So here you go. I'm letting you loose. All right. Here we are. So these are up for your interpretation. We have Jake. He is a two year old male, neutered Great Dane. He is presenting with acute vomiting, unproductive retching and abdominal distension. So we do two things with him. We do some serum chemistries, and here are our results. And so I'll just give you a second to look at those. And we're also going to do a venous blood gas. So here's all venous blood gas. So let's take a look at this and let's use those different one through five that we talked about. This is a venous blood gas. And see if you can come to a conclusion about what type of acid base disturbance this is. 

Okay, so I just popped it over here on the side so that you can look at it while we go through our steps. So what is the pH? We have an acidemia. Okay? So our pH is decreased. So our next question is, is our primary disturbance metabolic or respiratory? So if it was respiratory, we would expect our carbon dioxide to be high. And if it's metabolic, we would expect our bicarb and our base excess to be low. So we're going to say this is a primary metabolic acidosis. Do we, the next question is, do we have any compensation? And the answer is yes. We have a decrease in our PCO2, which means that we have respiratory compensation. Now we can calculate our anion gap by using our sodium, our potassium, our chloride, and our bicarbonate. And if we do that, we'll find that our anion gap is increased at 33, normal being 11 to 26. So that means we have more unmeasured anions in our in our circulation. So we have a high anion gap metabolic acidosis. So the question is why? And this kind of relates to what we just talked about being the most common. I'll give you a clue. So we've got some increased unmeasured anions and most likely they're going to be it's going to be lactate. Our glucose was normal. This is a big dog with two very classic clinical signs, unproductive retching and abdominal distension. So that should make you think of one disease. And it's very common to see an increased lactate in animals with this disease. So we measured Jake's lactate and it was 7.2. Now I would say that I have seen, particularly in animals with chronic dehydration, your lactate level may be normal, even though we're saying it's a lactic acidosis. So there isn't a 1 to 1 correlation with that. But certainly in this case, you know, the fact that the lactate is 7.2 is significant. So we can say that he has a lactic acidosis. But I'm sure as you deducted he had a gastric dilation volvulus causing a high anion gap metabolic acidosis. Okay. 

All right, let's go into case two. This is Jerry. He is a three year old male, neutered domestic shorthair, and he is presenting with straining to urinate and acute collapse. So here are his serum chemistries. Just give you a second to look over those. And here is a venous blood gas. So this is his venous blood gas. So again, we're going to go through those steps that we talked about to figure out what type of acid base disturbance this is. 

All right. So here are the values on the right hand side. So he has severe is azotemia. If we look at his pH now, we'll say that he's acidemic. And so the question is, is this a primary metabolic or respiratory in origin? So if this was metabolic in origin, we would expect a decrease in our bicarb and our base excess. If it was respiratory in origin, we would expect an increase in our CO2. So his bicarb and his base excess are low, which means that this is a primary metabolic origin. So he's got a primary metabolic acidosis. Do we have respiratory compensation? Remember, our PCO2 is going to go down, so our PCO2 is decreased. So, yes, we do have respiratory compensation. And if we calculate our anion gap, we'll find that our anion gap is increased at 34, normal being 12 to 25. He also, as an aside, has severe hyperkalemia and so hopefully you're starting to put things together to come up with a diagnosis with Jerry. So of course, answer the question is why? Well, he definitely has increase in his unmeasured anions, because we know that from his anion gap and we can say most likely lactate due to hypovolemia, but also he has severe is azotemia, so he likely has uremic acids circulating as well. The fact that he is hyperkalemic with azotemia, and remember he has this history of straining to urinate, suggests that he's got a decreased urinary excretion of BUN and creatinine and then also of the potassium. So he has a severe metabolic acidosis with an increased anion gap due to a urinary tract obstruction. So the good news is that we can fix him. If we relieve his urinary tract obstruction, then we should see a marked improvement in his acid base and in his azotemia once he's urinating again and once we're able to give him adequate fluids. 

All right. Let's go on to Georgia. So Georgia is a nine year old female spayed Labrador retriever, and she has a one month history of stridor with a nonproductive cough and most recently, an acute collapse. So this is her arterial blood gas measurement. She's again, She's a big dog, so we were able to get a arterial blood gas on her. All right. And so I just moved it over to the right again. So we know this is an arterial sample, which means that we can assess our oxygenation. But first, we are going to find out whether she has a acid base disturbance. So is her pH normal? The answer is no. Her pH is decreased. So she has an acidemia. Why she acidemic? Well, if we look at our PACO2 remember we would expect for acidemia for our PACO2 to be increased. And for an acidemia, if it was metabolic, we would suggest that our bicarb or our base ex, base excess would be decreased. So if we look at this panel for her, we'll find that her CO2 is increased, which indicates that this is a primary respiratory problem. So she's got a primary respiratory acid acidosis. Is there compensation? Well, our bicarb is increased. So, yes, there is some metabolic compensation. And that gives us a really interesting clue about how long this problem has been going on for this dog. Because remember that our metabolic compensation takes 4 to 5 days. So the fact that we're seeing metabolic compensation, we know that this dog's history has been going on for more than that period of time. She also is hypoxemic. So we can use our AA gradient or 120 rule to figure out whether or not she has hypoventilation or a primary pulmonary dysfunction. So our 120 rule, if we do that, we're going to add our 64 and our 54, which gives us 118, which is pretty much normal. So we're going to say this is normal. If we do our AA gradient, we're going to plug the numbers into our formula, and our AA gradient is just like a smidge high. Like both of these values are just a smidge off. But if you think about pulmonary dysfunction, we would really expect with a PAO2, if it was just pulmonary dysfunction, I would expect a much higher AA gradient and a much lower 120 rule if this was just from pulmonary dysfunction. So the fact that this is very close to 15 means to me that this is almost exclusively a ventilation problem. So she has a chronic respiratory acidemia with metabolic comp, compensation, and she has hypoxemia secondary to an upper airway obstruction. So she was a dog who had laryngeal paralysis. 

All right. We'll talk about Zoe. I think Zoe is our last one. So here we go. She is a 12 year old female female, spayed domestic, long hair cat, and she has a two month history of PUPD, weight loss, acute vomiting and anorexia. So here are her lab values. Just give you a second to look over the those. I know there's a few abnormalities there. All right. And then moving on.  Here is her venous blood gas analysis. Okay, so if we combine all that information on the right here, we can say that she has a significant hyperglycemia, she has a mild azotemia, and now we're going to get on to our blood gas. Her pH is decreased, which means that she has an acidemia. Is it metabolic or is it respiratory? We would expect with metabolic that our base excess and our bicarb would be decreased and we would expect with respiratory that our PCO2 would be increased. So in this situation, our bicarb and our base excess is decreased, which means that this is a primary metabolic disturbance. Then we're going to ask, is there any evidence of respiratory compensation? So our PCO2 is going to go in the same direction. It's going to decrease. And so, yes, we do see respiratory compensation. Then we can say, well, why? And we can look at that acidemia a little bit more and we can say that if we look at our anion gap, it is increased. Normal for a cat is 12 to 25 and her anion gap is 30. So that means that we have an increase in unmeasured anions. Why do we think? Let's look back at the full blood work on this Kitty. Let's look at that blood glucose. And she's a kitty that's had a history of PUPD and now has weight loss, vomiting and anorexia. And so I would say that in her case, most likely she has an increase in her unmeasured anions due to ketoacids. So she would be a diabetic ketoacidotic and also lactate because remember again she's azotemic, so I would be concerned about her perfusion and her circulating blood volume. We did a urine dipstick. She had three plus glucose and three plus ketones. So that supports that she has a metabolic acidosis with a high anion gap due to diabetic ketoacidosis. Okay. And that is our very last slide.