Thank you very much for joining me. I'm gonna talk things all today about blood gas boot camp. So we're gonna talk about sampling.
We'll touch a little bit on kind of arterial sampling and how that affects us looking at our blood gases, so our partial arterial oxygen content, and when we think about our PAO2FIO2 ratio. But we're mainly going to talk about acid base, it's quite a big topic, and so hopefully by the end of this lecture you'll be comfortable with looking at blood gases, going away and looking at those acid base and trying to decipher whether it's a respiratory or metabolic and whether there's actually a mixed based disorder as well. So let's start off with our sampling.
So I'm just going to touch on this very quickly. When we're doing our acid base, Venus is completely fine to do with this. The, the main things for this is that we get that sample to the machine as soon as possible.
So there's a period where it calibrates the slide or the or the cartridge that you've put in, and there'll be a little bit of time. Where that is starting to calibrate that, that's usually enough time for you to get a sample. If you've got a difficult sample, you might go slightly before that, but if you have got a patient that you know you'll be able to sample, they're not, you know, they're not anxious, and you've sampled them previously, or they've got a central lining for example.
Then just put pop your cartridge in and wait for that to calibrate, and get your sample then, so that there's less time where that is exposed to air, so, the longer that there's air bubbles or air exposure to that sample, or even just just, just that sample being left out is that you get changes to things like your lactate, your glucose will change, and more importantly, the blood gases, so things like your, partial arterial oxygen, your SAO2, your partial arterial content of carbon dioxide. So if we're using venous as well, this will be the same for this as well, so if you have a low, if you have abnormal results that you weren't expecting and you've had that sample out for a long time before you've put it into the cartridge to run, I would consider doing another sample. So these pre-heparinis syringes you can buy and they're basically they're lined with that that heparinized lithium heparin, and that just means when you take a sample, you only need to get the amount that you need.
So most machines will take 0.1 mLs. They might require more to figure out what your machine needs, and but for example, if you've got a patient you're sampling multiple times, like a diabetic ketoacidotic patient, er you have a small patient that has a low blood volume, and you don't want to be taking huge samples off and wasting all that sample.
The other thing that this does is that we're not transferring from a syringe into a lithium heparin tube where it's then also got that air exposure within the tube. So this allows us to to get rid of any gas bubbles, and then, and then put a cap on it as well, so they often come with a little cap. So put the cap on it so that there's less air exposure, less chances for those results to become erroneous.
The other thing about these is that they are actually for arterial sampling. So if you're doing an arterial sample for a blood gas, is that you leave that and they'll already be prefilled with air, 0.1 mils.
That is so that when you take your sample, when you hit your artery, you know you're in because that then the blood will come back through that. Once you've got your sample, then you can flick out your air. And cap it and for Venus you can get rid of that air, prior to sampling, and just so it's, you know, you don't have as much air to try and flick out as well.
With these as well, if you are, if for some reason your cartridge fails and you've already taken your sample, don't panic. If you put them on a little bit of on an ice pack, or if you've got like a fridge with like a little freeze compartment, you can put them in there, for for the minute or so while you're waiting for a new cartridge to run, and that hopefully will stop the, the processes of like those cell breakdowns that happen and cause an increased lactate or a decreased glucose, in changes to your, to your blood results. The other thing that's really important to note as well is that most, most of the blood gas machines, er, for example, Epoch are, calibrated to normal temperature ranges.
So if your patient has a temperature range outside of the normal temperature range, make sure that you input that into, The machine whilst you're waiting for your sample to run because it then will give you, it'll give you what the pH would be if it if it was just going off what a calibrated temperature was versus, The temperature of that patient and often there is a big difference, particularly if you've got a hypothermic or very hyperpyrexic patient, of over 40, you'll see that the temperature actually does make a difference to the pH, the PCO2, the PAO2. So it's just a quick brief rundown of sampling, venous samples you can get from anywhere. I'm try and think about like where we're sampling from, if we're getting multiple samples, maybe getting the central line in those patients.
And now on to kind of the nitty gritty of what we're looking at when we're looking at acid base. So we're just going to go over a brief recap of pH and what that is. So pH is a logarithmic scale that represents the concentration of hydrogenine, so within our body we have lots of hydrogenines.
And they're kept within this very tight range of 7.35 to 7.45.
Now, that 7.35 to 7.45 pH is actually representative of quite a big change in hydrogen ions, so.
I'm, when we are in 7.35 to 7.45, we're normal.
Anything above 7.2, anything, I'm below 7.2, I'm.
Sorry man, I just meant to say 7.45 to 7.6 is worrying, .
A pH of 6.8 and even up to 8, they're not really compatible with life. So if you, so once you get past those ranges of 6.8 and 8, often those patients will be comatose, and probably, you know, on their way out, they're probably in cardiopulmonary arrest or already dead if you're doing CPR and you've taken a blood gas.
So acid base is basically about balancing the acid, so hydrogen ions are an acid and base within the body, so things like bicarbonate. And what happens is that the body really works to to keep that in that 7.35 to 7.45 and tries to keep the same amount of acid as there is base.
Hydrogen ions will influence this, so if there are more hydrogen ions, because those hydrogen ions are acids, they will create a more acidic environment. If there is less, if there are less hydrogen ions, then there will be more base, so the, the, the body will be more alkalotic. And this is explained by an equation that was brought about in kind of in the early 1900s of the Henderson Hasselbach equation.
And so basically they just explained how I've just explained it there is that hydrogen ions are either donated or accepted by the body to create a more acidic environment or a more alkalotic environment, a base. So alkal alkalotic is the same as a base. And hydroines, are balanced within this system, and excreted through the kidneys.
So they're excreted, if you remember your, loop of Henley, your hydroines are actually, excreted or retained through that loop of Henley. So this is their equation, and it looks a bit intimidating when we just look at it like this. We, we know what a pH is, that's our logarithmic scale for our hydrogen ions.
And then we have our PKA. This is a dissociation constant of acid, so this is how much acid should constantly be disassociated within the body. This minus is then the concentration of conjugate base.
So again, we're looking at how much base we've got in the body. And then we have our concentration of acid. So how much base, how much acid, and how much within that is that in that constant.
So it's a bit overcomplicated really for what we want. We we're trying to do a boot camp here, right? So let's break it down further to what it actually looks like.
So again we have this disassociation constant, so 6.1 is a disassociation constant. I'm not sure why it says 6.1.
Bicarb is our, is our, our base. So bicarbonate again is excreted or retained through the kidneys. So the kidneys represent one half of this Henderson Hasselback equation of, of trying to maintain this balance.
0.3 is our carbon dioxide solubility constant, so, carbon dioxide is constantly soluble at 0.03.
So carbon dioxide is our other, this is our acid that is balancing against this base. So carbon dioxide is an acid. So the more carbon dioxide that we have, the more acidic we are, the less that we have, the more alkalotic we are.
So we get rid of carbon dioxide through our lungs, so we breathe carbon dioxide out. So if we want to get rid of more acid, we breathe out the carbon dioxide. We need more acid, we retain that, so this is when we become high .
Hypercapnia. So partial pressure of carbon dioxide is the other half of this equation. So this is what we basically need to remember that the Henderson Hasselback equation basically looks at the pH is kind of controlled by these two systems, by the kidneys and the and the.
And by the lungs to balance that bicarbonate and carbon dioxide, that base and that acid. So this is the bit that we're looking at. So when we have our patient and they are, you know, they're trying to balance their acid base, we have one side, we have our lungs, so we have our, acid, the carbon dioxide, plus water.
Water is created in respiration, right? Then we have on the other side, our kidneys, and this is our base, so we have our bicarbonate. And then we have H2CO3 as well, that's a byproduct of that, when, when we start to add things like hydrogen ions.
So when we have hydrogen ions, when we have too many of those hydrogen ions. We have an, we have a an alkalotic process, those hydroines start, to be donated, and they are combined and they make hydrogen . They create that water and our carbon dioxide that then get rid of.
There's hydrogen ions, so we get those rid of those through the lungs. When we have a patient that is too acidic, what happens now is that those proton, those hydrogen ions, which are acidic, will go to the kidneys. They're going to be excreted, H2CO3, and because they're being combined with that bicarbonates, we're getting rid of that.
Of those ho shrines. So these are called our buffer systems, and this is what our this is what Henderson Hasselback, their main theory is that the lungs and the kidneys are buffer systems within the body. We know that those are really crucial organs for us to live.
For many reasons, but especially for maintaining that acid-based balance, so. If we have too much acid, too much base, we're gonna try and get rid of that base through the kidneys. Too much acid.
So yeah, so too much bass. I'm And again, if we now have too, so now if we have too much base, we're gonna donate those hydrogen ions, we're gonna break down that H2CO3, give those hydrogen ions to the lungs. Where the lungs are going to create that H2O, that water, and get rid of that carbon dioxide.
And so now What we see Is that we might swing the other way because we might get rid of too much . Too many of those harsh lines. Sorry, we might retain too too many of those hydroines, and now we become acidic, so 7.25.
So this is where the theory kind of now becomes a little bit more complicated in that actually the kidneys and the lungs should only compensate and try and get that patient to what is considered normal between that 7.35 to 7.45.
They don't always do that. And that might be because they've overcompensated they've overshot the mark, or it might be because there's a mixed disorder. And so this is where it gets a little bit more complicated.
But what we look at is that when there's a primary metabolic process, so when you have a primary metabolic process, for whatever reason that is, it might be because. A patient has renal failure or hypovolemic shock, those kind of things, sepsis, all of those things are metabolic processes that can cause an alkalosis or an acidosis. So what we see now is that, OK, well the lungs are going to compensate for that because we know that the kidneys are responsible for that metabolic process, the lungs are responsible for that respiratory process.
So those res the respiratory compensation is going to be really rapid. We know that we can change our breathing rate, our respiration rate as quickly as possible. You know, our body immediately says, OK, we need to get rid of some of this acid or we need to retain some of this acid.
Let's start doing it now, let's start breathing, you know, becoming tachypneic, getting off all of that carbon dioxide, or I'm slowing down that breath, I'm becoming hypercapnic so we retain that acid. So it's a rapid onset and that is usually complete, that compensatory mechanism is complete within a couple of hours, unless that abnormality from the metabolic side is progressively getting, you know, is spiralling worse. So for example, like a septic patient might be continually getting worse.
So your respiratory side is constantly battling with that, but for the most part it's quick, and so what we start to see is that if we're seeing large differences between, what we should consider normal for a compensatory response, Is that actually it might be a mixed respiratory and metabolic process, so you can have a mixed, metabolic and respiratory process, you can also have a mixed metabolic process, you can have a mixed metabolic acidosis and a mixed metabolic alkalosis, and I'll come to that in a in a minute of how we might kind of decipher that. When we have a primary respiratory process, to think about things like your PLEs, your er aspiration pneumonias, diaphragmatic hernias, all those things are going to cause changes to the lung capacity, er, the ventilatory efforts of that patient. And whilst we can look at our arterial blood gases, this is where it's really useful to do the respiratory processes, is if you have a a question over whether that patient is able to er oxygenate and ventilate, you need to do an arterial sample.
With that comes increased risk of bleeding and increased risk of phlebitis, and they're also quite stressful, quite painful to do for these patients. So if that patient is, distressed in oxygen. You often need to take them out of oxygen for 5 minutes that they're on room air to be able to do things like your arterio, arteriolo, your AA gradient, so your, alveolar arterial, equation, or things like your PAO2, so your partial arterial of oxygen, ratio to your fraction of inspired oxygen.
So unless you know exactly how much that patient's getting, you do need to have them on room air, so. There's, there's advantages and disadvantages of both, if you're just looking at your PCO2, that, venous sample is about 3 millimetres of mercury out from what your arterial sample would be. So actually it's quite useful, whereas your oxygen, levels will be very different obviously in your venous compared to your arterial.
So anyway, so respiratory process, if you've got a primary respiratory process that's causing an increase or a decrease to your PCO2, so you've, you're having ventilatory changes, or potentially even things like ventilatory perfusion mismatch, that will. Then need to be compensated by that metabolic system, so by the kidneys, and if we're looking at Henderson Hasselback equation. And this can take hours to kick in, so again, the kidneys aren't immediately going to start filtering and get rid of stuff.
It will take them a couple of hours to start to get to get those messages, to start to know what to philtre, what, you know, what things they're gonna want to start to to retain and get rid of. And this can take 2 to 5 days to be complete. So when we look at the chart in a minute, you'll see how that actually kind of comes about, in what we're looking for for our compensatory response, and what's appropriate.
So respiratory, Is is very easy to remember whereas the respiratory the, the respiratory compensation is very easy to remember whereas the metabolic is a little bit more different because we again we have acute onset of respiratory, problems and we also have chronic respiratory problems, think about things like your westy lung, your pulmonary fibrosis. Over time, that will have needed a longer compensation and therefore you might allow more metabolic compensation for that. So this is the table that I'm talking about.
I'm, so for every, I'm, every 0.7 millimetres mercury, I'm. Of PCO2, we would expect to to correlate with 1 MEQ of or 1 millimole of bicarbonate.
So when we have a metabolic acidosis, our primary change is that our bicarbonate goes lower, so remember bicarbonate is a base. So the less base that we have, the more acidic we are. So bicarb is lost, the, the patient is acidotic.
What happens is that now, the patient needs to get rid of some of the acid, so the lungs kick in and the. And now the the lungs are getting rid of that carbon dioxide, so they'll be tachypnic. So if you think about .
You know, potential like trauma patients that you get in they're hypovolemic, they're in pain. They're often tachypnia because of the pain as well, but because of like hypovolemic shock and because of the lactate. Now what we see is we see a metabolic acidosis, we see a respiratory compensation where they're trying to blow off some of that acid.
And so you can kind of remember this about 1 to 1, as a ratio. So for every 1 of a bicarb, there should be just less than 1 of PCO2 and that's an appropriate mechanism. If you're having, if you're finding that you've got, you know, 2 millimetres of mercury PCO2 for every 1 bicarb, you've probably got a mixed disorder.
Metabolic alkalosis, remember, bicarbonate is a base, it's related to the metabolic system. More bicarbonate, more base. Our patient is now alkalotic, we have a metabolic alkalosis.
As a result of that, now the lungs want to retain the acid, so they retain the carbon dioxide. So again, for around less, just less than 1 to 1, that should happen, so the the body should retain that PCO2. Again, if you're seeing, so with our metabolic compensation, what you'll find is that they go the same, they go the same way even though it's slightly confusing because because PCO2, because that carbon dioxide is an acid, but they travel the same way if you're looking at them.
They both should go up or down, depending on anything. So then, as I said, we have acute respiratory acidosis and alkalosis and then chronic respiratory acidosis and alkalosis. So remember, carbon dioxide is a base, so if you have more like, sorry, carbon dioxide is an acid, so if you have more of your acid, you will have acidosis, so and you can see an acute and and chronic.
I'm that both of those trend up, the PCO2 trends up. I'm, and again, I'm. So this is where it's slightly different.
So for our acute, for every 1.5, so for every 10 millimetres of mercury of carb PCO2 that goes up, you should have 1.5 millimoles or milliequivalents per litre.
Of bicarb, so it's slightly easy to remember because it's it's kind of still a 1 to 1 ratio, and once we start to think about those patients that are chronic, and this is what it's really important to have our history with these patients and when we're taking them in and getting these blood gases. Is that actually we see a slightly increase in that, so for every 10 millimetres of mercury of PCO2 that goes up, we should have 3.5 milliequivalents per litre of bicarb that goes up, so slightly different in our acidosis.
And then to complicate things further, acute respiratory alkalosis, we allow for 2.5 mil equivalents, . Of bicarb, for every 10, and then with chronic again that goes up further, so 5.5 mill equivalents per litre of bicarb for every 10 millimetres mercury PCO2.
And again, they all go the same way when you're looking at your compensatory, so, if they trend the same way, then you probably have a compensatory mechanism unless it's largely different from, from this table, so for example, You have a 7 milliequivalents per litre bicarb for every 10 PCO2, you probably have a mixed base disorder. And that table is easy to find in books, you can look at it online if you want, and my emails at the end. I'm happy to send it as well.
So what that doesn't account for is all the other things that all the other mechanisms that go on in the body that that can influence our our pH and so some someone else came up with that actually base excess does tell us a lot about just the metabolic system, and the base excess is basically how much hydrogen titration is needed to return that pH to 7.4. It does bank on the PCO2 being at around 40 millimetre mercury, so this is where it downfalls slightly if you've got a, a, you know, vastly different PCO2, than your base excess might be, slightly.
Off kilter, but it does ignore, interstitial buffering, so between the lung and the kidneys, In the interstitium as well and that chronic and renal compensatory mechanism, so it is just looking at the metabolic system, without those buffer systems, so without the lungs and the kidneys, although like I said, there is some consideration that your machines will be calibrated for their PCO2 being at 40. So what we can do now is we can kind of add this into our Henderson Hasselback and this is going to make it easier for us to decide what's going on with these patients. So for example with this one, we have a pH that's high, so remember high is more base, so we have an alkalotic patient.
Our PCO2, so remember that is an acid, is high, so we have an acid respiratory acidosis. So now we're gonna go look at our bicarb. A bicarb is 42.2, so remember that's high, so that's more base.
So we have a metabolic alkalosis. So what we're seeing here is we might go, OK, well now we need to look at our compensatory responses. So we would suspect that if we have an alkalosis and we have a metabolic alkalosis in these because the bicarb's high, we probably have a primary metabolic alkalosis.
Let's just check with the base excess. So the base excess is 18.6.
The normal range, is much lower than that. It's like I'm. -5 to 5, and so the, the base excess is high.
So again, more base, more alkali, so we have a metabolic alkalosis. So it's it's fair to think now that we have a metabolic alkalosis with this patient. Now let's just see if we've got a a a a compensatory response with that PCO2 or if we actually have a mixed-based disorder.
And so I'm. So remember, so for every I'm. For every 1 milliequivalent of bicarb that's higher than the range, we're expecting just less than 1.
So our range of bicarb, I think goes up to, I think it's like 30. So let's just say it's 30. So 42.2, and it will be on the bottom of your thing.
So that's 12.2, our PCO2 goes up to 35. I'm on these ones, so.
57.8 takeaway. So 22.8, so we actually have more .
We have more than we want for that compensatory mechanism because we actually have like a 2:1 ratio for our PCO2 to our bicarbs, so we have a mixed based disorder here. That's why it's very important to check your compensatory mechanisms and so we have a mixed primary metabolic alkalosis and a respiratory acidosis. So we're talking about interstitial buffering, and these are all the things, this is a very good schematic on all these things that actually change, that logarithmic scale that change the pH.
So in the kidneys, we know that hydrogenines are exchanged, as well as bicarb. A nitrogen hydrant, IH NH4, and so other things, the liver as well are also in that, they also get rid of bicarbonate, they have urea which is acidic. Dietary intake and metabolism metabolism as well, have an effect on it, so carbon dioxide, again, carbon dioxide can create bicarbonate, if it's mixed with, oxyhydroxide, .
Again, by carbon dioxide is produced by the guts by that metabolism that's then excreted through the lungs. As well as that hydrogens are exchanged, so non-carbonate buffers as well, a haemoglobin, plasma proteins, phosphates, all of these things have influence, so I'm plasma proteins and phosphates. This is where now I'm Peter Stewart in the 80s kind of came in with this strong iron theory.
So a strong iron theory is quite a lot and I'm not gonna go into it too much because I don't want to blow your brains. But basically I'm just going to simplify it so that you understand that it's not just your lungs and your kidneys that have influence and when we're looking at our blood gases, let's go back to this one. You have all these other things on your blood, you know, when you run your acid-based bloods that come up with this, you have your electrolytes, you have your anion gap.
You have lactate, you have glucose, you have creatinine and uria, and all of these things have influence over your blood gases and over whether your patient has a metabolic acidosis or a metabolic alkalosis, so hopefully it's just helps you to understand it a little bit better. So his theory was very similar to Henderson Hasselback that electron neutrality must be maintained, that pH must be maintained. And the way that that is done is through electrolytes.
So you have your so you have with your strong ions, you have cations and anions, so we know that the most abundant cations are your sodium, potassium, and then also you have your hydrogen there as well. So they're the cations and then on the other side, there's ions, we have chloride. And then in addition to that, we have lactate, bicarbonate, and then our acids and, our albumen and things like that.
So, these are all independent, so things like, PCO2, your strong iron, so your electrolytes basically, and non-volatile weak acids are things like phosphate, lactate. And and albumin are all those non volatile weak acids that have some influence as well. And then dependent variables, so bicarbonate and hydrines, they exist within the body.
They're made through many processes, as you can see on this. They're made, you know, in that gastrointestinal system, they're made in the liver, they're made in the kidneys. So all of these, they, they already exist.
They're already dependent in the body, but independent things that can change as a result of. Diet, illness, pain, stress, that those kind of things will change, in this new electron neutrality equation. So this kind of how it formats out, is that you have kind of this electrolyte profile, so.
One side you have your sodium, potassium, magnesium, calcium. These are, these are the stronger of those electrolytes. And then on the other side, we have our weak acids, so our, that's where our anion gap comes in, so this anion gap accounts for these weak acids that aren't counted anywhere else, so things like our albumin, phosphate.
And then we have our bicarbonate and then our chloride as well. So, this is, I'm gonna move myself over here. So these are our unidentified ions, things like sulphate, ketones, urate, .
Weak acids, as well, so albumin, phosphate. And then our strong acids or ions, so chloride is an acid, you can remember that it's got like the little, it's a minus, so, this also includes lactate. So on this side of the profile we have kind of all those unmeasured things plus chloride.
On this side we have our strong cations, er and sodium is that major cation, so. Sodium and chloride are the two main players, which is why it's really important for our patients to have normal electrolyte balances, so a whole other lecture. I'm not gonna go into it, but it's really important when we're thinking about our electrolytes, we know that they cause problems to our like hearts, they cause arrhythmias and things like that.
So basically what we want to try and do is that we want to try and keep those in balance and sodium and chloride will move together and in order to move together what will often happen is that the anion gap will increase or that bicarbonate will increase, but they will move together. If they don't move together, this is where we get this imbalance in electron neutrality and and we get things like metabolic acidosis or alkalosis as a result. So when we're looking at, like I said, these unmeasured anines, these weak acids up here.
So again, the strong iron difference, this is what he wrote out as a strong iron difference, is that sodium and hydrogen equal are equal to chloride and and OH so. Now what we see together, I'm when we move this around is actually that sodium and chloride should move together and that's kind of the basics of this. I'm not gonna go into it too much, but basically they should just move together, they should move up or down together.
I'm And then the, the more interesting part that I found, obviously our sodium and our chloride have big influence, we want them to move together. If they don't move together it's going to cause imbalance and cause things like metabolic acidosis or alkalosis. But also what has influence on our metabolic acidosis or alkalosis is things like these weaker acids or anions, so things like phosphate, proteins like albumin.
So when we think about these patients that are critically ill, they have that loss of albumin. It is gonna cause an, it is gonna cause an alkalosis. So if we have a patient who has, An increase in proteins, so for example they're dehydrated, that is going to have influence because now they're going to have more proteins, they're going to their acids, they're weak acids, it will cause some form of acidosis that should resolve with things like fluid therapy.
And it's important to note as well with these ones that respiratory and immuno compensatory mechanisms aren't going to affect these, so this will be a separate issue and it's really really important to look at your albumin and your phosphate as well. So now if we have, more of these, so we have decrease in albumin. I'm, we are now going to have an alkalosis because we have a loss of proteins, we have a loss of those weak acids, and, and so now we're gonna have a patient that has a metabolic alkalosis.
So let's put it all together. This is the bit that is gonna take practise, and these, these are the steps that you should do every time. And hopefully it didn't like confuse you too much, but basically just to, to help you to put it together and why we're putting it together.
So we're going to confirm appropriate selection, you know, sample collection and handling, make sure that it's got no air bubbles, make sure it's been capped, make sure that we haven't been stabbing around in these patients or that the patient hasn't been stressed as well. Think about sampling techniques that are fear free, good cat handling, good dog handling, making sure they're on like things like non-slip mats. So that basically we're not skewing it with by having a higher lactate or higher glucose, things like that.
I'm, so the first thing we're gonna do and and what I did on that other one was that we're gonna look at our pH, so we're gonna see if it's normal, within that normal range. Is it aidemia, so is the pH lower, we know. The pH means that we've got more hydrogen ions confusingly, and then alkalemia is that we have less hydrogen ions, so that we have a higher pH is in the alkalemia.
So once we've done that, we've kind of seen what we've got with our pH where our body's at overall. We're now going to try and figure out where that's coming from. So we're gonna first, the first line down is the PCO2.
So we look at our respiratory component. So again, is it normal? Is it acidotic, remembering that carbon dioxide is an acid, so the more that we have, the more acidic we are.
Alkalotic process, so the less carbon dioxide, the more base essentially. So, so it's an alkalotic process or an acidic process, so we can say, OK, this has a respiratory acidosis or an alkalosis. We don't know yet if that's a compensatory.
Or if it's normal or if it's a mixed based disorder. We're then going to look at the metabolic components, so our bicarbonate and, or the base excess, so I like to look at both of them, and because sometimes the bicarbonate will be representative of a compensatory mechanism, but then your base excess will also show that you have a primary compensatory mechanism. So again, is it normal?
Is it acidic, remembering that bicarbonate is a base. So the more base we have, the more alkalotic we will be and the less bicarbonate, the less base, so the more acidic we will be. So then we're going to define the primary process.
So is it metabolic or is it respiratory? So what's causing a change in the same direction as the pH change, just the easiest way to look at it, which, which one is going the same direction as the pH. So which one is acidotic, the same as the pH?
And then we're going to look at their compensation. If we're seeing that we have an alkalosis and an acidosis in one and the other, is it because of compensation or is it because we have a mixed based disorder? So if the metabolic and respiratory er sides of the system move in the same direction, so they're both increasing in numbers, So that's your, your lungs and your kidneys from your PCO2 and your HDO3.
Then there must be some form of compensation. Remember your base excess might be increased and decreased aside from that, and that is giving you a that will tell you whether you have a metabolic component as well. So again, is that compensation as expected?
So is it within the time frame that I said, so remember rapid onset for the lungs to compensate 2 to 5 hours. And so if you're seeing this and this patient has been sick for a couple of days, that's not compensation anymore. That patient is now has a primary respiratory problem as well.
If it's kidneys, that are compensating, is it, is your condition acute or chronic? Is it an acidosis or an alkalosis? We know that we're going to have a slightly different one that increases that chronic, acute and chronic alkalosis are going to be slightly more that I'm.
2.5 to 5.5.
So is a compensation is accepted? Has it had time to occur is the big one. So if we're seeing a primary what we think is a primary respiratory problem, you know, if we're within that, you know, 2 to 5 day period, we might not see any compensation from the kidneys or barely any compensation from the kidneys.
And so it's really important to kind of consider that as well. And then we're going to consider mixed disorders. So as I said earlier, You can't have two respiratory disorders, you can't have a respiratory acidosis and alkalosis.
But you can actually have a mixed metabolic alkalosis and a mixed metabolic acidosis, and often what you where you'll see this difference such is in that base excess versus the bicarbonate. And you'll also see this with things like, changes to your chloride, your anion gap, I'm remembering those weak acids, and the, and the, and the chloride is an acid as well. So again, if there's a metabolic acidosis, look at the anion gap, see whether there's changes to your anion gap, is that increased or decreased.
Remember that that that is representative of those weak acids. So if there's a bigger anion gap, it might be as a result of those. So then you can go look at things like, you might have hyperchloremic because remember that that electron neutrality that's basically trying to stay within that little table.
If you've got an increase, . In anion gap, you've got to have got ridden, er you've got to have got rid of something somewhere, so often your chloride or your bicarbonate will have increased. If you have a normal iron gap, then actually what's happened now is that your hyper, you've got a a chloride that's increased, so your chloride has increased, separately to increase some of your sodium, and that's often present in, .
In patients with hypochloremic acidosis, so when I'm You have a normal iron gap and lots of chlorine. So the easiest way that I find to do this, to start out doing this, when you first start looking at blood gases and it will just take practise, is to use this tic tac to. And so basically you just format this, into, you don't need that bottom total, one, but you put PH, PCO2, bicarbonate and base excess on the left side, acid normal and base at the top.
And now what we do is we look at a set of bloods. So you can see here that it's got the pH at the top at 7.491 and then the pH with a T next to it is because it's been calibrated to a temperature of that patient and it's 7.487.
So it is a difference. So we use the temperature ones. So we know that that is high, so that means it's a base.
So we've got we've got an alkalotic process. Now we're gonna go to our PCO2, 5.18, we know more carbon dioxide is acid, so now we have a respiratory acidosis.
We don't know yet whether it's a primary aim or a compensatory mechanism yet. And so now we're gonna go to our bicarbonate. My bicarbonate is 3.91.
So again, more bicarbonate, more base. I'm, and so now we can kind of see from this, OK, our bicarbonate is moving the same way as the pH and therefore we have a metabolic alkalosis. And now we just need to see if we can kind of confirm that.
So again, our base excess. 15.8, remember that's separate to those buffer systems, but again, it is a base.
So we have a metabolic alkalosis. So let's see now whether our primary, whether our, our respiratory acidosis is a compensatory mechanism. So remember that we want kind of just a 1 to 1 ratio.
So you can see at the bottom here we've got those normal ranges, that's 23, . So it's a difference of 16.1.
And then for our respiratory, we have 51.8 take away, 38 is the range. So 13.8, so it's overshot the mark.
So it's just under 16. So that is an appropriate, compensatory response. And again, we would check how long that had been over, but it's likely that this one, you know, is a is an appropriate response.
And what will happen eventually is that, Because of that, carbon dioxide that is that the pH will actually start to creep down. This is a prime example of a metabolic alkalosis, it's probably one of the most common ones that you'll see. I'm And this is just the same one from the last last one there.
So it's got a high TCO2. So again, that's kind of related to your bicarbonate. So .
So those are high, which means you have an alkalotic and metabolic alkalosis. Your anion gap is normal, but what you see now, because it's trying to balance within that frame, is your anion gap's normal, your HCO3 is higher, your TCO2 is higher, and is creating less space within that electron neutrality. So what happens is we dump out those acids, we dump out that chloride.
To make room for that. So we also have a reduced sodium, so they've trended together and to try and maintain that electron neutrality. And this is often as a result of, obstruction.
So with these ones we might do a replacement therapy of 0.9% sodium chloride with additional potassium chloride in there. You can see that our potassium is also low as well, just so we can supplement back up, until we can get them onto a balanced isotonic crystalloid solution.
So hopefully that has made sense. Like I say, the tic tac toe is really useful. I'm to keep practising them with, and please feel free to email me any questions that you might have.
And if you want that slide on the compensatory mechanisms, I'm happy to send that out if you email me. And thank you very much for joining.