So good morning, everybody. We are on to part four of our clinical pathology lectures. And this morning, slash afternoon, slash evening, wherever you might be, we're going to talk about electrolytes and acid based analysis. I know that acid base analysis can be kind of scary topic. I know that's something that sometimes causes a lot of consternation. So hopefully today we'll break it down into some really nice, easy steps that make it a little less scary. 

And so just like we've done for all the other top topics, we're going to talk about electrolytes first, Then we're going to look at our venous blood gas and then our arterial blood gas interpretation. And all of that is going to be case based. So we're going to use real life cases to help us explain some of these concepts. And then at the end, we're going to test our knowledge. 

All right. So without further ado, let's get started with case one. Here is case one. And case one is Ruby. She is a two year old female spayed standard poodle. She's up to date on her vaccines and she has a 4 to 6 six week history of intermittent lethargy, anorexia and vomiting. The owners have also noticed that she's been losing weight. And for the last 24 hours prior to presentation, she's had severe lethargy and vomiting and she collapsed this morning, which is what triggered the owners to bring her in. 

So here are our physical exam findings and you might just want to note that her pulse rate is low, so she is bradycardic. She's a little hypothermic. Her mucous membranes are pale. And her CRT is prolonged with a poor pulse quality. And she's just a little bit on the skinnier side of normal.

So we're going to get started with some serum chemistries and we added in a urine specific gravity because we were able to get that at the same time. So I'm just going to give you a second to review these findings. Okay. I know there's a lot of changes here, so we're going to break it down a little bit more. So I've just highlighted on the right here the significant changes for Ruby. And so if we go through these sort of step by step, we'll see that she has an azotemia. So going back to lecture three, if you haven't seen that one yet, that one is all about serum chemistries relative to the kidneys and also urinalysis. So I encourage you to review that lecture if some of the things we're talking about with azotemia are unfamiliar. So as we can see, she is azotemic. And her urine specific gav, gravity is inappropriate. You know, if, if everything was normal, we would expect with azotemia for this urine specific gravity to, to be significantly increased. She also has hyponatremia, hypochloremia, and hyperkalemia. Her total CO2 is decreased and her anion gap or AG is increased. We're going to talk more about this coupling, so don't worry about that too much right now. She also is hypercalcemic. She's hypoglycemic and hypocholesterolemic. So this is a very, very classic panel. And not all of our patients with this disease present in this way. But when you see this blood panel, this should be one big disease jumping out at you. So just think about that for a second. 

But what we're going to do now is we're going to talk about our electrolytes. So let's talk first about sodium, because sodium is one of our main extracellular electrolytes. So it is our major extracellular cation. And sodium is really critical for maintaining our extracellular fluid volume. It's a primary determinant of our plasma osmolality or kind of concentration, if you like. And it maintains this osmotic gradient across our cell membranes. So remember that extracellularly we have a lot of sodium and we have all these different ways that sodium can pass through our cell membrane. And sodium, and to some extent chloride, which we'll talk about in a second, like to go with water. So wherever water goes, sodium follows and sort of vice versa. So I always like to think of water or fluid and sodium kind of hand-in-hand. So as I already mentioned, you know, we always going to look at our sodium relative to our hydration. And our hydration is going to be an estimation of our extracellular fluid volume. And as as I mentioned, most of the time, changes in sodium are going to be due to changes in our body water concentration. 

All right. So a little bit of some physiology. If you remember, back to physiology, our serum sodium is primarily controlled by our kidney. And there are two main hormones that help control sodium via the kidney. And that's going to be anti diuretic hormone or ADH and aldosterone, which is a mineralocorticoid, which is secreted by the adrenal glands. And both of these hormones, their role is to retain sodium and water. Okay. So again, you're retaining sodium. Water is going to follow. Now your body, water and sodium, there are two types of receptors in your body that are going to help control these factors. You have your Osmo receptors and your Baro receptors. So Osmo receptors, as the name suggests, you've got that Osmo right there. Osmo Receptors are going to be found in your hypothalamus, and they respond to increases in your plasma osmolality. And so what that means is that your sodium is going to be relatively increased compared to your water. So your plasma is getting concentrated, right? The water's coming out, the sodium staying there. So your plasma is more concentrated. And what that does is that stimulates your thirst. So if you think about kind of the way I always like to think about it is if you eat some really salty snacks, what happens? You get thirsty, right? So you take in a lot of sodium and you get thirsty and that stimulates your ADH release and then you start to retain water. Okay? So as you osmolality increases, it first of all, triggers an increase in your thirst, but then also you get concurrent increase in your ADH release. 

Now, your second type of receptor that can help control sodium and water, is, are the baroreceptors. So these are completely different and our baroreceptors are found in our major arteries. So such as in our aortic arch and our carotid arteries. And they respond to changes in our effective circulating volume or ECV. And so baroreceptors, Baro is derived from pressure. So essentially this is a pressure receptor. So as you become hypovolemic, so as your blood volume decreases, your baroreceptor is going to detect that because that's going to cause a subsequent decrease in pressure and that stimulates RAS. So that's our renin angiotensin aldosterone system. We're not going to go into a lot of detail about that. That is a really important physiologic process though, and this is a very brief overview right here. But if if renin angiotensin aldosterone system is unfamiliar to you, I would encourage you to just go back to your physiology textbooks and look at that, because that's something that's really important. But essentially what our RAS is doing is it's causing sodium and therefore water reabsorption. You're also going to stimulate vasoconstriction and as we mentioned, it's also going to increase thirst. And so all of these things are going to cause an increase in your ECV or your effective circulating volume. Now, what's really important is if you have your baroreceptors and your osmoreceptors triggered, you're always going to prioritize maintaining your extracellular volume. i'm sorry, your effective circulating volume over the osmolality or concentration of your plasma. So your body is always going to try to conserve that effective circulating volume because that's going to have a direct effect on your tissue perfusion. And your body is always going to try to maintain tissue perfusion. 

So let's look at a couple of instances where our sodium concentration in our blood may change. So hypernatremia so hyper, increased, natremia, sodium. So hypernatremia occurs when you lose water in excess of, of sodium. And so that's when you lose a hypotonic fluid. So you're losing water, but your sodium isn't being lost to the same degree. And this is the most common kind of sodium change that we see in animals. And it's usually accompanied by hypovolemia, which makes sense because we're losing fluid. So the big kinds of diseases that we think about when we see hypernatremia is if you have GI fluid loss. So from significant vomiting or diarrhea. Often with chronic kidney disease, we will see hypernatremia again because you're losing a hypotonic fluid and also with an acute kidney injury. Now, I'm just going to mention this because it's much less common, but it can happen would be if you had a pure water def, deficit. And that could be from water deprivation or a primary, adipsia. And I just have to tell you, kind of a cool story from a long time ago. There was a young boxer in our emergency room who presented with abnormal mentation who had profound hypernatremia. I think the dogs sodium concentration was over 170, if I remember, and no one could quite figure out why this dog was hypernatremic. And when we questioned the owner's a little bit more, it turned out that the dog had been peeing in the house. And so the way that they dealt with that, instead of house-training the dog, was taking the dog's water away. So there are some instances where a pure water deficit will cause hypernatremia, but this is a much less common situation. But I always remember that case. I saw that case probably 20 years ago, and I still remember it. 

All right. So what about hyponatremia? So that's when you have a low, less, hypo, natremia, sodium. So when you have a low blood sodium concentration, there are really sort of two main reasons why. The first is if you're gaining water or you're retaining water in excess, so more than your retaining sodium. So this happens with hypovolemia. And if you remember back to just a few slides ago, we talked about how your body is always going to try to maintain your ECV, your effective circulating volume over the osmolality or concentration of your plasma. So when you're hypovolemic, you're going to trigger water intake and then you're also going to retain that water. And so when you intake and retain water, you're going to dilute out your sodium. So when you measure your sodium in your plasma, that sodium concentration is going to be decreased. So what are the kinds of situations where that happens? So congestive heart failure is kind of a classic one where you have a decrease in your effective circulating volume. Body cavity effusions. So if you are third spacing fluids significantly into your abdomen or into your chest, or if you are excessively losing fluid through your GI tract or your urinary tract and you're drinking to replace that volume, but the sodium isn't being replaced. The other really important disease I just want to highlight is hypoadrenocorticism. Okay, so with hypoadrenocorticism, you have a decrease in your aldosterone concentration. Remember, aldosterone is a mineralic corticoid that is secreted by your adrenal cortex. And when your your aldosterone decreases, that decreases your sodium retention and increases your water intake. Now, the reason that your water intake increases and your urine becomes dilute is because you're excreting sodium into your urine and that causes an osmotic diuresis. So remember, with hypoadrenocorticism, often we will see a inappropriately dilute urine in the face of azotemia, even with normal renal function. 

Okay, so let's move on to our potassium. Now, we talked about how sodium is our major extracellular cation. So out here. Potassium, on the other hand, is our major intracellular cation. So remember that in our body, when we measure plasma, potassium, we're really only measuring a tiny fraction of our body potassium concentration because 98 to 99% of our potassium is located inside our cell. So intracellular. So there's a couple of different mechanisms that regulate our blood potassium concentration. One is very important, and that's our renal excretion. And if we remember back to aldosterone, we remember that aldosterone is going to do is it's going to reabsorb our sodium, and that's going to stimulate potassium excretion because of our sodium potassium exchange mechanism. So in hypoadrenocorticism where we have decreased aldosterone, we are going to decrease our potassium excretion. And so a plasma potassium increases. Another mechanism is if we start trans locating potassium that is in our extracellular fluid into our intracellular environment. So usually when this happens, this is by because of something that we're doing often. And the classic, classic example of this is giving a patient insulin. So for example, in an, in a patient who is a diabetic ketoacidotic, we're giving them insulin. And often what we find is as we give them insulin, our blood potassium concentration decreases quite significantly and then we have to address that. But insulin stimulates uptake of potassium by cells because the potassium goes with the glucose. And then other things can also affect this translocation. And I'm not going to get into too much detail because this is more complicated pathophysiology. But essentially, extracellular fluid volume and our pH can also affect translocation of potassium from extra to intracellular. 

All right. So let's talk about hyperkalemia, because hyperkalemia, so an increased potassium is, you know, one of those sometimes can be a very scary thing when we see it on our bloodwork because as we know, as your potassium increases that can make your heart very unhappy. And so the most common cause of hyperkalemia, if we look at all the animals that we see, is a decrease in our urinary excretion. So there's really two main causes of that. The first would be if we're not producing urine, so that would be a situation of an oliguric, so decreased urine or anuric, no urine, renal failure. So this is typically in acute situation, maybe a cat who's been exposed to lilies, a dog exposed to ethylene glycol or severe leptospirosis could be examples of an acute oliguric or anuric renal failure, which is going to result in hyperkalemia. The other big and very important differential, especially in our male cats, is is decreased urinary excretion and so specifically a lower urinary tract obstruction. So here you can see someone unblocking a cat  using a urinary catheter. But this is by far the most common cause of hyperkalemia in male cats. And then also, if you are an animal that has been hit by a car that can result in rupture of your urinary bladder and hyperkalemia as well. There are some other differentials as well, of course, and aldosterone deficiency. So again, we're coming back to hypoadrenocorticism, is going to cause potassium retention and sodium excretion. So we're retaining potassium, excreting sodium. And so we're going to see a change in those two values in our lab work. Now there's also a condition called Pseudo Addison's. And I'm not going to go through all the differentials because there are quite a few. But some of the classic ones are if you have a change in your effective circulating volume. So that would be if you have third spacing of fluid, so in particular ascites or pleural effusion. And then the other classic thing to think about is a whipworm infestation. And that we don't really know why whipworms cause a pseudo addisonian situation, but they can. So that's an important thing to remember. And then there are also the things that we give our patients, so drugs that we give our patients, that can also result in hyperkalemia. And so this is very classic in dogs in particular receiving angiotensin converting enzyme inhibitors. So that would be a drug like Enalapril. So a dog in congestive heart failure or an angiotensin two receptor blocker, which is a drug like Telmisartan, which we use a lot in dogs with protein losing nephropathy. And so these types of drugs will cause an increase in your, blood, blood potassium concentration. And the reason is that they're decreasing your aldosterone synthesis. And so, again, you're causing potassium retention and sodium excretion. 

What about hypokalemia? So a low blood potassium. So I would say that hypokalemia, in my clinical experience, we see more commonly in cats than in dogs. And most commonly, I would say we usually see it in all the cats with some kind of disease that is causing polyuria. So renal wasting. So potassium loss through the kidney is pretty common in CKD, especially in cats, but really any cause of polyuria. So anything that is causing you to produce excessive urine is going to promote kidney excretion of potassium. And so you may glycosuria with diabetes. And remember that often, cats with chronic kidney disease or other disease are going to have a decreased intake and most of your potassium you're intaking is coming, or all the potassium you're intaking, is coming from your food. So if you're a sick older kitty who's not eating well because of your CKD, you're wasting potassium through your kidney, but you're also not having any intake. And so that anorexia with your CKD is contributing to hyperkalemia. Sometimes as well, severe vomiting or diarrhea will cause significant GI loss. And then, as we already mentioned, insulin therapy, particularly in pets who often again on eating with diabetic ketoacidosis, when we start that insulin often will see a massive intracellular shift of potassium and that causes pretty profound hypokalemia. So this is something that we monitor very closely in our patients that we're treating for diabetic ketoacidosis. Another really cool diagnosis is hyperaldosteronism, which we see exclusively in cats, which is typically due to an adrenal tumor. And those cats can, the only thing they can present with sometimes as a profound hypokalemia. And then again, the drugs that we give our patients can also result in hypokalemia. So the classic was drug wise is a loop diuretic such as Furosemide, which we use pretty commonly in our heart failure patients. 

So let's move on to chloride. And chloride is our major extracellular anion. And I think what's helpful with Chloride is to think about chloride always going with sodium. So sodium chloride, like to go together. Right? Salt. That like stick, they like to go together. So in our body, sodium and chloride are found in a 1 to 1 ratio. So if you're generally speaking, what happens to your sodium is going to happen to your chloride as well. So there are some exclusions to that. And one thing that's really important to remember is that in animals that are receiving potassium bromide, which is an anti-epileptic medication, they will develop an artifactual increase in chloride. So the chloride is not increased, but bromide on chemistry analyzes is measured as chloride. So don't be surprised if you have a patient on potassium chloride sorry, potassium bromide that when you check that bloodwork, the chloride is 150, 160. They're not truly hyperchloremic, it it's just that the bromide is being measured. Sometimes we will see a low chloride due to chloride loss. Now in chloride loss, more than sodium loss. Now, in small animals, that's not very common that we see that. But one classic example would be vomiting of gastric contents. So if you remember in your stomach, you have a lot of hydrogen chloride. And so if you're losing a lot of hydrogen chloride and on this radiograph on the right, we have a gastric foreign body. So if that gastric foreign body was causing a pyloric outflow obstruction and we were vomiting gastric acid, that could result in hypochloremia. Now along with that, we would expect to also see a metabolic alkalosis, which we're going to talk about as well, but with losing the hydrogen as well as the chloride, and so as we lose hydrogen, our blood pH is going to increase. Okay. Now there is a formula that you can use to correct calcium. Sorry, excuse me. Correct chloride for sodium to give us more information about chloride. But that's kind of beyond the scope of of what we need to know here. 

All right, So let's go back to Ruby. So if we look back at Ruby's results, she has a hyponatremia slash hypochloremia. And, you know, one of our questions is, could this be due to loss? Well, it could. She did have some history of vomiting and then some more acute vomiting, but there's not really significant GI loss that we would expect with her. Could it be that she has a lack of aldosterone? So hypoadrenocorticism and there are other things on this lab panel that should be ringing a little bell in your head right now that's going to put hypoadrenocorticism pretty high on our list. We have a consistent presentation. She is a young female standard poodle, and she has some other clinpath findings that are very consistent with that. But don't worry. We're going to talk more about that in Lecture five so we can kind of put that slightly to the side at the moment. We also and probably most life threateningly, this dog, Ruby, has a pretty significant hyperkalemia. So the first question when I see a hyperkalemia is could it be an artifact? And what's really important to remember, and I've seen this happen many times, is that if you fill a purple top tube before you fill your serum separator, purple, purple top tubes contain potassium EDTA. And so if you contaminate, even with a small amount of potassium EDTA, you are going to falsely increase your serum potassium concentration. So you want to not do that. Okay? But in this case, you know that the other values and the fact that she was bradycardic on presentation suggests to me that this potassium is probably real. So I'm going to discount this. So the other question is, is it possible that this is due to an oliguric or anuric renal failure? So how can we figure that out? Well, let's look at our BUN and creatinine. Our BUN is 60, our creatinine is 2.7. Now, certainly, this is increased. But if you were a patient with oliguric or anuric renal failure, I would expect our BUN and creatinine to be much more severely increased. So that leaves us with the potential for hypoadrenocorticism, along with some of those other clinical pathology findings. And we had hypoglycemia, we had hypercholesterolemia, we had a mild hypoalbuminemia and we had hypercalcemia. And those things are all consistent with hypoadrenocorticism. 

So how else would we look at our sodium and potassium? And one of the values that I think is very useful when we look at sodium potassium is our sodium to potassium ratio. So this gives us more information than if we just look at sodium in isolation and then potassium in isolation. So specifically, we look at sodium potassium ratio when we're trying to evaluate for hypoadrenocorticisms. So sodium potassium ratio of less than 27 to 1 is suggestive of hypoadrenocorticism, and less than 24 to 1 is highly suggestive. Now, again, why is that? So when we have hypoadrenocorticism, we decrease aldosterone, we excrete sodium, we retain potassium, and we have volume depletion. Now, remember that we're looking at sodium to potassium, right? So we're basically taking our sodium and we're dividing it by our potassium. And so anything that affects our potassium is potentially going to cause a change in our sodium potassium ratio. So this is not 100% diagnostic for hypoadrenocorticism, but along with everything else, is suggestive of that disease. If we calculate Ruby's sodium potassium ratio, it's 17.7, which is really low, which again, along with everything else, is really pointing to hypoadrenocorticism, in her case. So how are we going to confirm that? We're going to do an ACTH stimulation test, but we're going to wait until next week to talk more about that. 

All right. So part two of our lecture is about our acid base analysis. And so we're going to spend some time now looking at acid base. Okay. So if we just have a serum chemistry to look at, we can get some information about our acid base status. Okay. And the way that we can do that is that most urine chemistries contain this TCO2 or bicarbonate value. And they also include an anion gap. Okay. So we can get some information about our acid base status here. But the best way to evaluate our acid base status is with a venous blood gas analysis. And so that's something that you have to run in the hospital. So you're pretty much all emergency critical care hospitals will have a blood gas analyzer. It's usually a handheld or there's another type of blood or gas analyzer that is used. But you know, general practitioners may not have access to this. Remember, though, that bicarbonate, so HCO3- is our most important buffer in our body. And if you go back to our physiology again, you'll remember this formula. And this formula is a very important formula. So this is our relationship between bicarbonate, hydrogen, the carbonic acid and H2O, so water and carbon dioxide. And remember that this is catalyzed by carbonic anhydrate. And so remember that these arrows go both ways. So this is a relationship that is in constant flux, trying to keep your body at a neutral pH, which is going to vary in which way it's going to go, whether it goes towards the left or goes with the right, depending on what your blood acid base status is. So that the problem with only looking at our serum chemistry is that we don't get information about our blood pH or the respiratory component of our acid base status. So the respiratory component, meaning the CO2. 

So if you're going to look at our total CO2 on our parameters here on our serum chemistry, you've always got to evaluate it in line with our anion gap. And in a second, we'll talk about how we can calculate that. But the anion gap is not necessarily written on every single serum chemistry analysis. But the good news is that if you have electrolytes and you have a total CO2 on your panel, you can calculate your anion gap. So what is the anion gap? So essentially what we're doing with our anion gap is estimating our unmeasured anions in our serum. And so this is helpful when we're trying to figure out a cause of a change in our blood pH. Specifically, what we're talking about when we talk about our anion gap and unmeasured anions is our metabolic acidosis. So as I already mentioned, remember that a body is going to do everything that it can to maintain a normal pH, because once our pH goes out of that very tight range, all our body systems start to get deranged. Our cellular metabolism changes, our organ function changes and everything kind of doesn't go well if you're outside of that range. So your body is always going to try to keep a normal or neutral pH. And that's really important to remember coming up and we'll go back to that in a second. So in order though, to maintain that electro neutrality, we can look at our cations. So remember that sodium and potassium are our major cations. There are also some unmeasured cations, but these unmeasured cations are pretty small in number, and we don't really consider them. So we kind of scratch this out of our formula, and then our cations need to match our anions. And so the anions that we think about in blood are chloride, bicarbonate, and then this other group of what we call unmeasured anions, and it's these unmeasured anions that are really important. So if we rearrange this formula, we get that our sodium plus our potassium minus our chloride plus our bicarbonate gives you that anion gap. Okay. So in Ruby's case, we have our sodium plus potassium. So 138 plus 7.8, minus chloride, 102, plus 9, our bicarbonate, and that gives you an anion gap of 34.8 or 35 if we round it up. So that means that we have an increase in our anion gap and an increase in our unmeasured anions. 

So our anion gap increases when our metabolic acidosis is caused by an accumulation of some kind of pathologic acid. Okay. So some acid that in a normal state wouldn't be there. So the big ones that we think about are, for example, DKA. We are going to see ketoacids. The most common one that we see in a lot of our patients is going to be lactate, and that is a result of cellular anaerobic metabolism. And that's usually due to decreased effective circulating volume due to dehydration or hypovolemia. In kidney failure, we will see an increase in uremic acids. And some things that you that animals might ingest that could do this would be something like ethylene glycol or salicylate. So let's look at lactic acid and lactate, because this is really the most common cause of metabolic acidosis in our patients. So why does lactic acid cause a metabolic acidosis? So if we break down lactic acid, we have hydrogen ions and unmeasured anion, which is lactate. Okay. So if we go back to our formula that that formula that we talked about earlier that's so important, as our hydrogen increases that hydrogen is going to bind with bicarbonate in the blood and is going to become carbonic acid. So as our hydrogen increases, our formula is shifting to the right, and that's using up bicarbonate. So our bicarbonate is going to decrease. Okay. So as our anion gap increases and bicarbonate decreases, we can say that in an instance such as that, if we don't have, say, a history of ethylene glycol or salicylate ingestion and or we're not a DKA, that that increase in anion and unmeasured anions can be attributed to lactic acid. Now, there are some instances which I'm not really going to talk about because it gets a little complicated, but there are situations where you can have a normal anion gap metabolic acidosis if you lose bicarbonate. So if you're just losing bicarbonate by your kidneys say and that would be something like a situation, like a renal tubular acidosis, you actually have a compensatory increase in your chloride, which keeps anion gap normal. But in the vast majority of cases of metabolic acidosis, you're going to have an increase in your anion gap due to an increase in one of these unmeasured anions. 

Okay, So let's now move to our venous blood gas and remember, the pH reflects our hydrogen concentration. And our hydrogen concentration is going to be determined by our ratio of bicarbonate to carbon dioxide. Now our venous blood gas, the nice thing about it, is that it provides additional information about pH, a partial pressure of CO2 or PCO2 that's dissolved in the blood, our bicarbonate concentration and our base excess or BE. So you'll often see that on a blood gas analysis. And basically that is just an estimation of the amount of base that's needed to be added to blood to achieve a normal pH. So that could be a positive value or a negative value depending on which way our base excess is going. And so that's going to reflect the metabolic portion of our acid base status. Now, you will see on your venous blood gas the partial pressure of oxygen or a PO2, but that is not useful to assess oxygenation. Okay, So the PO2 is not something we're going to look at to really assess oxygenation. That's something we're going to look at on our arterial blood gas. So I really don't typically pay very much attention to the p02. As I already mentioned, we need a specific in-clinic analyzer to look at blood pH and our venous blood gas. 

All right. So before we continue to get into venous blood gas analysis, let's just review some definitions. Okay? So we know what we're talking about when I start to introduce these concepts. So if your blood pH is decreased and in a dog, we would say a blood pH of less than 7.35, we describe that as acidemia. So an increase in our blood hydrogen concentration and a decrease in blood pH. Acidosis, on the other hand, is the process that is causing the acid accumulation or the loss of base. And this can be metabolic in origin or respiratory in origin. So there are two types of acidosis, a metabolic acidosis and a respiratory acidosis. Now, on the upside of that, we have alkalemia, and an alkalemia is an increase in blood pH. And in dogs, that's typically a pH greater than 7.45, and that's due to a decrease in our blood hydrogen concentration. And similarly to what we've already said, alkalosis is the process that is causing acid loss or base accumulation, and that also can be metabolic or respiratory. Okay. So the primary disturbance is the major or the primary the the primary thing that's driving the change in our pH. Okay. And then you often get a compensatory or secondary disturbance, which is the body's response to try to correct this primary disturbance. Because remember, your body is always going to want to retain homeostasis and is always going to try to bring your pH back to neutral. Okay. 

All right, so here is our blood gas in Ruby's case, this is a venous blood gas. So just kind of familiarize yourself here on the right with some of these values and some of the normal ranges. And we'll kind of go through this step by step to talk about how we're going to interpret a venous blood gas analysis. So these are the questions that you're going to ask yourself, and this is the order you're going to ask them every time. If you go out of order, you're going to get confused and you're not going to be able to figure it out. So you're always, always, always going to go in this order. So the first thing you're going to ask yourself is, is the pH normal. Okay. So in Ruby's case, the answer is no. And the pH is decreased, which means that she has and acidemia. The second question is going to be, is the primary disturbance metabolic? Which means something is changing with our bicarbonate or respiratory. Something is going to change with PCO2. So in dogs, if our bicarbonate is less than 20 or our base excess is neg, less than negative four, that indicates that the primary disturbance is metabolic. Conversely, if our PCO2 is increased so our PCO2 is greater than 46, that would suggest that this would be a respiratory disturbance. Okay. So in Ruby's case, she has acidemia, but we can further categorize that by saying that she has a metabolic acidosis. Her bicarbonate is decreased, her base excess is negative. Next, we want to know what is her body doing to try to correct this problem. So is there compensation? And so there are some rules to this. And this can get a little bit complicated if you have a mixed acid base disorder, which I'm not really going to get into, but there are situations where you have abnormalities in both your metabolic and your respiratory system, and then your bicarb and your PCO2 can kind of do whatever they want. But in a classic, straightforward venous gas interpretation, you're looking for compensation. And the rules for that are that your body never over compensates. So you're never going to have a metabolic acidosis that over compensates to an alkalemic pH. And generally speaking, your pH doesn't completely return to normal. So your pH may approach normal, but it's never going to completely return to normal. So primary metabolic disease, your respiratory change is going to be in the opposite direction. So remember that your PCO2 is increased with acidemia and so if you have an increase in your hydrogen ions, a decrease in your pH, you're going to tend to lose your PCO2 to maintain your pH at neutral. So if you're looking at the absolute value of your bicarbonate and your PCO2, they're going to move in the same, same direction for compensation. So a bicarbonate decreases, a PCO2 also decreases. Now, your lungs are really good at this, and so it happens very quickly. So in an animal with an acute primary metabolic problem, the lung compensation, can occur within a couple of minutes. So in in any animal with a metabolic acidosis, we should be assessing this PCO2 to look for a decrease as compensation. Now, just like we said, for metabolic, we have a respiratory change. If we have a primary respiratory problem, our metabolic change is similarly going to be in the opposite direction. So again, our PCO2 and bicarbonate are going to move in the same direction. So if our PCO2 increased, which would suggest a respiratory acidosis and we'll get to this more in a minute, our bicarbonate is similarly going to increase to try to maintain a neutral pH. Now, metabolic compensation takes a while. The kidney takes a minute to actually start to retain bicarbonate. And so it takes 4 to 5 days for that to happen. And that could be really useful when we're trying to figure out how long a problem has been around for. And we'll talk more about that coming up. If we look at this blood gas analysis, we'll see that there is some respiratory compensation occurring. The PCO2 is decreased. So we have a metabolic acidosis with some respiratory compensation. 

Okay. Now, there are some form formulas that you can use that try to predict whether or not that compensation is appropriate. And again, these are values I don't really want you to spend too much time worrying about. But for example, with a metabolic acidosis, we expect that every one mil equivalent per liter of decrease in bicarbonate is going to have a similar point seven millimeters of mercury decrease in our PCO2. So that's how you can figure out, like I was mentioning, a mixed disorder. So that's how you can figure out if the response you're seeing is appropriate or if there might be a mix problem where you have a respiratory and a metabolic disease. And sort of, I would say the classic thing when I think of that, would it be a dog with larpar, for example, that gets really hyperthermic and they have a upper airway obstruction, which we'll talk more about, that causes an increase in carbon dioxide. And then because of the hyperthermia, they have anaerobic cellular metabolism, which decreases their bicarbonate. So sometimes things don't go in the way you expect, but that's kind of a whole other thing. So in Ruby we have a increased or a high anion gap, metabolic acidosis, decreased bicarbonate, decreased pH with respiratory compensation. Our PCO2 has decreased as well. So what we could say in Ruby's case is that this is likely due to lactic acidosis due to hypovolemia and hypotension causing cellular anaerobic respiration. And ultimately she was diagnosed with hypoadrenocorticism. And the good news is that once we start giving her some fluids, we're going to resolve her hypovolemia. We are going to start to resolve her lactic acidosis and her pH will return to the normal range. All right.