drug induced and it can occur as a complication of other diseases such as GDVs. Moving on to cardiac output, cardiac output is defined as the volume of blood in mills per minute, which is ejected from the the ventricle. In combination with peripheral perfusion, cardiac output is probably the most useful cardiovascular parameter.
Having said that, direct measurement is actually really quite challenging. And in clinical practise, what's often sufficient is to just consider the influencing factors, and we've already seen this equation here, where cardiac outputs is is equal to the product of stroke volume and heart rate. There are a number of different ways we can measure cardiac output.
The, some of them are limited more to experimental settings. So for example, thermo dilution and placement of a swangans catheters into the pulmonary artery. And there are some more clinically based methods of cardiac output.
Including transesophageal Doppler, which we can see here, this patient has a probe into his oesophagus and it's, giving as a Doppler reading, and we actually have one of these in my place of work and we can use it in anaesthetized patients to get an idea of cardiac output. You can also use transesophageal echocardiography, where again, you're using an esophageal probe in an anaesthetized patient, but this time you're getting echo pictures and not just Doppler. You can use point of care ultrasound.
Which is probably one of the, the most clinically relevant, ways of at least gauging cardiac output. Lithium dilution, it has been commonly reported in a lot of clinical studies, but, it does require the equipment and placement of an arterial catheter. And we've already discussed how looking at the arterial wave form from an arterial catheter can give you a qualitative indication of cardiac output.
But there are also monitors out there which use the information from this to try and convert it and give you an absolute number of cardiac output. So hopefully I've illustrated to you that there are many different ways to monitor the cardiovascular system, and it's important to have an understanding of the patient's physiology and how we can actually use knowledge of the patient's physiology to help us work out what is going on, and use our monitors to their maximum potential, hopefully interpret the results and get, the best outcome for our patients. So brilliant.
Thank you very much, Becky. Absolutely brilliant webinar. I'll wait a couple of minutes and see if anybody has any questions.
And just to remind those listeners who would like to ask a question, just hover over the bottom toolbar on your screen, click the Q&A box and send it through and I can ask Becky. Really interesting video that you shown about the patients who've been deceased for 5 minutes, yet still had the capillary refill time. I find that one quite scary.
Yeah, it is quite scary. Yeah. And the mucous membranes still look quite pink as well.
Yeah, yeah, it looked almost pretty much normal. Yeah. No, I agree.
OK, in your browser there will be a feedback form that will pop up. If you could all fill that in, it will only take a couple of seconds, just ask 4 or 5 questions and we can feed back some info to Becky and also tailor the webinars to meet your needs, find out what you like, what you don't like, and if you could do that at the end, that would be great. We'll just stick around another couple of minutes to see if there are any questions, do feel free to ask to get the most out of the webinar that you can.
I think all of the slides on the ECG complexes are all particularly quite interesting. So they're really difficult to to understand and to interpret all the different complexes. Yeah, especially I find with cats, all of the examples I gave were based on on dog ECGs just because they're a little bit easier to interpret, but, .
Cats have minuscule ECG complexes and especially with a lot of our anaesthetic monitors at least, they're so heavily filtered so that they can work, well with all of the other electrical interference which is going on. It makes it very, very difficult to for us to actually interpret what's happening. So even now I still struggle when it comes to cat arrhythmias.
Yeah. Where I work, we do a lot of four limb CTs when we're placing the ECG on, obviously we can't have it on in the imaging on the forelimbs. So we tend to put them on the hind limbs and then one on the ear, but we don't always pick up a good traits.
Is there anything you would do to alter that? So sometimes just a simple changing of which leads you're using, can help. Most often people are using lead 2 under anaesthesia.
So obviously, you've got your traditional sort of like 6 lead ECGs, lead 123, AVF and I I forget the other ones because I never use them. But the, the three main ones are lead 12, and 3. And in anaesthesia, we, we're often looking at lead 2 because of the traditional configuration.
We're applying the ECG. But obviously, as, as you said, that sometimes we can't use that traditional methods. So, simply just changing from lead to to one of the other leads can help, and I'm often flicking through to see basically which is the best trace that I've got.
OK, so just flick through and see which one. OK. And also just changing the size of the trace as well sometimes, .
And it's just finding, working your way around the, the anaesthetic monitor, but most of them will allow you to make the trace bigger, which just makes it a little bit more easy to see. And even if the monitor, then sometimes the monitors still can't give you a heart rate, but at least you can see what the, the trace is yourself. Yeah, true.
Excellent, thank you very much. You're welcome. It doesn't look like we have any questions coming through from our listeners.
Everybody must be happy with the info you've given. So in that case, we'll start to wrap up. So thank you everybody for listening tonight and thank you very much to you, Becky.
It's absolutely brilliant webinar and I hope you can go and enjoy the rest of your evening now.